Impaired Blood Pressure Research Articles

Blood Pressure Non-Dipping and Obstructive Sleep Apnea Syndrome: A Meta-Analysis.

Aim: We examined the reduced blood pressure (BP) nocturnal fall in patients with obstructive sleep apnea (OSA) by a meta-analysis including studies that provided data on prevalence rates of non-dipping (ND) pattern during 24-h ambulatory blood pressure monitoring (ABPM). Design: The PubMed, OVID-MEDLINE, and Cochrane CENTRAL literature databases were searched for appropriate articles without temporal restriction up to April 2019 through focused and sensitive search methods. Studies were identified by crossing the search terms as follows: “obstructive sleep apnea”, “sleep quality”, “non dipping”, “reduced nocturnal BP fall”, “circadian BP variation”, “night-time BP”, and “ambulatory blood pressure monitoring”. Results: Meta-analysis included 1562 patients with OSA from different clinical settings and 957 non-OSA controls from 14 studies. ND pattern prevalence in patients with OSA widely varied among studies (36.0–90.0%). This was also the case for non-OSA controls (33.0% to 69.0%). Overall, the ND pattern, assessed as an event rate in the pooled OSA population, was 59.1% (confidence interval (CI): 52.0–65.0%). Meta-analysis of the seven studies comparing the prevalence of ND pattern in participants with OSA and controls showed that OSA entails a significantly increased risk of ND (Odds ratio (OR) = 1.47, CI: 1.07–1.89, p < 0.01). After the exclusion of patients with mild OSA, OR increased to 1.67 (CI: 1.21–2.28, p < 0.001). Conclusions: The present meta-analysis, extending previous information on the relationship between OSA and impaired BP dipping, based on single studies, suggests that this condition increases by approximately 1.5 times the likelihood of ND, which is a pattern associated with a greater cardiovascular risk than normal BP dipping.

Abstract P139: Cytochrome B5 Reductase 3 Biases Activation of Soluble Guanylyl Cyclase in Resistance Arteries

Soluble guanylyl cyclase (sGC) heme oxidation (Fe 3+ ) leading to apo-sGC formation diminishes the ability of nitric oxide (NO) to bind sGC and generate intracellular cGMP levels needed for downstream protein kinase G activation and vessel relaxation. While several studies suggest that pathological oxidative stress drives sGC heme oxidation and apo-sGC formation, we report for the first time that resistance arteries, but not conduit arteries, contain a previously unrecognized pool of heme oxidized and/or apo-sGC in non-stressed conditions that can be activated independent of NO. Specifically, our vascular reactivity studies indicate that systemic resistance and pulmonary arteries are responsive to NO-independent sGC activator BAY 58-2667 at 2-3 log-fold lower concentrations than that of conduit aorta and renal arteries (n=4-5/ vascular bed). Further, mesenteric arteries treated with 1μM MitoTempol, a superoxide dismutase mimetic and mitochondrial anti-oxidant, show a decreased responsiveness to BAY 58-2667 (n=3-5/group). Notably, we have published evidence that cytochrome b5 reductase 3 (CYB5R3) acts as an sGC heme reductase (Fe 3+ -&gt; Fe 2+ ) in cultured vascular smooth muscle cells. We recently performed vasoreactivity studies in transgenic CYB5R3 overexpression (OE CYB5R3) mice and show these mice have a significantly decreased responsiveness to BAY 58-2667 compared to controls irrespective of vascular bed (n=4-6/ group). Additionally, OE CYB5R3 mice exhibit a ~7mmHg decrease in pulse pressure and impaired blood pressure reduction in response to an acute injection of BAY 58-2667 as compared to controls (n=5/ group). Combined, these data indicate that mitochondria derived-reactive oxygen species and expression of CYB5R3 serve as a rheostat for modulating sensitivity to sGC activator BAY 58-2667 and vascular responsiveness in resistance arteries. Importantly, these results provide valuable insight into sGC activator therapy for treatment of hypertension and other cardiovascular related diseases.

