Maximum Decrease In Systolic Blood Pressure Research Articles

Impact of Quantity and Type of Dietary Protein on Cardiovascular Disease Risk Factors Using Standard and Network Meta-analyses of Randomized Controlled Trials.

Higher protein diets (HPDs) have shown favorable outcomes on weight maintenance and body-composition management; however, their protective effects against cardiovascular diseases (CVDs) remain uncertain and contentious. Furthermore, it is important to consider the influence of other macronutrients in the diet and type of dietary protein when studying HPDs, because this aspect has been overlooked in previous studies. We assessed the impacts of quantity and type of dietary protein on CVD risk factors. A database search was conducted in PubMed, Embase, CINAHL, Web of Science, and Cochrane Library and a total of 100 articles met the eligibility criteria. Extracted data from 100 articles were analyzed using standard meta-analysis, and 41 articles were also analyzed using network meta-analysis. In the standard meta-analysis, an HPD had significant favorable effects on systolic blood pressure (SBP) (mean difference [MD] = -1.51 mmHg; 95% CI: -2.77, -0.25), diastolic blood pressure (DBP) (MD = -1.08 mmHg; 95% CI: -1.81, -0.35), and flow-mediated dilation (MD = 0.78%; 95% CI: 0.09, 1.47) compared with lower protein diets. The further network meta-analysis supported that the high-protein, high-carbohydrate, low-fat diet was the most recommended diet to ensure a maximum decrease in SBP, DBP, total cholesterol (TC), and low-density-lipoprotein cholesterol (LDL-C). In comparison to animal-protein-rich diets, plant-protein-rich diets (PPRs) exhibited a significant favorable effects on improving TC (MD = -0.12 mmol/L; 95% CI: -0.19, -0.05), triglyceride (MD = -0.05 mmol/L; 95% CI: -0.09, -0.01), LDL-C (MD = -0.11 mmol/L; 95% CI: -0.18, -0.04), and high-density-lipoprotein cholesterol (MD = 0.03 mmol/L; 95% CI: 0.02, 0.04) levels. Consumption of HPDs and PPRs supports improvements in vascular health and lipid-lipoprotein profiles, respectively. Furthermore, macronutrient composition should be carefully designed in the dietary approach to maximize the effectiveness of HPDs in improving CVD risk factors. PROSPERO registration no. CRD42022369931.

Differences in correlations of depression and anhedonia with cardiovascular sympathetic functions during a head-up tilt test in drug-naïve Parkinson's disease patients.

Depression is a symptom of Parkinson's disease (PD) and may be correlated with cardiovascular sympathetic function. Anhedonia is an element of depression, but these symptoms can emerge independently in PD. A correlation of anhedonia with cardiovascular sympathetic function has rarely been examined. To compare correlations of depression and anhedonia with cardiovascular sympathetic function in drug-naive PD patients. Assessments of depression (Self-rating Depression Scale; SDS), anhedonia (Snaith-Hamilton Pleasure Scale; SHAPS), myocardial 123I-MIBG (123I-meta-iodobenzylguanidine) scintigraphy (heart to mediastinum (H/M) ratios in early and delayed images), and head-up tilt test (HUT) up to 60° for 10min were performed in 45 drug-naïve PD patients. During the HUT, blood pressure was measured every minute and the maximum decrease in systolic blood pressure (SBP) was determined. Plasma noradrenaline (NA) and arginine vasopressin (AVP) levels were examined at baseline and 10min after tilt, with subsequent calculation of increases in plasma NA and AVP levels in this 10min. Correlation coefficients were calculated among these assessment parameters. SDS significantly correlated with % maximum decrease in SBP (r = 0.344, p = 0.02), but not with H/M ratios in both images and increases in plasma NA and AVP levels. SHAPS did not correlate with the change in SBP, H/M ratios in both images, or plasma NA and AVP levels. Depression was correlated with the % maximum decrease in SBP during a 10-min HUT, but anhedonia did not show this relationship. This suggests that depression and anhedonia may have different pathophysiological backgrounds in drug-naïve PD patients.

Effects of exogenous glucagon-like peptide-1 on the blood pressure, heart rate, mesenteric blood flow, and glycemic responses to intraduodenal glucose in healthy older subjects.

Studies relating to the cardiovascular effects of glucagon-like peptide-1 (GLP-1) and its agonists, which slow gastric emptying, have not discriminated between fasting and postprandial, blood pressure (BP) and heart rate (HR). To determine whether exogenous GLP-1 modulates the effects of an intraduodenal (ID) glucose infusion on BP, HR, and splanchnic blood flow in healthy older subjects. A double-blind randomized trial was conducted. Community-dwelling residents attended a clinical research laboratory. Ten healthy "older" subjects (9 male, 1 female; age 73.2 ± 1.5 y) were studied. Intravenous infusion of GLP-1 (0.9 pmol/kg/min), or saline (0.9%) for 90 min (t = -30-60 min). Between t = 0-60 min, ID glucose was infused at 3 kcal/min. BP, HR, superior mesenteric artery (SMA) flow, blood glucose, and serum insulin were measured. During the fasting period (t = -30-0 min), GLP-1 had no effect on BP or HR. In response to ID glucose (t = 0-60 min), systolic BP decreased (P < .001), and both HR (P < .001) and SMA flow (P < .05) increased, on both days. GLP-1 attenuated the maximum decrease in systolic BP (P < .05), tended to increase HR (P = .09), and increased SMA flow (P < .01). GLP-1 diminished the glycemic response (P < .05). In healthy older subjects, acute administration of GLP-1 attenuates the hypotensive response to ID glucose, and potentiates the increase in SMA flow.

