Marked Elevation Of Blood Pressure Research Articles

Abstract P370: Dementia Does Not Increase Mortality in Patients Admitted for Hypertensive Emergency.

Objectives: Hypertensive Emergency is an acute, marked elevation in blood pressure that is associated with signs of target-organ damage. We sought to determine the outcome of hypertensive emergency in patients with dementia. Methods: Using the 2020 National Inpatient Sample Database (NIS), we conducted a retrospective analysis of patients admitted for Hypertensive Emergency as a principal diagnosis according to ICD-10 codes. Our primary outcome was inpatient mortality. Secondary outcomes include acute kidney injury (AKI), cerebrovascular accident (CVA), myocardial infarction (MI), acute hypoxic respiratory failure, length of hospital stays, and hospital charges between groups. (Patient with or without Dementia) Results: A total of 59690 patients were admitted for hypertensive emergency. Of those, 4.3% had a history of dementia. Patients with a history of dementia were older (80 years, 95% CI 79 – 81 VS 59 years, 95% CI 58 – 59). There was no statistically significant difference in inpatient mortality (p=0.1363), acute kidney injury (p=0.7461), cerebrovascular accident (p=0.7712), myocardial infarction (p=0.1517), and acute hypoxic respiratory failure (p=0.3088). Patients with dementia had increased length of hospital stays (6 days, 95% CI 5 – 6 VS 4 days, 95% CI 3 – 4) and total hospital charges ($55,302.18, 95 % CI $49,669.87 - $60,934.5 VS $46,685.84, 95% CI $45,231.38 - $48,140.3) Conclusion: This study shows that there is no difference in in-hospital mortality when comparing patients with dementia and the general population admitted for a hypertensive emergency. Patients with dementia had increased length of hospital stays and charges.

High-Dose Nitroglycerin Bolus and Non-Invasive Ventilation Prevent Intubation or ICU Admission on Hypertensive Emergency and Acute Pulmonary Edema: Sympathetic Crashing Acute Pulmonary Edema (SCAPE) Treatment on STEMI Patient: A Case Report

Highlight: 1. SCAPE could lead to respiratory failure when not treated promptly. 2. High-dose NTG and NIV support can be used as an alternative treatment to overcome hypertensive emergency and pulmonary edema, thus preventing the need for endotracheal intubation and ICU admission. - Background: A marked elevation in blood pressure that causes acute heart failure and fluid accumulation in the lungs is known as sympathetic crashing acute pulmonary edema (SCAPE). Here, we present a SCAPE patient with severe respiratory failure who was successfully treated with high-dose nitroglycerin (NTG) bolus and non-invasive ventilation (NIV). Case summary: A 48-year-old male was referred to our center with typical chest pain and dyspnea. Physical and additional examination found hypertensive emergency (196/66 mmHg), acute pulmonary edema, and acute heart failure, accompanied by anterior STEMI and severe respiratory failure (P/F ratio of 72) in need of intubation. He was given 2 mg intravenous NTG bolus twice supported with NIV, diuretics followed by the primary percutaneous coronary intervention (PCI) stenting in mid left anterior descending (LAD). The patient recovered from acute pulmonary edema, and the P/F ratio improved from 72 to 321 without intubation. Discussion: SCAPE could lead to respiratory failure requiring intubation and intensive care unit (ICU) admission when not treated promptly. The administration of large doses of NTG and NIV was safe and resulted in a speedy improvement in symptoms. Conclusion: SCAPE can be resolved without invasive procedures, using high-dose NTG and NIV support to overcome hypertensive emergency and pulmonary edema.

