scholarly journals Effects of Experimental Sleep Restriction on Ambulatory and Sleep Blood Pressure in Healthy Young Adults: A Randomized Crossover Study

Hypertension ◽  
2021 ◽  
Author(s):  
Naima Covassin ◽  
Jan Bukartyk ◽  
Prachi Singh ◽  
Andrew D. Calvin ◽  
Erik K. St Louis ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Weight Maintenance ◽  
Cardiovascular Effects ◽  
Sleep Time ◽  
Sleep Restriction ◽  
Plasma Norepinephrine ◽  
Post Hoc ◽  
Persistent Elevation ◽  
Randomized Crossover Study ◽  
Cardiovascular Biomarkers

Although insufficient sleep is associated with increased cardiovascular risk, evidence of a causal relationship is lacking. We investigated the effects of prolonged sleep restriction on 24-hour ambulatory blood pressure (BP) and other cardiovascular measures in 20 healthy young participants (aged 23.4±4.8 years, 9 females), who underwent a randomized, controlled, crossover, 16-day inpatient study consisting of 4 days of acclimation, 9 days of sleep restriction (4 hours of sleep/night) or control sleep (9 hours), and 3 days of recovery. Subjects consumed a weight maintenance diet with controlled nutrient composition throughout. A 24-hour BP (primary outcome) and cardiovascular biomarkers were measured repeatedly. Polysomnographic monitoring was continuous. Comparing sleep restriction versus control sleep, 24-hour mean BP was higher (adjusted mean difference, day 12: 2.1 mm Hg [95% CI, 0.6–3.6], corrected P =0.016), endothelial function was attenuated ( P <0.001), and plasma norepinephrine increased ( P =0.011). Despite increased deep sleep, BP was elevated while asleep during sleep restriction and recovery. Post hoc analysis revealed that 24-hour BP, wakefulness, and sleep BP increased during experimental and recovery phases of sleep restriction only in women, in whom 24-hour and sleep systolic BP increased by 8.0 (5.1–10.8) and 11.3 (5.9–16.7) mm Hg, respectively (both P <0.001). Shortened sleep causes persistent elevation in 24-hour and sleep-time BP. Pressor effects are evident despite closely controlled food intake and weight, suggesting that they are primarily driven by the shortened sleep duration. BP increases are especially striking and sustained in women, possibly suggesting lack of adaptation to sleep loss and thus greater vulnerability to its adverse cardiovascular effects.

Cardiovascular and neuroendocrine responses to baroreceptor denervation in baboons

1990 ◽  
Vol 258 (4) ◽  
pp. R930-R938 ◽  
Author(s):  
R. E. Shade ◽  
V. S. Bishop ◽  
J. R. Haywood ◽  
C. K. Hamm
Keyword(s):  
Blood Pressure ◽  
Aortic Arch ◽  
Carotid Sinus ◽  
Cardiovascular Effects ◽  
Plasma Renin ◽  
Plasma Norepinephrine ◽  
Arterial Blood ◽  
Bilateral Carotid ◽  
Vasopressin Secretion ◽  
Blood Pressure Responses

The purpose of this study was to describe the hormonal and blood pressure responses to partial (carotid sinus) and complete (carotid sinus + aortic arch) baroreceptor denervation in baboons. Experiments were performed in eight adult male baboons maintained on a tether system for the continuous measurement of mean arterial blood pressure (MAP) and heart rate (HR). Bilateral carotid sinus denervation (CSD) immediately increased MAP from 83 +/- 2.2 to 124 +/- 7.3 mmHg. MAP gradually decreased over the next 14 days to intact levels. There were also transient decreases in HR variability and increases in blood pressure variability after CSD. Subsequent denervation of the aortic arch to produce sinoaortic denervation (SAD) resulted in another abrupt large increase in MAP followed by a small but significant increase in MAP of 11 mmHg that was maintained for up to 4 wk after SAD. The short-term variability of HR and blood pressure was chronically decreased and increased, respectively, after SAD. Plasma renin activity, vasopressin, and epinephrine were not changed from intact levels either after CSD or SAD. Plasma norepinephrine was only transiently increased by CSD and chronically elevated by 72% over intact levels after SAD. Thus CSD in the baboon does not produce a sustained increase in MAP. SAD chronically increases MAP and is associated with evidence for an increased sympathetic tone. There is no indication that either increased renin secretion or vasopressin secretion contributes to the chronic cardiovascular effects of SAD in baboons.

