Abstract P154: Hypertension in Obese African American Women is Not Caused by Increased Sympathetic Activity

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Cyndya A Shibao ◽  
Alejandro Marinos ◽  
Jorge E Celedonio ◽  
Luis E Okamoto ◽  
Amy C Arnold ◽  
...  

African American (AA) women have the highest prevalence of hypertension and obesity in the United States. We tested the hypothesis that sympathetic activity contributes to hypertension in obese AA women, as we previously shown to be the case in Caucasians. We studied 42 obese women (16 whites, body mass index (BMI) 36± 4 kg/m 2 , 44% with diagnosis of hypertension (HTN) and 26 AA, BMI 35± 4 kg/m 2 , 46% HTN). Anti-HTN medications were discontinued for 2 weeks prior to the study day. All subjects underwent complete autonomic blockade with the ganglionic blockade trimethaphan at doses of 4 mg/min. Autonomic blockade was evaluated by the lack of heart rate changes in response to ~25 mm Hg increase in blood pressure produced by a bolus infusion of the alpha 1 adrenergic agonist, phenylephrine and the decrease in norepinephrine levels. Results: Plasma norepinephrine significantly decreased during trimethaphan infusion (from baseline 253±1107 to 61±29 pg/ml, trimethaphan). The decrease in mean arterial blood pressure (MAP) produced by trimethaphan was greater in obese HTN compared with normotensive (NTN) Caucasians (-27±10 vs. -15±8 mm Hg, P=0.016). In contrast, no difference in the decrease in MAP induced by trimethaphan was found between HTN and NTN obese AA women (-16±11 vs. -12±10, P=0.451, figure ). Heart rate increased similarly with trimethaphan between HTN and NTN caucasians (+9.1± 6 vs. 16± 9, P=0.109) and AA women (+22± 7 vs. 21±12 bpm, P=0.760). MAP remained elevated in HTN obese AA women during trimethaphan infusion (84±15 vs. 72±9.8 mm Hg in NTN AA, P=0.021). Conclusion: Sympathetic activity does not contribute to hypertension in AA women

1993 ◽  
Vol 264 (1) ◽  
pp. R79-R84 ◽  
Author(s):  
J. N. Stinner ◽  
D. L. Ely

The pressor response to normal daily behaviors and acute stress was studied in black racer snakes (Coluber constrictor) at 30 degrees C. In addition, hematological changes during the stress response were assessed. Mean nighttime systemic arterial blood pressure (SABP) in undisturbed snakes was lower than daytime pressure (26 +/- 3 vs. 32 +/- 9 mmHg, P < 0.001). When snakes were fed mice, SABP increased 3.5- to 4-fold and heart rate increased approximately 3-fold above resting values within approximately 30 s (peak SABP, 99 +/- 18 mmHg; peak heart rate, 99 +/- 12 beats/min). Killing and ingesting the mice required 6-15 min, during which time mean SABP and heart rate were 84 +/- 16 mmHg and 92 +/- 12 beats/min. Pulmonary blood pressure also increased but remained 40-50 mmHg lower than SABP. During stress elicited by tapping the snakes for 5-8 min, heart rate was 94 +/- 6 beats/min but SABP averaged only 44 +/- 11 mmHg. Plasma norepinephrine and epinephrine increased 51- and 26-fold. Plasma glucose increased 58%, hematocrit increased 19%, and plasma volume decreased 19%. It is concluded that blood pressure is markedly affected by behavior and that the sympathetic nervous system appears to play a key role.


2010 ◽  
Vol 12 (2) ◽  
pp. 149-155 ◽  
Author(s):  
Jacquelyn Y. Taylor ◽  
Yan V. Sun ◽  
Steven C. Hunt ◽  
Sharon L.R. Kardia

African American women have the highest prevalence of hypertension and obesity of any group in the United States. African American girls have the highest incidence of obesity of any groups of children in the nation, and diagnoses of hypertension have been rising among this group. Because both genetic heredity and body mass index (BMI) are important risk factors for hypertension, this study examined the gene-BMI interaction for hypertension across the lifespan in two generations of African American women. Participants comprised of 868 African American women in the parent cohort and 322 in the offspring cohort from the Hypertension Genetic Epidemiology Network (HyperGEN) study, part of the Family Blood Pressure Program (FBPP). A total of 115 single-nucleotide polymorphisms (SNPs) were evaluated among the parent cohort and 491 among the offspring cohort for tests of SNP-BMI interaction using methods of false discovery rate (FDR; <.20) and examination of minor allele frequency (MAF; >.05) and Hardy-Weinberg equilibrium (>.10). One SNP (located in the CAPN 13 gene, rs1879282) passed adjustments for the multiple testing mentioned above and had a significant (p < .01) gene-BMI interaction on both systolic blood pressure (SBP) and diastolic blood pressure (DBP) among African American female offspring. The rs1879282 SNP is located on chromosome 2 on the calpain (CAPN) 13 gene, which is part of a family of cytosolic calcium-activated proteases involved in apoptosis, cell division, modulation of integrin—cytoskeletal interactions, and synaptic plasticity. This SNP was not available for testing in the African American parent cohort.