Fleet Enema-Induced Autonomic Dysreflexia in a Spinal Cord Injured Patient

Background and aim: Autonomic dysreflexia (AD) is an uncommon yet life-threatening and preventable condition. AD classically presents with hypertension, headache, bradycardia, flushing of the face, diaphoresis, malaise, nausea, and blurring of vision. One of the trigger factors is the neurogenic bowel. This clinical report highlights the use of fleet enema in spinal cord injured patients that can cause autonomic response and lead to severe complications. Methods: A 33-year-old man with 3 months post-traumatic Cervical 5 AIS (American Spinal Injury Association) B was admitted for active rehabilitation. Despite the use of tablet Bisacodyl, his neurogenic bowel remains unregulated. Consequently, he was given a fleet enema for bowel programme management and successfully been regulated. On the next bowel day, he presented with sudden onset of blurring of vision and light-headedness after given fleet enema, accompanied by marked elevation of blood pressure, ranging from 130 – 140/ 90 – 100 mmHg (baseline during admission 80 – 90/ 50 – 60 mmHg) with a heart rate 50 – 60 bpm. The condition worsened as 20 minutes later, he developed a sudden generalised tonic-clonic seizure for 10 seconds, which aborted spontaneously. Results: Pre-ictal blood pressure significantly showed a more significant rise in the SBP, up to 40 mmHg. Computed tomography (CT) brain revealed no abnormality. A series of infection markers pre- and post-event showed normal value. However, the result of metabolic level post-event appeared to be higher in phosphate level 1.80 mmol/L, low calcium level 2.0 mmol/L, and borderline high level of sodium 146 mmol/L. Conclusion: This case illustrates the usage of fleet enema can cause AD, as it has been reported that it may irritate the bowel. Hence, a seizure is also a part of AD complications. On top of that, it also led to an electrolytes imbalance which triggered the seizure. Fleet enema, which contains monobasic sodium phosphate, may result in electrolytes imbalances such as hyperphosphataemia, hypernatraemia, and hypocalcaemia. This needs to be highlighted the proper use of fleet enema in neurogenic bowel management.

Transfusion-Associated Circulatory Overload (Taco) Presentations In Pediatric Patients

Abstract Introduction/Objective Limited literature exists regarding Transfusion Associated Circulatory Overload(TACO) in children. Its clinical expressions compared to those in adults remains to be fully explored. We report two TACO cases in children <18 months of age describing their clinical presentations compared to those in older patients. Methods/Case Report Case series Results (if a Case Study enter NA) Case 1: 1.13 kg 18 day old male neonate (27 weeks premature) with anemia requiring hemotherapy(HT). He received 35 ml aliquot of Red Blood Cells(RBCs) which he tolerated well on postoperative day(POD) 1 after bowel surgery. On POD 2, he was transfused RBCs(18 mls). Within 15 minutes of HT initiation, marked elevations in blood pressure(BP) were noted. Workup for a suspected transfusion reaction(STR) was initiated. Blood Bank studies revealed vital sign value(VSV) changes similarly seen in adults with TACO(Transfusion: 52; 2311, 2012). NT-proBNP levels post HT were markedly elevated (8,000 and 64,000 pg/ml).Case 2: 17 month old(11 kg) female with a three weeks prior history of COVID-19 admitted with fever/dehydration and subsequently diagnosed with multisystem inflammatory syndrome in children (MIS-C). Intravenous immunoglobulin(IVIG) infusion ordered and within 20 minutes of starting IVIG, she developed grunting. STR workup showed post HT BP/temperature elevations/chest X-ray with increased interstitial markings. Of note she had also received 1070 ml of intravenous fluids within 48 hours prior to HT. Elevated NT-proBNP levels pre/post HT were measured(17,121 pg/ml and 19, 824 pg/ml respectively). Symptoms improved with diuretics. Conclusion Children experiencing TACO can clinically manifest similarly as in adults with respect to BP elevations and pulmonary changes. Grunting may be an underappreciated manifestation of TACO in pts < 18 months of age. IVIG infusions used in the treatment of patients with MIS-C may present problematic fluid challenges. Recognition of and mitigation strategies for TACO risk factors in such patients may enhance HT safety in this vulnerable patient population.