Mechanisms involved in central cardiovascular effects of prostaglandin F2 alpha

1982 ◽  
Vol 242 (5) ◽  
pp. R545-R551 ◽  
Author(s):  
G. Feuerstein ◽  
C. J. Helke ◽  
R. L. Zerbe ◽  
D. M. Jacobowitz ◽  
I. J. Kopin
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Rectal Temperature ◽  
Cardiovascular Effects ◽  
Plasma Norepinephrine ◽  
Central Administration ◽  
Prostaglandin F2 Alpha ◽  
Arterial Blood ◽  
Norepinephrine Concentration ◽  
Bilateral Vagotomy

Prostaglandin F2 alpha (PGF2 alpha) injected into the cerebroventricular system (icv) of halothane-anesthetized rats increased the arterial blood pressure, heart rate, and rectal temperature. These effects were accompanied by a preferential increase in plasma norepinephrine concentration. Plasma levels of epinephrine, renin, and vasopressin were not changed in the PGF2 alpha-icv-treated rats. Bilateral vagotomy did not affect the PGF2 alpha-induced hypertension and tachycardia nor was there any change in the selective increase in plasma norepinephrine concentration. Hexamethonium pretreatment suppressed, in a dose-response manner, the increases in blood pressure, heart rate, and rectal temperature in response to PGF2 alpha-icv. Plasma norepinephrine and epinephrine levels were not altered by PGF2 alpha-icv in hexamethonium-treated rats, but plasma vasopressin concentration was markedly elevated in all hexamethonium-infused rats. These results suggest that selective central activation of the sympathetic nervous system underlies the profound cardiovascular and temperature responses elicited by central administration of PGF2 alpha.

scholarly journals Increased superoxide levels in ganglia and sympathoexcitation are involved in sarafotoxin 6c-induced hypertension

2008 ◽  
Vol 295 (5) ◽  
pp. R1546-R1554 ◽  
Author(s):  
Melissa Li ◽  
Xiaoling Dai ◽  
Stephanie Watts ◽  
David Kreulen ◽  
Gregory Fink
Keyword(s):  
Blood Pressure ◽  
Sympathetic Innervation ◽  
Sympathetic Ganglia ◽  
Plasma Norepinephrine ◽  
Sprague Dawley ◽  
Surgical Ablation ◽  
Arterial Blood ◽  
Sprague Dawley Rats ◽  
Induced Hypertension ◽  
Hypertension Development

Endothelin (ET) type B receptors (ETBR) are expressed in multiple tissues and perform different functions depending on their location. ETBR mediate endothelium-dependent vasodilation, clearance of circulating ET, and diuretic effects; all of these should produce a fall in arterial blood pressure. However, we recently showed that chronic activation of ETBR in rats with the selective agonist sarafotoxin 6c (S6c) causes sustained hypertension. We have proposed that one mechanism of this effect is constriction of capacitance vessels. The current study was performed to determine whether S6c hypertension is caused by increased generation of reactive oxygen species (ROS) and/or activation of the sympathetic nervous system. The model used was continuous 5-day infusion of S6c into male Sprague-Dawley rats. No changes in superoxide anion levels in arteries and veins were found in hypertensive S6c-treated rats. However, superoxide levels were increased in sympathetic ganglia from S6c-treated rats. In addition, superoxide levels in ganglia increased progressively the longer the animals received S6c. Treatment with the antioxidant tempol impaired S6c-induced hypertension and decreased superoxide levels in ganglia. Acute ganglion blockade lowered blood pressure more in S6c-treated rats than in vehicle-treated rats. Although plasma norepinephrine levels were not increased in S6c hypertension, surgical ablation of the celiac ganglion plexus, which provides most of the sympathetic innervation to the splanchnic organs, significantly attenuated hypertension development. The results suggest that S6c-induced hypertension is partially mediated by sympathoexcitation to the splanchnic organs driven by increased oxidative stress in prevertebral sympathetic ganglia.

High disease activity is associated with higher blood pressure in recent onset rheumatoid arthritis patients, post-hoc analyses of IMPROVED study

2021 ◽  
Vol 28 (Supplement_1) ◽  
Author(s):  
M Gegenava ◽  
SA Bergstra ◽  
H Maassen ◽  
CF Allaart
Keyword(s):  
Rheumatoid Arthritis ◽  
Blood Pressure ◽  
Disease Activity ◽  
Classification Criteria ◽  
Recent Onset ◽  
American College Of Rheumatology ◽  
Cardiovascular Morbidity And Mortality ◽  
The Difference ◽  
Post Hoc ◽  
Acpa Status