Abstract P2063: Isolated Noradrenergic Failure Due Tocongenital Cyb561 Deficiency

CYB561 generates ascorbic acid, a cofactor for the function of dopamine-beta-hydroxylase (DBH), the enzyme that converts dopamine to norepinephrine. We report a novel genetic defect in the CYB561 gene and provide the clinical characteristics of CYB561 deficiency. We evaluated 4 patients referred for life-long disabling orthostatic hypotension and performed whole genome sequencing of the CYB561 gene. Patients had disabling orthostatic hypotension (OH) since infancy and impaired blood pressure response to the Valsalva maneuver (VM) with exaggerated phase 2 hypotension and absence of phase 2 late recovery and phase 4 blood pressure overshoot consistent with sympathetic failure. Heart rate ratio to sinus arrhythmia and the VM, however, were normal. Plasma norepinephrine and metabolites were undetectable, and plasma dopamine and metabolites were normal. Droxidopa restored norepinephrine and improved orthostatic hypotension. Patients 1 and 2 were sisters and were homozygous for a nonsense mutation in Exon 2, c.131G&gt;A, p.Trp44 (Circ Res 2018). Their brother (patient 3) died at age 16 and his DNA was not available. Patient 4 was compound heterozygous; one allele had a mutation in Exon 2, c157C&gt;T, p.His.53Tyr, and the other had an Exon 2 deletion. In conclusion, CYB561 deficiency is characterized by isolated sympathetic noradrenergic failure with disabling orthostatic hypotension since infancy, but with normal sympathetic cholinergic (sweating) and parasympathetic (heart rate regulation) functions. The genetic defect differed between patients; we report a novel case of CYB561 deficiency due to compound heterozygosity, with a gene deletion in one allele, and a missense mutation in the other. These patients highlight the critical role of CYB561 in sympathetic function and cardiovascular regulation.

Impaired orthostatic blood pressure stabilization and reduced hemoglobin in chronic kidney disease.

Impaired orthostatic blood pressure (BP) stabilization is prevalent in patients with chronic kidney disease (CKD) and is associated with adverse outcomes. We aimed to test the hypothesis that reduced hemoglobin is an important contributor to orthostatic intolerance in CKD in the present study. This study included 262 patients with non-dialysis-dependent CKD. Seated and standing BP was measured, and orthostatic BP reduction was calculated for both systolic BP (∆ SBP) and diastolic BP (∆ DBP). The association between orthostatic BP reduction and hemoglobin was determined by multiple linear regression models. We also performed mediation analysis to test to what extent the effect of renal dysfunction on impaired orthostatic BP stabilization can be explained by reduced hemoglobin. The mean age of the patients was 57.7 (±14.5)years, and 61.5% were male. Both ∆ SBP and ∆ DBP correlated negatively with estimated glomerular filtration rate (eGFR). With adjustment for age and sex, hemoglobin level was negatively associated with ∆ SBP (β=-1.4, SE=0.4, P<.001) and ∆ DBP (β=-0.6, SE=0.2, P=.009). The associations remained significant with further adjustment for additional covariates. When eGFR was introduced as a covariate, it did not eliminate the significance (both P<.05). The associations remained essentially unchanged in a sensitivity analysis excluding those with concurrent erythropoietin use. Mediation analysis demonstrated that reduced hemoglobin accounted for 35.4% (P=.004) of the effect of eGFR on ∆ SBP and 47.7% (P=.032) on ∆ DBP. Our study suggests that reduced hemoglobin is a potentially important contributor to the development of orthostatic hypotension in CKD.

BLOOD PRESSURE PROFILE, CATECHOLAMINE PHENOTYPE AND TARGET ORGAN DAMAGE IN PHEOCHROMOCYTOMA/PARAGANGLIOMA

Objective: Impaired diurnal blood pressure (BP) variability is related to higher cardiovascular risk. The aim of the study was to assess diurnal variability of BP and its relation to target organ damage (TOD) and catecholamine phenotype in a consecutive sample of pheochromocytoma/paraganglioma (PPGL). Design and method: We included 179 patients with PPGL (96 females). All patients underwent 24 h ambulatory blood pressure monitoring (SpaceLabs 90207) to determine dipping status. Differences in plasma metanephrine or urine adrenaline were used to distinguish catecholamine biochemical phenotype. To evaluate TOD, renal functions, presence of left ventricle hypertrophy (LVH) and, in the subgroup (N = 111) carotid-femoral PWV, were assessed. Structural equation modelling was used to find the relationship among nocturnal dipping, catecholamine phenotype and TOD parameters. Results: According to the nocturnal dipping, patients were divided into the three groups –dippers (28%), non-dippers (40%) and reverse dippers (32%). Reverse dippers were older (P < 0.05), with a higher proportion of noradrenergic phenotype (P < 0.05), a higher prevalence of diabetes mellitus (P < 0.05), sustained arterial hypertension (P < 0.01) and its duration (P < 0.05) as opposed to the other groups. All parameters of TOD were more pronounced only in reverse dippers, in comparison with non-dippers and dippers. The presence of noradrenergic biochemical phenotype (=absence of adrenaline production) was associated with reverse dipping and TOD (LVH and PWV). Conclusions: Only patients with reverse dipping had more significant TOD compared to other groups. The noradrenergic biochemical phenotype plays an important role not only in impaired diurnal BP variability, but also, independently from dipping status, in more pronounced TOD of heart and vessels. Supported by the Ministry of Health of the Czech Republic, grant no. 16–30345A.