POSSIBLE ROLE OF THE INVASIVE ARTERIAL BLOOD PRESSURE MEASUREMENT IN SEVERE RESISTANT HYPERTENSION AND GENERALISED ATHEROSCLEROSIS

Objective: In severe resistant hypertension, a generalised atherosclerosis with high arterial stiffness present significant challenge for clinicians to obtain the realistic non-invasive blood pressure measurements and adjust antihypertensive treatment successfully. Design and method: Several patients with generalised atherosclerosis and severe resistant hypertension of the renovascular and renoparenchymal aetiology were referred to our Excellence centre. After performing ambulatory blood pressure monitoring (ABPM) and testing for non-compliance, often we still don’t reach target blood pressure. Due to generally expressed atherosclerosis, daily oscillometer technique could not be reliable in these set of patients. Invasive arterial blood pressure measurements via intra-arterial radial line were recorded for 24-hours and the consecutive non-invasive blood pressure was measured on the ipsilateral arm by oscillatory method. Results: In 3 patients, hypertension was renovascular and renoparenchymal (serum creatinine 134–219 micromol/l, oGF CDK-EPI 47 ml/min). The blood pressure values obtained by oscillatory method ranged from 170/100 mmHg to 230/120 mmHg. Generalised atherosclerosis with obstructive coronary and carotid artery disease, stenosis of iliac arteries, a hemodynamically important renal artery stenosis and subclavian artery stenosis was present in all 3 patients; one had comorbid periaortitis. Two patients were treated with six and one with five antihypertensives in maximum doses, at least one being a diuretic, and with at least one antihypertensive drug exceeding maximum dose. The difference in blood pressure measurements by the invasive vs. non-invasive method ranged from -20/10 mmHg to -50/30 mmHg. In 2 patients, marked blood pressure elevations (+40/20 mmHg) were triggered by elevated sympathycotonus. At discharge, doses of antihypertensive drugs could be lowered or stayed in the same range and a short-acting anxiolytic was added. Conclusions: In patients with severe resistant hypertension and generalised atherosclerosis, after excluding non-adherence, invasive blood pressure technique could be helpful in determining the relative difference to non-invasive measurements and safely adjusting antihypertensive therapy.

Blood Pressure Response During Resistance Training of Different Work-to-Rest Ratio.

Paulo, AC, Tricoli, V, Queiroz, ACC, Laurentino, G, and Forjaz, CLM. Blood pressure response during resistance training of different work-to-rest ratio. J Strength Cond Res 33(2): 399-407, 2019-Changes in the work-to-rest ratio (W:R) of resistance training protocols (RTPs) (i.e., decreasing work or increasing rest) reduce the marked elevation in blood pressure (BP) that occurs during RTP execution. However, whether changes in RTP structure without changing W:R can change BP responses to RTP is unknown. To investigate the effect of different structures of rest intervals and number of repetitions per set on BP response among RTP equated and nonequated for W:R, 20 normotensive participants (25 ± 4 years) performed 4 different RTP of the leg extension exercise with the same work but different W:R structures. Two protocols followed the recommendations for cardiovascular disorders: (a) HIGHW:R-3×15:44s-3×15:44s (set×reps:rest between sets), which has high W:R (45reps:88s) and (b) LOWW:R-3×15:88s-3×15:88s, which has low W:R (45reps:176s). The other 2 protocols were W:R-equated to LOWW:R (45reps:176s): (c) LOWW:R-9×5:22s and (d) LOWW:R-45×1:4s. Systolic BP (ΔSBP) and diastolic BP (ΔDBP) were assessed by finger photoplethysmography. There were significant main effects for ΔSBP after RTP (p ≤ 0.05): HIGHW:R-3×15:44s = LOWW:R-3×15:88s > LOWW:R-45×1:4s > LOWW:R-9×5:22s (+87 ± 5 and +84 ± 5 vs. +61 ± 4 vs. 57 ± 4 mm Hg). For ΔDBP, there was a significant interaction between RTP and moment (p ≤ 0.05). Thus, HIGHW:R-3×15:44 > LOWW:R-3×15:88s > LOWW:R-45×1:4s > LOWW:R-9×5:22s (+53 ± 5 vs. +49 ± 5 vs. +44 ± 4 vs. +38 ± 3 mm Hg). HIGHW:R-3×15:44s produced the highest increase in ΔDBP, and LOWW:R-9×5:22s produced the lowest increase in ΔSBP and ΔDBP. Our findings may help the development of RTP protocols that may mitigate pressure peaks without changing important exercise variables (i.e., volume or duration).