Abstract Funding Acknowledgements Type of funding sources: None. Background Rheumatoid arthritis (RA) is a chronic autoimmune disease with a high prevalence of cardiovascular morbidity and mortality. Purpose: purpose of our project was to investigate the association between disease activity and systolic and diastolic blood pressure (SBP, DBP) in patients with recent-onset rheumatoid arthritis (RA 2010 criteria) or undifferentiated arthritis (UA) who were treated to target disease activity score (DAS)&lt;1.6 in the IMPROVED study. Methods: The associations between disease activity and SBP/DBP were tested for 610 patients (364 RA, 246 UA), cross-sectionally and over time. GEE analyses were performed with both SBP and DBP as outcome measures and disease activity categories (DAS&lt;1.6;&gt;1.6 but ≤2.4; &gt;2.4), CRP level, treatment arms or the number of visits on a certain drug as potential predictors in separate analyses. Separate analyses tested potential contributions of gender, anti-cyclic citrullinated peptide antibodies (ACPA) status, and fulfilling the 2010 ACR/EULAR (American college of rheumatology/ European league against rheumatism) classification criteria. In addition association of BP with various levels of disease activity was tested with T-test. Results: At the baseline mean (SD) SBP was 133 (20) and DBP mean (SD) was 80 (10).  SBP &gt; 140mm Hg was observed in 40% of patients and DBP &gt; 90 mm Hg  in 21% of patients. SBP and DBP statistically significantly decreased during 5 years follow up (mainly during year 1), but the difference in mm Hg was small. Estimates from GEE analysis showed that patients with high DAS &gt;2.4 (HDAS) had a statistically significantly higher SBP (average 3 mm Hg higher, 95% CI 1.7; 4.2, p &lt; 0.01), than the patients in with DAS ≤2.4. ANOVA analyses showed a statistically significant association between SBP and DAS. In addition, post hoc analyses showed that patients with HDAS had a statistically significantly higher  SBP (mean (SD) 132 (19) than the patients with DAS &lt; 1.6 (remission) (mean (SD) 129 (20), p &lt; 0.01), and patients in LDAS but DAS≥1.6 had a statistically significantly higher SBP (mean (SD) 131 (19) than the patients in remission (mean (SD)  129 (20), p = 0.02) (Figure 1), whereas no association was found between DAS category and DBP. Gender, ACPA status or fulfilling the 2010 classification criteria did not influence the relation between DAS and blood pressure. Conclusions: In patients with RA or UA, a higher DAS is associated with higher blood pressure, but the clinical impact is unclear. Abstract Figure 1

Long term habitual vigorous physical activity is associated with lower visit-to-visit systolic blood pressure variability

2020 ◽  
Author(s):  
Xiaoyong Xu ◽  
Xianghong Meng ◽  
Shin-ichi Oka
Keyword(s):  
Physical Activity ◽  
Blood Pressure ◽  
Standard Deviation ◽  
Systolic Blood Pressure ◽  
Blood Pressure Variability ◽  
Vigorous Physical Activity ◽  
Systolic Blood Pressure Variability ◽  
Average Real Variability ◽  
Post Hoc

Abstract Objective Our work aimed to investigate the association between vigorous physical activity and visit-to-visit systolic blood pressure variability (BPV). Methods We conducted a post hoc analysis of SPRINT (Systolic Blood Pressure Intervention Trial), a well-characterized cohort of participants randomized to intensive (&lt;120 mmHg) or standard (&lt;140 mmHg) SBP targets. We assessed whether patients with hypertension who habitually engage in vigorous physical activity would have lower visit-to-visit systolic BPV compared with those who do not engage in vigorous physical activity. Visit-to-visit systolic BPV was calculated by standard deviation (SD), average real variability (ARV), and standard deviation independent of the mean (SDIM) using measurements taken during the 1-, 2-, 3-, 6-, 9- and 12-month study visits. A medical history questionnaire assessed vigorous physical activity, which was divided into three categories according to the frequency of vigorous physical activity. Results A total of 7571 participants were eligible for analysis (34.8% female, mean age 67.9±9.3 years). During a follow-up of 1-year, vigorous physical activity could significantly reduce SD, ARV, and SDIM across increasing frequency of vigorous physical activity. There were negative linear trends between frequency of vigorous physical activity and visit-to-visit systolic BPV. Conclusions Long-term engagement in vigorous physical activity was associated with lower visit-to-visit systolic BPV.

Effect of chronic left ventricular failure on beta-endorphin

1992 ◽  
Vol 73 (6) ◽  
pp. 2675-2680 ◽  
Author(s):  
E. Mellow ◽  
E. Redei ◽  
K. Marzo ◽  
J. R. Wilson
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Chronic Heart Failure ◽  
Left Ventricular ◽  
Plasma Norepinephrine ◽  
Endogenous Opiates ◽  
Beta Endorphin ◽  
Arterial Blood ◽  
Norepinephrine Concentration ◽  
C 30