1995 ◽  
Vol 268 (6) ◽  
pp. H2232-H2238 ◽  
Author(s):  
J. K. Triedman ◽  
M. H. Perrott ◽  
R. J. Cohen ◽  
J. P. Saul

Fourier-based techniques are mathematically noncausal and are therefore limited in their application to feedback-containing systems, such as the cardiovascular system. In this study, a mathematically causal time domain technique, autoregressive moving average (ARMA) analysis, was used to parameterize the relations of respiration and arterial blood pressure to heart rate in eight humans before and during total cardiac autonomic blockade. Impulse-response curves thus generated showed the relation of respiration to heart rate to be characterized by an immediate increase in heart rate of 9.1 +/- 1.8 beats.min-1.l-1, followed by a transient mild decrease in heart rate to -1.2 +/- 0.5 beats.min-1.l-1 below baseline. The relation of blood pressure to heart rate was characterized by a slower decrease in heart rate of -0.5 +/- 0.1 beats.min-1.mmHg-1, followed by a gradual return to baseline. Both of these relations nearly disappeared after autonomic blockade, indicating autonomic mediation. Maximum values obtained from the respiration to heart rate impulse responses were also well correlated with frequency domain measures of high-frequency "vagal" heart rate control (r = 0.88). ARMA analysis may be useful as a time domain representation of autonomic heart rate control for cardiovascular modeling.


1997 ◽  
Vol 272 (1) ◽  
pp. H448-H461 ◽  
Author(s):  
T. J. Mullen ◽  
M. L. Appel ◽  
R. Mukkamala ◽  
J. M. Mathias ◽  
R. J. Cohen

We applied system identification to the analysis of fluctuations in heart rate (HR), arterial blood pressure (ABP), and instantaneous lung volume (ILV) to characterize quantitatively the physiological mechanisms responsible for the couplings between these variables. We characterized two autonomically mediated coupling mechanisms [the heart rate baroreflex (HR baroreflex) and respiratory sinus arrhythmia (ILV-HR)] and two mechanically mediated coupling mechanisms [the blood pressure wavelet generated with each cardiac contraction (circulatory mechanics) and the direct mechanical effects of respiration on blood pressure (ILV⇢ABP)]. We evaluated the method in humans studied in the supine and standing postures under control conditions and under conditions of beta-sympathetic and parasympathetic pharmacological blockades. Combined beta-sympathetic and parasympathetic blockade abolished the autonomically mediated couplings while preserving the mechanically mediated coupling. Selective autonomic blockade and postural changes also altered the couplings in a manner consistent with known physiological mechanisms. System identification is an “inverse-modeling” technique that provides a means for creating a closed-loop model of cardiovascular regulation for an individual subject without altering the underlying physiological control mechanisms.


1980 ◽  
Vol 58 (1) ◽  
pp. 37-43 ◽  
Author(s):  
R. D. S. Watson ◽  
C. A. Hamilton ◽  
D. H. Jones ◽  
J. L. Reid ◽  
T. J. Stallard ◽  
...  

1. Forearm venous plasma noradrenaline, heart rate and intra-arterial blood pressure were measured sequentially during and after upright bicycle exercise in five normotensive and six hypertensive patients. 2. Plasma noradrenaline increased significantly between 4 and 8 min during exercise. 3. On stopping exercise blood pressure and heart rate decreased rapidly whilst plasma noradrenaline increased in each subject to reach a maximum at a median time of 108 s after exercise. 4. Plasma noradrenaline decreased in five of six normotensive patients between the end of exercise and 2 min after exercise performed in the supine position. 5. Evidence in favour of a reflex increase in sympathetic activity after upright exercise is discussed.