Beneficial Effects of Different Flavonoids on Vascular and Renal Function in L-NAME Hypertensive Rats.

Background: we have evaluated the antihypertensive effect of several flavonoid extracts in a rat model of arterial hypertension caused by chronic administration (6 weeks) of the nitric oxide synthesis inhibitor, L-NAME. Methods: Sprague Dawley rats received L-NAME alone or L-NAME plus flavonoid-rich vegetal extracts (Lemon, Grapefruit + Bitter Orange, and Cocoa) or purified flavonoids (Apigenin and Diosmin) for 6 weeks. Results: L-NAME treatment resulted in a marked elevation of blood pressure, and treatment with Apigenin, Lemon Extract, and Grapefruit + Bitter Orange extracts significantly reduced the elevated blood pressure of these animals. Apigenin and some of these flavonoids also ameliorated nitric oxide-dependent and -independent aortic vasodilation and elevated nitrite urinary excretion. End-organ abnormalities such as cardiac infarcts, hyaline arteriopathy and fibrinoid necrosis in coronary arteries and aorta were improved by these treatments, reducing the end-organ vascular damage. Conclusions: the flavonoids included in this study, specially apigenin, may be used as functional food ingredients with potential therapeutic benefit in arterial hypertension.

Smooth Muscle PPARγ Mutation Causes Salt‐sensitive Hypertension

Systemic loss of peroxisome proliferator‐activated receptor‐γ (PPARγ) function causes hypertension, whereas its activation lowers blood pressure largely via PPARγ activity in the vasculature. We have recently shown that loss of PPARγ in smooth muscle cells increases mesenteric myogenic tone, promotes vascular remodeling, and predisposes to deoxycorticosterone acetate (DOCA)‐salt‐induced hypertension in mice. However, it is unclear whether these effects were attributable to altered salt sensitivity. In this study, we examined the role of smooth muscle PPARγ in regulating renal function and salt‐sensitivity. Transgenic mice expressing dominant negative PPARγ in smooth muscle cells (S‐P467L) and non‐transgenic littermates (NT) were fed normal chow diet (containing 0.3% salt) or a 4% salt diet for a total of 8 weeks and metabolic cage studies were performed at baseline, 3 weeks, 6 weeks, and at the end of the protocol. S‐P467L and NT mice had similar food intake, feces weight, and weight gain on high salt diet throughout the study. While 24‐hour water intake tripled in both strains (6.3 ± 0.21 mL S‐P467L vs. 5.9 ± 0.40 mL NT, n=7) when they were switched to high salt diet from normal chow, S‐P467L mice excreted 32% less urine in the third week (24‐hour urine 1.96 ± 0.13 mL S‐ P467L vs. 2.90 ± 0.17 mL NT, two‐way ANOVA p<0.01). In order to assess renal function, mice were subjected to a bolus i.p. injection of normal saline equal to 10% of their body weight and the urine volume excreted in the subsequent 4 hours were plotted as a percentage of saline injected. We observed a marked decline in their capacity to excrete this volume challenge in S‐ P467L mice (28.2 ± 2.1% S‐P467L vs. 39.9 ± 5.1% NT, p<0.05) in the third week of high salt diet. Because nitric oxide (NO) is known to regulate sodium and water balance, we determined daily renal NO production as indicated by 24‐hour urinary nitrate/nitrite. Three‐week dietary salt induced a 4‐fold increase in urinary NO metabolites in NT mice, but this was blunted in S‐P467L mice (2.82 ± 0.19 μmoL/24 hours S‐P467L vs. 4.42 ± 0.27 μmoL/24 hours NT, p<0.01). In parallel with these renal phenotypes, S‐P467L mice developed marked elevation of blood pressure that peaked in the third week of high salt feeding (telemetry systolic pressure 136.4 ± 3.4 mmHg S‐P467L vs. 124.2 ± 2.4 mmHg NT, p<0.01) and remained elevated throughout the study. At the end of 8 weeks, vascular function was assessed in freshly isolated carotid and basilar arteries, and flow cytometry analysis was performed in single cell suspensions of aorta and kidney tissues. S‐P467L mice, but not NT littermates, exhibited severe impairment of acetylcholine‐ and sodium nitroprusside‐induced vascular relaxation in the carotid and basilar arteries in response to high salt. CD45+ total leukocytes, CD3+ T cells, CD4+/CD8+ T cell subsets, and F4/80+ monocytes/macrophages were not altered in the aortas but were paradoxically reduced in the kidneys of S‐P467L mice in response to high salt. These data indicate that loss of PPARγ in smooth muscle cells predispose to impaired vascular relaxation, renal dysfunction, and salt‐sensitive hypertension. This study highlights the significance of vascular PPARγ in regulating systemic physiological responses.Support or Funding InformationNIH and AHA Grants