Stimulation of endogenous opiate secretion worsens circulatory dysfunction in several forms of shock, in part by inhibiting sympathetic activity. To investigate whether endogenous opiates have a similar effect in chronic heart failure (HF), we measured beta-endorphin concentrations and hemodynamic responses to naloxone infusion (2 mg/kg bolus + 2 mg.kg-1 x h-1) in six control (C) dogs and eight dogs with low-output HF produced by 3 wk of rapid ventricular pacing. The dogs with HF exhibited reduced arterial blood pressure (C, 123 +/- 4 vs. HF, 85 +/- 7 mmHg; P < 0.01) and cardiac outputs (C, 179 +/- 14 vs. HF, 76 +/- 2 ml.min-1 x kg-1; P < 0.01) and elevated plasma norepinephrine concentrations (C, 99 +/- 12 vs. HF, 996 +/- 178 pg/ml; P < 0.01) but normal beta-endorphin concentrations (C, 30 +/- 11 vs. HF, 34 +/- 12 pg/ml; P = NS). Naloxone produced similar transitory increases in blood pressure (C, 14 +/- 5 vs. HF, 26 +/- 25%) and cardiac output (C, 37 +/- 13 vs. HF, 22 +/- 15%) in both groups (both P = NS). No significant changes in norepinephrine concentration or systemic vascular resistance were observed in either group. These findings suggest that beta-endorphin secretion does not exacerbate circulatory dysfunction in chronic heart failure.

scholarly journals Dietary Quercetin and Kaempferol: Bioavailability and Potential Cardiovascular-Related Bioactivity in Humans

Nutrients ◽  
2019 ◽  
Vol 11 (10) ◽  
pp. 2288 ◽  
Author(s):  
Wijdan M. Dabeek ◽  
Melissa Ventura Marra
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Vegetable Intake ◽  
Cardiovascular Effects ◽  
Fruit And Vegetable Intake ◽  
Food Sources ◽  
Free Form ◽  
Kaempferol Glycoside ◽  
Plant Sources ◽  
Reduced Risk

Fruit and vegetable intake has been associated with a reduced risk of cardiovascular disease. Quercetin and kaempferol are among the most ubiquitous polyphenols in fruit and vegetables. Most of the quercetin and kaempferol in plants is attached to sugar moieties rather than in the free form. The types and attachments of sugars impact bioavailability, and thus bioactivity. This article aims to review the current literature on the bioavailability of quercetin and kaempferol from food sources and evaluate the potential cardiovascular effects in humans. Foods with the highest concentrations of quercetin and kaempferol in plants are not necessarily the most bioavailable sources. Glucoside conjugates which are found in onions appear to have the highest bioavailability in humans. The absorbed quercetin and kaempferol are rapidly metabolized in the liver and circulate as methyl, glucuronide, and sulfate metabolites. These metabolites can be measured in the blood and urine to assess bioactivity in human trials. The optimal effective dose of quercetin reported to have beneficial effect of lowering blood pressure and inflammation is 500 mg of the aglycone form. Few clinical studies have examined the potential cardiovascular effects of high intakes of quercetin- and kaempferol-rich plants. However, it is possible that a lower dosage from plant sources could be effective due to of its higher bioavailability compared to the aglycone form. Studies are needed to evaluate the potential cardiovascular benefits of plants rich in quercetin and kaempferol glycoside conjugates.

Effects of S-adenosyl-methionine on plasma norepinephrine, blood pressure, and heart rate in healthy volunteers

1986 ◽  
Vol 17 (2) ◽  
pp. 111-118 ◽  
Author(s):  
Michael A. Sherer ◽  
Giulio L. Cantoni ◽  
Robert N. Golden ◽  
Matthew V. Rudorfer ◽  
William Z. Potter
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Healthy Volunteers ◽  
Plasma Norepinephrine ◽  
Adenosyl Methionine

Increased Pressor Responsiveness to Enkephalin in Spontaneously Hypertensive Rats: The Role of Vasopressin

1980 ◽  
Vol 59 (s6) ◽  
pp. 235s-237s ◽  
Author(s):  
R. W. Rockhold ◽  
J. T. Crofton ◽  
L. Share
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Pressor Response ◽  
Cardiovascular Effects ◽  
Hypertensive Rats ◽  
Methionine Enkephalin ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto Rats ◽  
Wistar Kyoto

1. The cardiovascular effects of an enkephalin analogue were examined in spontaneously hypertensive and normotensive Wistar-Kyoto rats. (D-Ala2)-methionine enkephalin caused a biphasic increase in blood pressure and an increase in heart rate after intracerebroventricular injection. 2. The initial pressor response to (D-Ala2)-methionine enkephalin was greater in hypertensive than in normotensive rats. No difference was noted between groups during the secondary pressor response. Heart rate increases paralleled the secondary increase in blood pressure. 3. Naloxone pretreatment abolished the secondary increase in blood pressure and the tachycardia, but did not blunt the initial pressor response in female Wistar-Kyoto rats. 4. Plasma levels of arginine vasopressin were depressed during the plateau phase of the pressor response in hypertensive rats given intracerebroventricular (d-Ala2)-methionine enkephalin. 5. The results suggest that the cardiovascular effects of central enkephalin are not due to vasopressin, but may involve activation of the sympathetic nervous system.

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