NOCTURNAL BLOOD PRESSURE DROP IN PATIENTS WITH RECENT ON SET OF DIABETES MELLITUS TYPE 2 AND ITS ASSOCIATION WITH MICROVASCULAR CORONARY PERFUSION

Objective:Abolishment of the normal circadian blood pressure (BP) pattern is frequently observed in patients with diabetes mellitus (DM) and has been associated with autonomic neuropathy and vascular dysfunction. However, it remains unclear whether impaired BP dipping is observed concordantly with D

Is Aberrant Reno-Renal Reflex Control of Blood Pressure a Contributor to Chronic Intermittent Hypoxia-Induced Hypertension?

Renal sensory nerves are important in the regulation of body fluid and electrolyte homeostasis, and blood pressure. Activation of renal mechanoreceptor afferents triggers a negative feedback reno-renal reflex that leads to the inhibition of sympathetic nervous outflow. Conversely, activation of renal chemoreceptor afferents elicits reflex sympathoexcitation. Dysregulation of reno-renal reflexes by suppression of the inhibitory reflex and/or activation of the excitatory reflex impairs blood pressure control, predisposing to hypertension. Obstructive sleep apnoea syndrome (OSAS) is causally related to hypertension. Renal denervation in patients with OSAS or in experimental models of chronic intermittent hypoxia (CIH), a cardinal feature of OSAS due to recurrent apnoeas (pauses in breathing), results in a decrease in circulating norepinephrine levels and attenuation of hypertension. The mechanism of the beneficial effect of renal denervation on blood pressure control in models of CIH and OSAS is not fully understood, since renal denervation interrupts renal afferent signaling to the brain and sympathetic efferent signals to the kidneys. Herein, we consider the currently proposed mechanisms involved in the development of hypertension in CIH disease models with a focus on oxidative and inflammatory mediators in the kidneys and their potential influence on renal afferent control of blood pressure, with wider consideration of the evidence available from a variety of hypertension models. We draw focus to the potential contribution of aberrant renal afferent signaling in the development, maintenance and progression of high blood pressure, which may have relevance to CIH-induced hypertension.

Blood Pressure Profile, Catecholamine Phenotype, and Target Organ Damage in Pheochromocytoma/Paraganglioma.

Impaired diurnal blood pressure (BP) variability is related to higher cardiovascular risk. To assess diurnal variability of BP and its relation to target organ damage (TOD) and catecholamine phenotype in a consecutive sample of pheochromocytoma/paraganglioma (PPGL). We included 179 patients with PPGL All patients underwent 24 hours of ambulatory BP monitoring to determine dipping status. Differences in plasma metanephrine or urine adrenaline were used to distinguish catecholamine biochemical phenotype. To evaluate TOD, renal functions, presence of left ventricle hypertrophy (LVH), and the subgroup (n = 111) carotid-femoral pulse wave velocity (PWV) were assessed. Structural equation modeling was used to find the relationship among nocturnal dipping, catecholamine phenotype, and TOD parameters. According to the nocturnal dipping, patients were divided into the three groups: dippers (28%), nondippers (40%), and reverse dippers (32%). Reverse dippers were older (P < 0.05), with a higher proportion of noradrenergic (NA) phenotype (P < 0.05), a higher prevalence of diabetes mellitus (P < 0.05), and sustained arterial hypertension (P < 0.01) and its duration (P < 0.05), as opposed to the other groups. All parameters of TOD were more pronounced only in reverse dippers compared with nondippers and dippers. The presence of NA phenotype (=absence of adrenaline production) was associated with reverse dipping and TOD (LVH and PWV). Patients with reverse dipping had more substantial TOD compared with other groups. The NA phenotype plays an important role, not only in impaired diurnal BP variability but also independently from dipping status in more pronounced TOD of heart and vessels.