Neurological disorders in hypertensive patients

Hypertension is one of the most common vascular diseases. The brain as target organs in hypertension is damaged more often and earlier. Neurological complications due to hypertension are frequently hyperdiagnosed in Russian neurological practice. Thus, headache, dizziness, impaired recall of recent events, nocturnal sleep disorders, and many other complaints in a hypertensive patient are usually regarded as a manifestation of dyscirculatory encephalopathy. At the same time headaches (tension headache and migraine) in hypertensive patients are predominantly primary; headache associated with dramatic marked elevations in blood pressure is encountered in only a small number of patients. The role of cerebrovascular diseases in the development of dizziness in hypertensive patients is also overestimated. The vast majority of cases, patients with this complaint are in fact identified to have benign paroxysmal postural vertigo, Mеniеre’s disease, vestibular neuronitis, or vestibular migraine. Psychogenic disorders or multisensory insufficiency are generally responsible for non-systemic vertigo in hypertensive patients. Chronic cerebral circulatory insufficiency may cause non-systemic vertigo as a subjective equivalent of postural instability. Cognitive impairments (CIs) are the most common and earliest manifestation of cerebrovascular lesion in hypertension. In most cases, CIs in hypertension were vascular and associated with cerebrovascular lesion due to lacunar infarcts and leukoaraiosis. However, mixed CIs frequently occur when hypertensive patients are also found to have signs of a degenerative disease, most commonly in Alzheimer’s disease.

Prevention of Hypertensive Crises in Rats Induced by Acute and Chronic Norepinephrine Excess

Calcium Channel Blockers (CCBs), competitive α-adrenoceptor blockers, and phenoxybenzamine (POB) are used for preoperative treatment of pheochromocytomas. We analyzed the protection from hypertensive crisis provided by these drugs during acute and chronic norepinephrine excess. To ensure adaptive changes during chronic norepinephrine (NE) excess, we continuously exposed male Wistar rats to NE for 3 weeks (osmotic pumps). Afterwards, blood pressure (BP) was continuously measured while NE boli (0-1000 μg/kg, i. v.) were administered before and after antihypertensive treatment in anesthetized and catheterized rats. A single dose of urapidil (10 mg/kg), nitrendipine (600 μg/kg) and POB (10 mg/kg) lowered BP from 212 ± 12 mmHg by 52 ± 7%, 31 ± 9%, and 50 ± 6%, respectively. With NE boli a maximum BP of 235 ± 29, 240 ± 30 and 138 ± 3 mmHg was measured in urapidil, nitrendipine, and POB treated animals (p<0.05). The number of hypertensive episodes (delta BP >30 mmHg) was 3 (3), 1.5 (0-3), and 0 (0-1) (p<0.05). Because of inferiority, urapidil was excluded from further testing. Chronically NE exposed rats were treated with POB (10 mg/kg/d), nifedipine (10 mg/kg/d), or vehicle for 7 days. Marked BP elevations were observed at baseline (167 ± 7, 210 ± 7 , and 217 ± 7 mmHg, p<0.01) and maximum blood pressure was 220 ± 32, 282 ± 26, and 268 ± 40 mmHg (p<0.001) with NE boli. Further stabilization was achieved combining POB pretreatment with a continuous nifedipine infusion, which effectively prevented BP elevations during NE excess. POB was the most effective drug used in monotherapy, but BP stabilization was superior using a combination of POB pretreatment with a continuous nifedipine infusion in this model.