Pharmacokinetic–Pharmacodynamic Modeling of the Antihypertensive Effect of Eprosartan in Black and White Hypertensive Patients

It is well recognized that many antihypertensive drugs exhibit large interindividual variability in effect and that this wide range of patient response to antihypertensive drugs is a major problem in achieving blood pressure (BP) control. Variability in both drug concentration and drug effect may cause the heterogeneity in antihypertensive drug response. However, for most antihypertensive drugs, no clear relationship between drug concentration and its effect on BP has been reported. This study aimed to describe the relationship between eprosartan exposure and its effect on the systolic blood pressure (SBP) using population pharmacokinetic-pharmacodynamic modeling. Interindividual variability in pharmacokinetics and pharmacodynamics was quantified and the influence of covariates on this relationship was evaluated. Eprosartan plasma concentrations and SBP measurements were determined in 86 mildly hypertensive patients from the ROTATE study aged 48.1±7.6years with different ethnic backgrounds (33 White Dutch, 41 Creole Surinamese, 12 Hindustani Surinamese). In 12 of these patients, pharmacokinetics were densely sampled and 24-h ambulatory BP measurements were obtained. Data were analyzed using nonlinear mixed effects modeling. Eprosartan concentration-time profiles were adequately described with a two-compartment pharmacokinetic model with zero-order absorption. A log-linear relationship was used to describe the relationship between concentration and the decrease in SBP. A hypothetical effect compartment was used to describe hysteresis in the drug effect. Approximately 80% of the maximum decrease in SBP was observed after 24days. Interindividual variability in drug response was 65% and decreased to 14% when ethnicity was added as covariate. Creole Surinamese exhibited no drug response in contrast to White Dutch and Hindustani Surinamese [-2.6mmHg per (ng/ml)]. The developed pharmacokinetic-pharmacodynamic model allows the quantification and explanation of variability in SBP between individuals with ethnicity as a useful determinant of responsiveness to eprosartan.

Genetic Variations in the α 2A -Adrenoreceptor Are Associated With Blood Pressure Response to the Agonist Dexmedetomidine

α(2A)-Adrenoceptors (α(2A)-ARs) have important roles in sympathetic cardiovascular regulation. Variants of ADRA2A affect gene transcription and expression and are associated with insulin release and risk for type 2 diabetes. We examined whether ADRA2A variants are also associated with cardiovascular responses to the selective α(2)-AR-agonist dexmedetomidine. Seventy-three healthy subjects participated in a placebo-controlled, single-blind study. After 3 infusions of placebo, subjects received 3 incremental infusions of dexmedetomidine (cumulative dose, 0.4 μg/kg). Primary outcomes were changes in systolic blood pressure (SBP) and plasma norepinephrine concentrations, measured as difference of the area-under-the-curve during placebo and dexmedetomidine infusions (ΔAUC). We used multiple linear regression analysis to examine the associations between 9 ADRA2A tagging variants and 5 inferred haplotypes and ΔAUC after adjustment for covariates. Homozygous carriers of rs553668 and the corresponding haplotype 4, previously associated with increased α(2A)-AR expression, had a 2.2-fold greater decrease in AUC(SBP) after dexmedetomidine (adjusted P=0.006); similarly, the maximum decrease in SBP was 24.7±8.1 mm Hg compared with 13.6±5.9 mm Hg in carriers of the wild-type allele (P=0.007). Carriers of haplotype 3, previously associated with reduced α(2A)-AR expression, had a 44% smaller decrease in AUC(SBP) (P=0.013). Haplotype information significantly improved the model predicting the decrease in SBP (P<0.001). There were similar but nonsignificant trends for diastolic blood pressure and heart rate. Genotypes were not significantly associated with norepinephrine responses. Common ADRA2A variants are associated with the hypotensive response to dexmedetomidine. Effects of specific variants/haplotypes in vivo are compatible with their known effects on gene expression in vitro.