Impact of analgesics on macro‐ and microcirculatory responses to hemorrhage

BACKGROUNDPeripheral vasoconstriction in responseto hemorrhage is critical for blood pressure compensation and vital organperfusion. Opiates and ketamine have been demonstrated to have direct vasoactive effects, but effects on peripheral vasoconstriction response to hemorrhage are unknown for these analgesics. We hypothesize that opioid(fentanyl) impairs blood pressure compensation following hemorrhage due toblunted peripheral vasoconstriction, while ketamine preserves pressure compensation and vasoconstriction.METHODSprague Dawley rats(11–13wk) were randomly assigned to saline (control), fentanyl, or ketamine‐treated groups (n = 9 for each group). Rats were anesthetized within actin and the spinotrapezius muscles were prepared for microcirculatory observation. The arcade arterioles were topically challenged with saline, fentanyl, or ketamine at concentrations relevant to analgesic doses and vascular responses were recorded. After procedurally‐challenged arteriolar diameters returned to baseline, 30% of total blood volumes were removed during a 25 min period. Ten minutes after hemorrhage, rats were treated with a single intravenous(IV) injection of an analgesic dose of fentanyl or ketamine or a comparable volume of saline. Blood pressure, respiratory rate, and arteriolar responses were recorded throughout the experiment.RESULTSBaseline parameters were not different among groups (Table 1). Topical fentanyl induced vasodilation (17 ± 2%, p &lt; 0.01)but ketamine caused vasoconstriction (−15 ± 4%; p &lt; 0.01). IV ketamine and fentanyl failed to affect blood pressure compensation compared with the control group (Figure A). Neither saline nor ketamine altered respiratory rate. However, IV fentanyl induced a prolonged suppression in respiratory rate (&gt;10 minutes, with a peak inhibition at 57 ± 8% of baseline, Figure B). A persistent and similar arteriolar constriction to hemorrhage was observed in the control and ketamine treated groups. However, this compensatory vasoconstriction was absent in the fentanyl‐treated group, which instead exhibited continuous vasodilation (peak change 42 ± 10% of baseline immediately after injection, p &lt;0.01, Figure C). While no mortality occurred with IV saline or ketamine, fentanyl caused an 18% mortality.CONCLUSIONThese results indicate that ketamine preserves, but fentanyl impairs, respiration and peripheral vasoconstrictor response to hemorrhage, although minor effects on initial compensation of systemic hemodynamics appear to be similar. The study suggests that microcirculatory responses may be more sensitive than systemichemo dynamics to predict outcomes during pain management following hemorrhage.Support or Funding InformationThis study was funded by the US Army Medical and Materiel Command, Clinical and Rehabilitative Medicine Research Program.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Spinal Cord Disruption Is Associated with a Loss of Cushing-Like Blood Pressure Interactions.

The capacity of the cerebrovasculature to buffer changes in blood pressure (BP) likely plays an important role in the prevention of stroke, which is three- to fourfold more common after spinal cord injury (SCI). Although the directional relationship between BP and cerebral blood flow (CBF) has traditionally been thought to travel solely from BP to CBF, a Cushing-like mechanism functioning in the inverse direction, in which changes in CBF influence BP, has recently been revealed using Granger causality analysis. Although both CBF buffering of BP and the Cushing-like mechanism are influenced by the sympathetic nervous system, we do not understand the impact of disruption of descending sympathetic pathways within the spinal cord, caused by cervical SCI on these regulatory systems. We hypothesized that people with cervical SCI would have greater BP to CBF transmission, as well as a reduced Cushing-like mechanism. The directional relationships between mean arterial BP (MAP; Finometer® PRO) and middle cerebral artery blood velocity (MCAv; transcranial Doppler) were assessed at rest in 14 cervical SCI subjects and 16 uninjured individuals using Granger causality analysis, while also accounting for end-tidal CO2 tension. Those with SCI exhibited 66% increased forward MAP→MCAv information transmission as compared with the uninjured group (p = 0.0003), indicating reduced cerebrovascular buffering of BP, and did not have a predominant backward Cushing-like MCAv→MAP phenotype. These results indicate that both forward and backward communication between BP and CBF are influenced by SCI, which may be associated with impaired cerebrovascular BP buffering after SCI as well as widespread BP instability.