1993 ◽  
Vol 264 (2) ◽  
pp. R262-R267
Author(s):  
J. Michalicek ◽  
G. Campbell

Mean arterial blood pressure (P(a)) and heart rate (HR) were studied in normal conscious cane toads (Bufo marinus) or in autonomically blocked animals treated variously with bretylium, atropine, phentolamine, and propranolol. Partial or total autonomic blockade had no effect on resting values of the variables tested, with the exception that atropine treatment of bretylium-treated toads caused an increase of heart rate by 5.3 +/- 1.3 beats/min. In graded hemorrhage, aliquots of blood (1.68 ml/100 g body wt) were removed at 60-min intervals. There was extensive plasma recruitment, and blood could be removed up to 10.08 ml/100 g without inducing cardiovascular shock. Each hemorrhage caused an initial transient decrease in P(a) and increase in HR followed by recovery toward prehemorrhage values. Repeated hemorrhage caused a progressive rise in basal HR and fall in basal P(a). The effects of drug treatments suggest that transient increases in HR may be caused by the release of adrenal catecholamines. In addition, hemorrhage may increase sympathetic tone so that basal HR becomes elevated, which, together with sympathetic vasoconstriction, limits the progressive fall of basal P(a).


2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Maryam H Al Mansi ◽  
YenJun Chuang ◽  
Puliyur S MohanKumar ◽  
Sheba M J MohanKumar

Abstract Cardiovascular diseases are the leading causes of mortality among men and women. With the new blood pressure guidelines from the American Heart Association, almost half of the United States population has hypertension (45.6%). The reasons for this high prevalence of hypertension in our population could be several, but the effect of emerging contaminants are overlooked and understudied. Bisphenol-A (BPA) is a widely used plasticizing agent that contaminates the environment. Most humans are exposed to BPA on a daily basis and urine levels of this endocrine disrupting chemical (EDC) are positively correlated with hypertension. The FDA banned the use of BPA in baby bottles in 2012, however, it is still being used in food containers and plastics. Currently, several BPA analogs such as bisphenol-S (BPS) and bisphenol-F (BPF) are used to replace BPA in the plastic industry. But their physiological effects are not clear. In order to study the effects of these EDCs on the development of hypertension, we exposed pregnant Sprague Dawley (SD) rats to saline, 5 µg/Kg BW of BPA, BPS or 1µg/kg BW of BPF. The offspring were allowed to reach adulthood before implantation with a radiotelemeter (Data Sciences International; HD-S10) in the femoral artery for undisturbed monitoring of systolic, diastolic and mean arterial blood pressure and heart rate. Recordings were measured once a week for 11 weeks over 24 hours to establish day and night readings. Night-time systolic BP was significantly elevated in BPA, BPF and BPS exposed rats compared to control. During the day, systolic BP was significantly higher in the BPA group compared to control. Diastolic BP was elevated in the BPS and BPF groups. Heart rate was elevated the most in the BPS group. These results indicate that prenatal exposure to low levels of BPA analogs has a profound effect on hypertension.


2018 ◽  
Vol 125 (6) ◽  
pp. 1804-1811 ◽  
Author(s):  
Timothée Fontolliet ◽  
Vincent Pichot ◽  
Aurélien Bringard ◽  
Nazzareno Fagoni ◽  
Alessandra Adami ◽  
...  

We performed the first analysis of heart rate variability (HRV) at rest and during exercise under full autonomic blockade on the same subjects, to test the conjecture that vagal tone withdrawal occurs at exercise onset. We hypothesized that between rest and exercise there would be 1) no differences in total power (PTOT) under parasympathetic blockade, 2) a PTOT fall under β1-sympathetic blockade, and 3) no differences in PTOT under blockade of both autonomic nervous system branches. Seven men [24 (3) yr, mean (SD)] performed 5-min cycling (80 W) supine, preceded by 5-min rest during control and with administration of atropine, metoprolol, and atropine + metoprolol (double blockade). Heart rate and arterial blood pressure were continuously recorded. HRV and blood pressure variability were determined by power spectral analysis, and baroreflex sensitivity was determined by the sequence method. At rest, PTOT and the powers of low- and high-frequency components of HRV (LF and HF, respectively) were dramatically decreased with atropine and double blockade compared with control and metoprolol, with no effects on LF-to-HF ratio and on the normalized LF (LFnu) and HF (HFnu). During exercise, patterns were the same as at rest. Comparing exercise with rest, PTOT varied as hypothesized. For systolic and diastolic blood pressure, resting PTOT was the same in all conditions. During exercise, in all conditions, PTOT was lower than in control. Baroreflex sensitivity decreased under atropine and double blockade at rest and under control and metoprolol during exercise. The results support the hypothesis that vagal suppression determined disappearance of HRV during exercise. NEW & NOTEWORTHY This study provides the first demonstration, by systematic analysis of heart rate variability at rest and during exercise under full autonomic blockade on the same subjects, that suppression of vagal activity is responsible for the disappearance of spontaneous heart rate variability during exercise. This finding supports previous hypotheses on the role of vagal withdrawal in the control of the rapid cardiovascular response at exercise onset.