Mice Overexpressing Both Human Angiotensinogen and Human Renin as a Model of Superimposed Preeclampsia on Chronic Hypertension

Preeclampsia is the major cause of maternal and fetal mortality/morbidity. Because hypertension is an important risk factor for preeclampsia, we investigated whether hypertensive mice that overexpress human renin and angiotensinogen develop superimposed preeclampsia. Given that the mechanisms underlying this disease are still poorly understood, animal models are of great use for elucidation. Blood pressure and proteinuria were measured by telemetry and ELISA, respectively. Heart function was evaluated by echocardiography, whereas pathological cardiac hypertrophy-related genes were assessed by real-time PCR. Soluble fms-like tyrosine kinase 1 plasma concentrations were quantitated by ELISA and placental expression by real-time PCR. Transgenic mice develop de novo proteinuria during gestation and marked blood pressure elevation, which are hallmarks of superimposed preeclampsia on chronic hypertension. Abnormal placentation present in these mothers produced a significant decrease in pup and placental weight and was associated with an increased placental expression of soluble fms-like tyrosine kinase 1. We also found heightened circulating levels of this receptor, when adjusted for placental mass, as has been observed in women who suffer from preeclampsia. Cardiac hypertrophy could be observed in the transgenic mice and was exacerbated by gestation. As a result, heart function was significantly decreased, and markers of pathological hypertrophy were increased. Our data, thus, confirm the characterization of a new model of superimposed preeclampsia on chronic hypertension. Because chronically hypertensive women are at risk of developing the pathology, our model reflects a clinical reality and is, thus, an excellent tool to elucidate the molecular mechanisms triggering this disease.

Diagnosis of pheochromocytoma in the setting of Parkinson disease

A 59-year-old man with a 7-year history of Parkinson disease (PD) presented with episodes of sudden, severe headaches with neck pain, tachycardia, sweating and pallor. During these episodes, the patient showed marked elevations in blood pressure, regardless of posture. This was unusual, given that he had no prior history of hypertension. The array of symptoms raised suspicions of pheochromocytoma, but diagnosis was challenging, as the standard diagnostic biochemical tests were confounded by dopaminergic medications. Further work-up revealed left adrenal medullary hyperplasia. Several reports exist of pseudopheochromocytoma in patients on dopaminergic therapy, but this is the first documented case of pheochromocytoma syndrome due to adrenal medullary hyperplasia in a patient with PD. This case highlights the challenges of performing a diagnostic work-up in a PD patient with symptoms suggestive of pheochromocytoma, and illustrates the utility of (123)I-metaiodobenzylguanidine ((123)I-MIBG) single-photon emission CT in making a diagnosis.Investigations. Physical examination, laboratory tests, abdominal MRI scan, abdominal (123)I-MIBG scan, abdominal (18)F-fluorodeoxyglucose PET scan. Pheochromocytoma syndrome due to adrenal medullary hyperplasia.Management. Surgical excision of the left adrenal gland.