Rapid Development of Nitrate Tolerance in Healthy Volunteers

Nitrate tolerance is characterized by a loss of nitroglycerin (NTG) vasodilating and hypotensive effects during continuous administration, but is difficult to detect clinically. We hypothesized that the decrease in arterial blood pressure (BP) and the reflex sympathetic activation and tachycardia due to baroreflex deactivation associated with rapid intravenous (i.v.) infusion of NTG would be decreased during continuous NTG patch therapy as a result of tolerance to transdermal NTG. Sympathetic activation was measured as the change in amplitude of low-frequency (66-129 mHz) oscillations in BP and heart rate (HR) recorded by a noninvasive method. Eleven healthy male volunteers received rapid i.v. infusion of 0.45 mg NTG in 1 min on 3 consecutive days: before NTG patch, after 22.5 h of patch therapy, and 22.5 h after patch removal. The maximum decrease in systolic BP (SBP) and maximum reflex tachycardia as well as the sympathetic activation produced by i.v. NTG were compared during each of the three study periods. The maximum decrease in SBP was 38 +/- 8 mm Hg before NTG patch and 27 +/- 15 mm Hg during NTG patch (p < 0.05), with return to baseline values (37 +/- 13 mm Hg) after patch removal. There was no significant change in amplitude of reflex tachycardia among study periods. However, low-frequency oscillations in SBP increased by 40 +/- 31% in the absence of NTG patch and by only 9 +/- 35% after 22.5 h of patch therapy (p < 0.05). Patch removal resulted in a significant rebound increase in these oscillations (70 +/- 51%; p < 0.05 vs. baseline).(ABSTRACT TRUNCATED AT 250 WORDS)

Rapid Development of Nitrate Tolerance in Healthy Volunteers

Summary: Nitrate tolerance is characterized by a loss of nitroglycerin (NTG) vasodilating and hypotensive effects during continuous administration, but is difficult to detect clinically. We hypothesized that the decrease in arterial blood pressure (BP) and the reflex sympathetic activation and tachycardia due to baroreflex deactivation associated with rapid intravenous (i.v.) infusion of NTG would be decreased during continuous NTG patch therapy as a result of tolerance to transdermal NTG. Sympathetic activation was measured as the change in amplitude of lowfrequency (66-129 mHz) oscillations in BP and heart rate (HR) recorded by a noninvasive method. Eleven healthy male volunteers received rapid i.v. infusion of 0.45 mg NTG in 1 min on 3 consecutive days: before NTG patch, after 22.5 h of patch therapy, and 22.5 h after patch removal. The maximum decrease in systolic BP (SBP) and maximum reflex tachycardia as well as the sympathetic activation produced by i.v. NTG were compared during each of the three study periods. The maximum decrease in SBP was 38 ± 8 mm Hg before NTG patch and 27 ± 15 mm Hg during NTG patch (p < 0.05), with return to baseline values (37 ± 13 mm Hg) after patch removal. There was no significant change in amplitude of reflex tachycardia among study periods. However, low-frequency oscillations in SBP increased by 40 ± 31% in the absence of NTG patch and by only 9 ± 35% after 22.5 h of patch therapy (p < 0.05). Patch removal resulted in a significant rebound increase in these oscillations (70 ± 51%; p < 0.05 vs. baseline). Similar results were noted when sympathetic activation was assessed as the change in lowfrequency oscillations in HR. We conclude that nitrate tolerance develops rapidly and can be assessed by the change in BP and HR oscillations produced by i.v. NTG administration.

Differentiation between renovascular and essential hypertension by means of changes in single kidney 99mTc-DTPA clearance induced by angiotensin-converting enzyme inhibition.

Blood pressure (BP), plasma renin concentration (PRC), and 99mTc-labeled diethylenetriaminepenta acetate (DTPA) renography with determination of single kidney 99mTc-DTPA clearance and parenchymal mean transit time (MTT) were measured in exactly the same way on two consecutive days in 14 patients with renovascular hypertension (RVH), unilateral renal artery stenosis in nine and bilateral stenosis in five, and ten patients with essential hypertension (EH). The examination on day 1 served as a control for day 2 during which captopril (25 mg) was given orally one hour before measurements of PRC and DTPA clearance. Blood pressure was reduced by captopril in both groups, but the maximum decrease in systolic BP was slightly more pronounced (P less than .01) in RVH (22%, median) than EH (13%). Plasma renin concentration increased to a much greater extent (P less than .01) after captopril in RVH (366%) than in EH (46%), Single kidney 99mTc-DTPA clearance was significantly (P less than .01) reduced (-39.5%) and MTT considerably prolonged (170%) on the affected/most affected side in RVH, but both parameters were only slightly changed or unchanged on the unaffected/least affected side (-6.5%, -2% respectively) and were not significantly changed in any of the sides in EH. The degree of renal artery stenosis was significantly correlated to the increase in PRC (rho = -0.786, n = 14 patients, P less than .01), to the reduction in single kidney 99mTc-DTPA clearance (rho = 0.729, n = 19 kidneys, P less than .01) and to the prolongation in MTT (rho = -0.785, n = 16 kidneys, P less than .01). By analysis of the captopril-induced changes in 99mTc-DTPA clearance and MTT, it was possible to predict the existence of a moderate to several renal artery stenosis in arterial hypertension with a very high degree of probability, and the use of changes in 99mTc-DTPA clearance and MTT after angiotensin-converting enzyme (ACE) inhibition may become a valuable tool in differentiation between RVH and EH.