Pharmacological Review on Uricosuric activity

The naturally available uricosuric agents are Tinospora cardifolia, Allium sepa, Cajanus Cajan, Piper nigrum etc., Natural medicinal plants having no side effects are more preferred when compared to synthetic medications. Uricosuric agents increase the urinary excretion of uric acid hence the natural uricosuric agent is preferred to prevent many diseases like gout, arthritis, kidney stones etc., without side effect. Uricosuric medications are the substances that increase the excretion of uric acid in urine, thus reducing the concentration of uric acid in blood plasma. Prolonged and untreated hyperuricemia results into gout, a severe inflammatory condition. Sustain hyperuricemia leads to impaired blood pressure control, renal impairment and nephropathy. The common factors for deposition of uric acid in blood are drinking alcohol and taking high purine diet. The various screening methods for the uricosuric activity are uricosuric activity in mice, Potassium oxonate induced activity, and Phenol red excretion methods are explained in this review.

Impaired nocturnal blood pressure dipping in patients with type 2 diabetes mellitus.

Hypertension is a common comorbidity of type 2 diabetes mellitus (T2DM). Both conditions are associated with an increased cardiovascular risk, which is reduced by tight blood pressure (BP) and glycemic control. However, nondipping BP status continues to be an enduring cardiovascular risk factor in T2DM. Cardiovascular autonomic neuropathy and endothelial dysfunction have been proposed as potential mechanisms. This study tested the hypothesis that microvascular disease rather than cardiovascular autonomic neuropathy interferes with the physiological nocturnal BP reduction. Cardiovascular autonomic function and baroreflex sensitivity were determined in 22 type 2 diabetic patients with (DM+) and 23 diabetic patients without (DM-) manifest microvascular disease. BP dipping status was assessed from 24-hour ambulatory BP measurements. Sixteen nondiabetic subjects served as controls (CTRL). Cardiovascular autonomic function was normal in all subjects. Baroreflex sensitivity was lower in DM- compared with CTRL (7.7 ± 3.3 vs. 12.3 ± 8.3 ms·mm Hg-1; P < 0.05) and was further reduced in DM + (4.6 ± 2.0 ms·mm Hg-1; P < 0.01 vs. DM- and CTRL). The nocturnal decline in systolic and diastolic BP was blunted in DM- (12% and 14% vs. 17% and 19% in CTRL; P < 0.05) and even more so in DM+ (8% and 11%; P < 0.05 vs. DM- and P < 0.001 vs. CTRL). A nocturnal reduction in pulse pressure was observed in CTRL and DM- but not in DM+ (P < 0.05 vs. DM- and P < 0.01 vs. CTRL). In T2DM, progression of microvascular disease interferes with the normal nocturnal BP decline and coincides with a persistently increased pulse pressure and reduced baroreflex sensitivity, contributing to their increased cardiovascular risk.

A14339 Impaired systolic blood pressure recovery after standing is associated with arterial stiffening and baroreceptor dysfunction in patients with life-style related disease

Objectives: To investigate whether arterial stiffening and baroreceptor dysfunction is associated with impaired blood pressure recovery after standing, which is considered to be a severe condition of orthostatic hypotension (OH). Methods: A total of 1056 patients with life-style related disease were included in the study. During the sit-to-stand test (consist of sitting position, 30 seconds [initial phase] and 90 seconds [late phase] after standing up), we measured blood pressure and heart rate variability (HRV) as an index of baroreceptor function (LF and HF: low and high frequency component). The patients were divided into 4 groups according to the response of orthostatic systolic blood pressure (SBP) change (Non-OH: SBP change > -20 both in the initial and the late phase, late-OH: SBP change ≤ -20 only in the late phase, initial-OH: SBP change ≤ -20 only in the initial phase, sustained-OH: SBP change ≤ -20 both in the initial and the late phase). We measured cardio-ankle vascular index (CAVI) as an index of arterial stiffness. Results: Mean age of the patients was 66.5 ± 11.9 years. Initial-OH and sustained-OH showed significant higher CAVI compared with non-OH (9.03 ± 1.25 versus 8.65 ± 1.48, p = 0.024; 9.35 ± 1.17 versus 8.65 ± 1.48, p = 0.010, respectively). Sustained-OH showed significant lower LF than non-OH both in the initial and the late phase (2.10 ± 0.50 versus 2.31 ± 0.44, p = 0.008; 1.67 ± 0.52 versus 1.95 ± 0.53, p = 0.005, respectively). Sustained-OH showed significant lower HF than non-OH in the late phase (1.39 ± 0.60 versus 1.68 ± 0.58, p = 0.005). Conclusion: Impaired SBP recovery after standing was associated with arterial stiffening and blunted autonomic nervous response. Patients with impaired SBP recovery after standing should be aware of severe arterial stiffening and baroreceptor dysfunction.