2001 ◽  
Vol 94 (2) ◽  
pp. 252-258 ◽  
Author(s):  
Peter Kienbaum ◽  
Thorsten Heuter ◽  
Goran Pavlakovic ◽  
Martin C. Michel ◽  
Jürgen Peters

Background S(+)-Ketamine is reported to exert twofold greater analgesic and hypnotic effects but a shorter recovery time in comparison with racemic ketamine, indicating possible differential effects of stereoisomers. However, cardiovascular regulation during S(+)-ketamine anesthesia has not been studied. Muscle sympathetic activity (MSA) may be an indicator of the underlying alterations of sympathetic outflow. Whether S(+)-ketamine decreases MSA in a similar manner as the racemate is not known. Thus, the authors tested the hypothesis that S(+)-ketamine changes MSA and the muscle sympathetic response to a hypotensive challenge. Methods Muscle sympathetic activity was recorded by microneurography in the peroneal nerve of six healthy participants before and during anesthesia with S(+)-ketamine (670 microg/kg intravenously followed by 15 microg x kg(-1) x min(-1)). Catecholamine and ketamine plasma concentrations, heart rate, and arterial blood pressure were also determined. MSA responses to a hypotensive challenge were assessed by injection of sodium nitroprusside (2-10 microg/kg) before and during S(+)-ketamine anesthesia. In the final step, increased arterial pressure observed during anesthesia with S(+)-ketamine was adjusted to preanesthetic values by sodium nitroprusside infusion (1-6 microg x kg(-1) x min(-1)). Results Anesthesia with S(+)-ketamine (ketamine plasma concentration 713 +/- 295 microg/l) significantly increased MSA burst frequency (mean +/- SD; 18 +/- 6 to 35 +/- 11 bursts/min) and burst incidence (32 +/- 10 to 48 +/- 15 bursts/100 heartbeats) and was associated with a doubling of norepinephrine plasma concentration (from 159 +/- 52 to 373 +/- 136 pg/ml) parallel to the increase in MSA. Heart rate and arterial blood pressure also significantly increased. When increased arterial pressure during S(+)-ketamine was decreased to awake values with sodium nitroprusside, MSA increased further (to 53 +/- 24 bursts/min and 60 +/- 20 bursts/100 heartbeats, respectively). The MSA increase in response to the hypotensive challenge was fully maintained during anesthesia with S(+)-ketamine. Conclusions S(+)-Ketamine increases efferent sympathetic outflow to muscle. Despite increased MSA and arterial pressure during S(+)-ketamine anesthesia, the increase in MSA in response to arterial hypotension is maintained.


1999 ◽  
Vol 276 (6) ◽  
pp. R1608-R1616 ◽  
Author(s):  
Bernat Kocsis ◽  
Tomas Karlsson ◽  
B. Gunnar Wallin

Partial coherence analysis was used to evaluate the extent to which coherence between resting muscle sympathetic activity (MSA) in different pairs of limbs in humans is explained by the common baroreceptor input and by other noncardiac-related factors. Multiunit MSA in two or three nerves, arterial blood pressure, and electrocardiogram were recorded simultaneously. Correlated MSA consisted of a sharp periodic component at the heart rate and a wideband component of relatively low power distributed between 0 and 2–2.5 Hz. Quantitative analysis revealed stronger coupling between MSAs in close limbs than in distant limbs (peak coherence leg-leg, 0.94 ± 0.03; arm-leg, 0.76 ± 0.11). Furthermore, the wideband component, unaffected by partialization with circulatory signals, was significantly stronger between leg-leg (0.67 ± 0.10) than between arm-leg pairs (0.29 ± 0.10), i.e., noncardiac-related components explained 71% of leg-leg and 38% of arm-leg coherences at the frequency of the heart. Our results indicate that nonuniform relationship exists between resting sympathetic outflow to muscles in close and distant extremities which is, however, partially masked by the effect of the common rhythmic baroreceptor input.


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