Parsing Risk for the Use of Selective Serotonin Reuptake Inhibitors in Pregnancy

Parsing Risk for the Use of Selective Serotonin Reuptake Inhibitors in Pregnancy

Treatment of hypertension in acute ischemic stroke

Blood pressure fluctuation early in the course of ischemic stroke is a proven independent predictor of morbidity and mortality. Both high and low systolic blood pressures have a detrimental effect on the neurologic outcome. Current guidelines support permissive hypertension in the early course of acute ischemic stroke. For patients with marked elevation in blood pressure, a reasonable goal would be to lower blood pressure by 15% during the first 24 hours after onset of stroke. The level of blood pressure that would mandate such treatment is not known, but consensus exists that medications should be withheld unless the systolic blood pressure is greater than 220 mm Hg or the diastolic blood pressure is greater than 120 mm Hg. For patients undergoing intravenous thrombolysis for acute ischemic stroke, it is recommended that the blood pressure be reduced and maintained below 185 mm Hg systolic for the first 24 hours. The first-line drugs for lowering of blood pressure remain labetalol, nicardipine, and sodium nitroprusside. These recommendations are based on consensus rather than evidence, however. Comorbid conditions such as myocardial infarction, left ventricular failure, aortic dissection, preeclampsia, or eclampsia would override the guidelines for permissive hypertension; a lower blood pressure would be preferred in these conditions. Children with acute strokes should be managed in the same way as adults, with extrapolated lowering of blood pressures, until further evidence emerges. Current research focuses on both hemodynamic augmentation of low blood pressures and the effects of further lowering the blood pressure after acute ischemic stroke. Until more definitive data are available, a cautious approach to the treatment of arterial hypertension is generally recommended.

Cardiorespiratory and cerebrovascular responses to hyperoxic and hypoxic rebreathing: Effects of acclimatization to high altitude

We examined the cardiorespiratory and cerebrovascular responses to hyperoxic and hypoxic rebreathing at low attitude and high altitude. We measured ventilation, middle cerebral artery blood flow velocity (MCAv) and arterial blood pressure in conditions of eucapnia, hypocapnia (voluntary hyperventilation) and during hyperoxic and hypoxic rebreathing firstly at low altitude (1400 m) then again at high altitude (3840 m) in five individuals, following 9 days at altitude >5000 m. High altitude was associated with elevations in the blood pressure response to hyperoxic rebreathing, whilst cerebrovascular reactivity was reduced and ventilatory sensitivity was unchanged. During hypoxic rebreathing, whilst ventilatory and blood pressure reactivity were increased (vs. low altitude and hyperoxic rebreathing), cerebrovascular reactivity was preserved. In conclusion, at high altitude there was an enhancement in peripheral but not central chemosensitivity to CO(2); and during hypoxic rebreathing, marked elevations in blood pressure may restore some of the reduction in cerebrovascular CO(2) reactivity, potentially reflecting a pressure-passive relationship in the brain offsetting sympathetic-induced cerebral vasoconstriction.

Oxidative Stress Causes Renal Dopamine D1 Receptor Dysfunction and Salt-Sensitive Hypertension in Sprague-Dawley Rats

Renal dopamine plays an important role in maintaining sodium homeostasis and blood pressure (BP) during increased sodium intake. The present study was carried out to determine whether renal dopamine D1 receptor (D1R) dysfunction contributes to increase in salt sensitivity during oxidative stress. Male Sprague-Dawley rats, divided into various groups, received tap water (vehicle); 1% NaCl (high salt [HS]); L-buthionine sulfoximine (BSO), an oxidant; and HS plus BSO with or without Tempol, an antioxidant, for 12 days. Compared with vehicle, HS intake increased urinary dopamine production and decreased basal renal Na/K-ATPase activity but did not affect BP. BSO-treated rats exhibited oxidative stress and a mild increase in BP. In these rats, D1R expression and G protein coupling were reduced, and SKF38393, a D1R agonist, failed to inhibit Na/K-ATPase activity and promote sodium excretion. Concomitant administration of BSO and HS caused oxidative stress, D1R dysfunction, and a marked increase in BP. Although renal dopamine production was increased, it failed to reduce the basal Na/K-ATPase activity in these animals. Treatment of BSO plus HS rats with Tempol decreased oxidative stress and restored endogenous, as well as exogenous, D1R agonist-mediated Na/K-ATPase inhibition and normalized BP. In conclusion, during HS intake, the increased dopamine production via Na/K-ATPase inhibition prevents an increase in BP. During oxidative stress, D1R function is defective, and there is mild hypertension. However, in the presence of oxidative stress, HS intake causes marked elevation in BP, which results from a defective renal D1R function leading to the failure of dopamine to inhibit Na/K-ATPase and promote sodium excretion.