Does Obstructive Sleep Apnea Influence Blood Pressure and Arterial Stiffness in Response to Antihypertensive Treatment?

Untreated obstructive sleep apnea (OSA) is common in patients with hypertension and may impair blood pressure (BP) and target-organ damage responses to antihypertensive therapy. In this study, we recruited hypertensive patients who underwent treatment with a 30-day regimen of hydrochlorothiazide 25 mg plus enalapril (20 mg BID) or losartan (50 mg BID) and were assessed with a baseline clinical evaluation, polysomnography, 24-hour ambulatory BP monitoring, and carotid-femoral pulse wave velocity. All the examinations except for polysomnography were repeated at 6 and 18 months of follow-up. We studied 94 hypertensive patients (mean age, 55±9 years). The frequency of OSA was 55%. Compared with baseline, we did not observe significant differences between groups in 24-hour BP, daytime systolic and diastolic BPs, or night-time systolic BP at 6 and 18 months. The BP control rate at 24 hours (<130/80 mm Hg) was similar between the groups (baseline, 42.3% versus 45.2%; 6 months, 46.9% versus 57.5%; 18 months, 66.7% versus 61.5%). However, patients with OSA had higher night-time diastolic BP decrease than did the non-OSA group (6 months, -4.9±11.8 versus -0.3±10.3 mm Hg; 18 months, -6.7±11.1 versus -1.2±10.6 mm Hg; P=0.027). There were no differences in the number and class of antihypertensive medications prescribed during follow-up. In terms of arterial stiffness, patients with OSA had higher pulse wave velocity than did patients without OSA at baseline (10.3±1.9 versus 9.2±1.7 m/s; P=0.024), but both groups had similar decreases in pulse wave velocity during follow-up. In conclusion, with combined antihypertensive treatment aimed at controlling BP, hypertensive patients with OSA had similar 24-hour BP and arterial stiffness to those without OSA.

Cardiovascular Responses During Resistance Exercise in Patients With Parkinson Disease

BackgroundPatients with Parkinson disease (PD) present cardiovascular autonomic dysfunction that impairs blood pressure control. However, cardiovascular responses during resistance exercise are unknown in these patients. ObjectiveTo investigate cardiovascular responses during resistance exercise performed with different muscle masses in patients with PD. DesignProspective, repeated-measures. SettingExercise Hemodynamic Laboratory, School of Physical Education and Sport, University of São Paulo. ParticipantsThirteen patients with PD (4 women, 62.7 ± 1.3 years, stages 2-3 of the modified Hoehn and Yahr scale; “on” state of medication) and 13 paired control patients without PD (7 women, 66.2 ± 2.0 years). InterventionsBoth groups performed, in a random order, bilateral and unilateral knee extension exercises (2 sets, 10-12 maximal repetition, 2-minute intervals). Main Outcome MeasurementsSystolic blood pressure (SBP) and heart rate (HR) were assessed before (pre) and during the exercises. ResultsIndependent of set and exercise type, SBP and HR increases were significantly lower in PD than the control group (combined values: +45 ± 2 versus +73 ± 4 mm Hg and +18 ± 1 versus +31 ± 2 bpm, P = .003 and .007, respectively). Independently of group and set, the SBP increase was greater in the bilateral than the unilateral exercise (combined values: +63 ± 4 versus +54 ± 3 mm Hg, P = .002), whereas the HR increase was similar. In addition, independently of group and exercise type, the SBP increase was greater in the second than the first set (combined values: +56 ± 4 versus +61 ± 4 mm Hg, P = .04), whereas the HR increases were similar. ConclusionsPatients with PD present attenuated increases in SBP and HR during resistance exercise in comparison with healthy subjects. These results support that resistance exercise is safe and well tolerated for patients with PD from a cardiovascular point of view supporting its recommendation for this population. Level of EvidenceII

Impairments in Hemodynamic Responses to Orthostasis Associated with Frailty: Results from The Irish Longitudinal Study on Ageing (TILDA).

To characterize the relationships between orthostatic blood pressure (BP) and heart rate recovery and frailty in an older population. Cross-sectional study. Two health centers in the Republic of Ireland. The Irish Longitudinal Study on Ageing participants aged 50 and older (N=4,334). Continuous noninvasive BP responses during active standing were captured using digital photoplethysmography. Frailty was assessed using the Cardiovascular Health Study criteria. Linear mixed models (random intercept) with piecewise splines were used to model differences in rate of BP and heart rate recovery. Ninety-three (2.2%) participants were frail, and 1,366 (31.5%) were prefrail. Adjusting for age and sex, frailty was associated with a slower rate of systolic BP recovery 10 to 20 seconds after standing (frailty by time = -4.12, 95% confidence interval=-5.53 to -2.72) and with subsequent deficits in BP 20 to 50 seconds after standing. Similar results were seen for diastolic BP and heart rate. Further adjustment for health behaviors, morbidities, and medications reduced, but did not attenuate, these associations. Of the 5 frailty criteria, only slow gait speed was consistently related to impaired BP and heart rate responses in the full model. Frailty, particularly slow gait speed, was associated with slower rate of BP and heart rate recovery after active standing. Impaired BP recovery may be a marker of physiological frailty.

Abstract P334: The Effects of Inadequate Sleep on Blood Pressure and Endothelial Inflammation in Women: Findings From the American Heart Association Go Red for Women Strategically Focused Research Network

Background: Insufficient sleep impairs blood pressure regulation. However, the effects of milder, highly prevalent but frequently neglected sleep disturbances, including poor sleep quality and insomnia, on vascular health in women are unclear. We investigated whether poor sleep patterns are associated with blood pressure and endothelial inflammation in a diverse sample of women. Methods: Women who participated in the ongoing AHA Go Red for Women Strategically Focused Research Network population project were studied (n=323, 57% minority, mean age=39 + 17 y, range=20-79 y). Sleep duration, sleep quality, and time to sleep onset were assessed using the Pittsburgh Sleep Quality Index (score &gt; 5=poor sleep quality). Risk for obstructive sleep apnea (OSA) was evaluated using the Berlin questionnaire, and insomnia was assessed using the Insomnia Severity Index (ISI). In a subset of women who participated in the basic study (n=28), sleep duration was assessed objectively using actigraphy and endothelial inflammation was assessed directly in harvested endothelial cells by measuring nuclear translocation of nuclear factor kappa B (NFκB). Vascular reactivity was measured by brachial artery flow-mediated dilation (FMD). Systolic and diastolic blood pressure (SBP and DPB) were measured by trained personnel. Multivariate linear regressions were used to evaluate associations between sleep patterns and blood pressure, NFκB and FMD. Results: Mean sleep duration was 6.8 ± 1.3 h/night in the population study and 7.5 ± 1.1 h/night in the basic study. In the population study sample, 50% had poor sleep quality (25% in the basic study), and 37% had some level of insomnia (15% in the basic study). SBP was associated directly with poor sleep quality, and DBP with OSA risk after adjusting for confounders (p=0.04 and p=0.08, respectively). Poor sleep quality was associated with endothelial NFκB activation (β=30.6; p=0.03). Insomnia and longer time to sleep onset were also associated with endothelial NFκB activation (β=27.6; p=0.002 and β=8.26; p=0.02, respectively). Sleep patterns were not associated with FMD. Conclusions: These findings provide direct evidence that common but frequently neglected sleep disturbances such as poor sleep quality and insomnia are associated with increased blood pressure and vascular inflammation even in the absence of sleep deprivation in women.

Physical Exercise-Induced Cardiovascular and Thermoregulatory Adjustments Are Impaired in Rats Subjected to Cutaneous Artery Denervation.