Effects of short-term and subchronic lead poisoning on nitric oxide methabolites and vascular responsiveness in rat

Chronic exposure to low levels of lead results in sustained hypertension in humans and experimental animals. The mechanism of lead-induced hypertension remains unclear. We investigated the short-term (4 and 8 weeks) and subchronic (12 weeks) effects of lead treatment on responsiveness of vascular adrenergic system and level of nitric oxide metabolites, that is, total nitrates and nitrites (NOx). Male Sprague–Dawley rats were treated with lead acetate (100 ppm in drinking water) for 12 weeks. Short-term lead administration resulted in marked elevation of blood pressure accompanied by significant reduction in serum NOx levels. In contrast, after subchronic lead administration the trend of decrease in NOx levels somehow reversed despite further increase in blood pressure. Both short-term and subchronic lead administration resulted in significant differences in vascular reactivity with respect to either vasoconstrictor (phenylephrine and clonidine) or vasodilator (isoproterenol) agents. We conclude that vascular adrenergic system and nitric oxide pathway change in short-term and subchronic phases of lead poisoning.

Effects of angiotensin-converting-enzyme inhibitors in combination with diuretics on blood pressure and renal injury in nitricoxide-deficiency-induced hypertension in rats

The present study investigates the effects of chronic administration of ACEIs (angiotensin-converting-enzyme inhibitors; either zofenopril or enalapril) in combination with a diruetic (hydrochlorothiazide) on BP (blood pressure) increase and renal injury induced by L-NAME (NG-nitro-L-arginine methyl ester), an inhibitor of NO (nitric oxide) synthesis. Rats were untreated or received L-NAME alone, L-NAME+zofenopril+hydrochlorothiazide or L-NAME+enalapril+hydrochlorothiazide for 8 weeks. L-NAME treatment resulted in marked elevation in BP and mortality. Treatment with either ACEI and diuretic prevented the increase in BP induced by L-NAME, reduced the death rate and improved excretory parameters. Renal injury in the L-NAME group was severe, but, in the groups treated with either ACEI and diuretic, glomerular and tubulointerstitial lesions were not observed and the intensity, number and size of vessels affected was reduced. However, the efficacy of zofenopril+diuretic was superior to that of enalapril+diuretic in reducing vascular alterations. Oxidative stress indices and the expression of NO synthase and nitrotyrosine were normalized by the treatments. In conclusion, the combined treatment of zofenopril or enalapril with hydrochlorothiazide completely prevented the development of arterial hypertension induced by L-NAME. Renal morphological and functional alterations in the hypertensive animals were also almost completely normalized, but the treatment with zofenopril+diuretic produced a more complete organ protection. The protective effect is related to an activation of endothelial NO synthase expression and to a normalization of the oxidative stress parameters due to the inhibition of angiotensin II.

Cardiac tamponade associated with an elevated arterial blood pressure

A 30-year-old male presented with acute pericarditis and a moderate pericardial effusion. His condition deteriorated suddenly with a marked elevation in blood pressure. The hypertension was erroneously correlated with a low probability of cardiac tamponade, leading to a delay in performing an echocardiogram. The echocardiogram subsequently showed features of cardiac tamponade. Severe elevation of blood pressure in a patient with cardiac tamponade is a rare and under-recognized disorder. This condition is discussed here.

What Causes the Acute Blood Pressure Elevation After Stroke?

To the Editor: In an insightful editorial1 to a recently published paper by Mattle et al,2 Lindsberg raises a central question as to why blood pressure increases in the acute phase of stroke. The Cushing reflex is suggested as a possible mechanism because it results in sympathetic nervous system activation; however, this reflex is typically described as occurring in the face of raised intracranial tension.3 The purpose of this letter is to suggest that the central nervous system (CNS) ischemic response may be responsible for the marked sympathoexcitation leading to marked blood pressure elevation in acute stroke. This reflex leads to marked activation of the sympathetic nervous system …