This study aimed to investigate the chronic effects of caudal artery denervation on morphometric parameters of the tail vascular smooth muscle and on physical exercise-induced thermoregulatory and cardiovascular adjustments in rats. Male Wistar rats were subjected to caudal artery denervation or the sham procedure. Approximately 26–28 days after these procedures, their thermoregulatory and cardiovascular parameters were evaluated at rest and during or following a fatiguing treadmill run. At the end of the experiments, the rats were euthanized, and samples of their tails were removed to evaluate morphometric parameters of the vascular smooth muscle surrounding the caudal artery. Denervated rats showed morphological adaptations, including increased arterial wall thickness and wall-to-lumen ratios. In resting rats and following the fatiguing exercise, caudal artery denervation barely affected the thermoregulatory and cardiovascular parameters evaluated. By contrast, caudal artery denervation attenuated the increase in tail skin temperature, decreased the spontaneous baroreflex sensitivity, and exacerbated the increases in mean arterial pressure in exercising rats. The increased wall-to-lumen ratio of denervated rats correlated negatively with the maximum tail skin temperature attained or cutaneous heat loss sensitivity but correlated positively with the maximum diastolic blood pressure attained during exercise. In conclusion, cutaneous denervation induces vascular remodeling characterized by morphological adaptations of the tail vascular smooth muscle. This vascular remodeling likely underlies the impaired tail heat loss and blood pressure adjustments in denervated rats subjected to physical exercise. Therefore, we have highlighted the importance of cutaneous vascular innervation integrity in thermal and cardiovascular control in stress-challenged rats. In this sense, our findings advance the understanding of thermoregulatory and cardiovascular system reactions after a sustained cutaneous vascular innervation injury, which is essential for the treatment of some diseases, such as Parkinson's disease and type 1 and type 2 diabetes mellitus.

Poor sleep is responsible for the impaired nocturnal blood pressure dipping in elderly hypertensive: A cross-sectional study of elderly

ABSTRACTObjective: This study was aimed to assess whether sleep disorder was associated with an increased risk of less nocturnal blood pressure (BP) dipping in elderly patients with hypertension.Methods: Cases were 1006 patients, aged >60 years, who were admitted to hospital with diagnosed hypertension during 2016–2017, and were divided into three groups with the systolic nocturnal BP dipping of 10%, and 0% as the cut-off value. The patients’ sleep was evaluated by Pittsburgh sleep quality index (PSQI).Results: Compared to non-dipper BP rhythm patients (n = 382) and dipper BP rhythm patients (n = 132), reverse dipper patients (n = 492) exhibited higher PSQI score and had higher scores on six components with the exception of use sleep drug (p < 0.05). Multivariate logistic regression indicated that poor sleep, which was defined as high score of PSQI or its seven components, was associated with prevalence of reverse dipper in elderly hypertensive (odds ratio (OR) = 1.17, (95% confidence interval (CI), 1.13–1.21, p < 0.05) after adjusting for risk factors of hypertension. Multiple linear regression analysis showed that there was a significant negative correlation between PSQI score (include its seven components) and nocturnal BP dipping value after adjusting for risk factors of hypertension (β = −0.584, p < 0.001).Conclusions: In elderly patients with hypertension, poor sleep quality individuals were more prone to reverse dipper BP rhythm. Even adjusting for the effect of known risk factors of hypertension, poor sleep may contribute to attenuated BP dipping in elderly hypertensive.

Recovery of the cardiac autonomic nervous and vascular system after maximal cardiopulmonary exercise testing in recreational athletes.

The body's adaptation to physical exercise is modulated by sympathetic and parasympathetic (vagal) branches of the autonomic nervous system (ANS). Heart rate variability (HRV), the beat-to-beat variation of the heart, is a proxy measure for ANS activity, whereas blood pressure (BP) is an indicator for cardiovascular function. Impaired vagal activity and lower BP is already described after exercise. However, inconsistent results exist about how long vagal recovery takes and how long post-exercise hypotension persists. Therefore, the aim of this study was to assess HRV and BP 1h after maximal cardiopulmonary exercise testing (CPET). HRV (Polar RS800CX), peripheral and central BP (Mobil-O-Graph®) were prospectively studied in 107 healthy volunteers (47 female, median age 29.0years) in supine position, before and 60min after maximal CPET. One hour after terminating CPET measures of HRV were still impaired and post-exercise BP was significantly reduced suggesting an improved vascular function compared to pre levels. HRV parameters post-exercise were 34.7% (RMSSD), 67.2% (pNN50), 57.2% (HF), and 42.7% (LF) lower compared to pre-exercise levels (for all p < 0.001). Median reduction in BP was 5mmHg for systolic BP (p < 0.001), and 4mmHg for diastolic BP (p = 0.016) and central systolic post-exercise (p = 0.005). One hour after terminating strenuous exercise, autonomic nervous regulation seems to be postponed which is reflected in reduced HRV, whereas the early recovery of the vasculature, post-exercise hypotension, is still preserved over the recovery period of 1 h.