Stress-induced Changes In Blood Pressure Research Articles

Wearable Technology to Detect Stress-Induced Blood Pressure Changes: The Next Chapter in Ambulatory Blood Pressure Monitoring?

Wearable Technology to Detect Stress-Induced Blood Pressure Changes: The Next Chapter in Ambulatory Blood Pressure Monitoring?

Abstract 505: Effects of Etamicastat, a Selective Peripheral Dopamine-β-Hydroxylase Inhibitor, Upon Stress-induced Changes in Blood Pressure in the SHR

Stressors induce an overactivation of the sympathetic nervous system (SNS) that triggers several changes in the body as a response to stress. These changes include vasoconstriction and increase in heart rate, which results in raised blood pressure (BP). Etamicastat is a selective dopamine-β-hydroxylase (DβH) inhibitor that decreases norepinephrine levels in peripheral sympathetically innervated tissues. Cardiovascular parameters were measured after a single oral administration of etamicastat (30 mg/kg) 9 h post-administration in male spontaneously hypertensive rats (SHR) by radio-telemetry or tail-cuff recording. Telemetered recording was performed in both restrained and unrestrained animals. Etamicastat treatment had no effect on heart rate (HR, beats/min) in any recording method. HR measured in unrestrained SHR instrumented with radio-telemetry probes (305±5) consistently yielded HR values significantly lower than restrained animals (362±11) or those recorded by tail-cuff (393±7). On the other hand, single-dose oral etamicastat treatment decrease in mean arterial pressure (MAP, mm Hg) was -14.0±2.0 from 153.3±4.0 in telemetered unrestrained animals, -26.1±5.1 from 182.8±6.4 in telemetry-implanted restrained SHR and -47.9±7.0 from 183.4±9.5 recorded by tail-cuff method. In addition, a power spectral analysis was performed to evaluate BP variability (BPV), in SHR implanted with radio-telemetry probes, at high frequency (HF: 1-2 Hz), low frequency (LF: 0.2-0.6 Hz) and very low frequency (VLF: 0.02-0.2 Hz). The stressor (i.e., cage restrainement) increased the ratio LF/HF-BPV in untreated SHR from 5.23±1.24 to 10.03±1.75, which results from the activation of the SNS. Treatment with etamicastat decreased the ratio LF/HF-BPV in stressed SHR from 10.03±1.75 to 4.46±0.68 and in non-stressed SHR from 5.23±1.24 to 2.23±0.39. In conclusion, etamicastat treatment reduces (1) high BP in SHR, (2) the stress-induced increase in SNS drive and (3) the stress-induced increase in BP.

Adrenergic Genetic Mechanisms in Hypertension and Hypertensive Kidney Disease

Catecholamine secretory traits were significantly heritable, as were stress-induced blood pressure changes. Tyrosine hydroxylase (TH) is the rate-limiting enzyme in catecholamine biosynthesis. In the tyrosine hyroxylase promoter, significant associations were found for urinary catecholamine excretion and for blood pressure response to stress. TH promoter haplotype 2 (TGGG) showed pleiotropy, increasing both norepinephrine excretion and blood pressure during stress. In hypertension, 2 independent case-control studies (1,266 subjects with 53% women and 927 subjects with 24% women) replicated the effect of C-824T in the determination of blood pressure. Chromogranin A (CHGA) plays a fundamental role in the biogenesis of catecholamine secretory granules. Changes in the storage and release of CHGA in clinical and experimental hypertension prompted us to study whether genetic variation at the CHGA locus might contribute to alterations in autonomic function, and hence hypertension and its target organ consequences such as hypertensive kidney disease (nephrosclerosis). Systematic polymorphism discovery across the human CHGA locus revealed such regulatory regions as the proximal promoter and 3'-UTR. In chromaffin cell-transfected CHGA 3'-UTR and promoter/luciferase reporter plasmids, the functional consequences of the regulatory/non-coding allelic variants were documented. Variants in both the proximal promoter and the 3'-UTR displayed statistical associations with hypertension and hypertensive end stage renal disease. Therefore, I would like to review the common genetic variation in TH and CHGA as a cause of inter-individual variation in sympathetic activity, and ultimately blood pressure and hypertensive kidney disease.

Effects of Concord grape juice on ambulatory blood pressure in prehypertension and stage 1 hypertension

Consumption of flavonoid-containing foods may be useful for the management of hypertension. We investigated whether 100% Concord grape juice lowers blood pressure in patients with prehypertension and stage 1 hypertension. We conducted a double-blind crossover study to compare the effects of grape juice (7 mL · kg⁻¹ · d⁻¹) and matched placebo beverage on 24-h ambulatory blood pressure, stress-induced changes in blood pressure, and biochemical profile. Participants consumed each beverage for 8 wk with a 4-wk rest period between beverages. They ceased consumption of grapes and other flavonoid-containing beverages throughout the study. We enrolled 64 otherwise healthy patients taking no antihypertensive medications (31% women, 42% black, age 43 ± 12 y). Baseline mean (± SD) cuff blood pressure was 138 ± 7 (systolic)/82 ± 7 (diastolic) mm Hg. No effects on the primary endpoint of 24-h mean systolic blood pressure, diastolic blood pressure, or stress-induced changes in blood pressure were observed. A secondary endpoint was nocturnal dip in systolic pressure. At baseline, nocturnal pressure was 8.3 ± 7.1% lower at night than during daytime. The mean nocturnal dip increased 1.4 percentage points after grape juice and decreased 2.3 percentage points after placebo (P = 0.005). Fasting blood glucose was 91 ± 10 mg/dL at baseline for the entire cohort. Glucose decreased 2 mg/dL after consumption of grape juice and increased 1 mg/dL after consuming the placebo (P = 0.03). We observed no effect of grape juice on ambulatory blood pressure in this cohort of relatively healthy individuals with modestly elevated blood pressure. Secondary analyses suggested favorable effects on nocturnal dip and glucose homeostasis that may merit further investigation. This trial was registered at clinicaltrials.gov as NCT00302809.

Adrenergic Polymorphism and the Human Stress Response

Tyrosine hydroxylase (TH) is the rate-limiting enzyme in catecholamine biosynthesis. Does common genetic variation at human TH alter autonomic activity and predispose to cardiovascular disease? We undertook systematic polymorphism discovery at the TH locus, and then tested variants for contributions to sympathetic function and blood pressure. We resequenced 80 ethnically diverse individuals across the TH locus. One hundred seventy-two twin pairs were evaluated for sympathetic traits, including catecholamine production and environmental (cold) stress responses. To evaluate hypertension, we genotyped subjects selected from the most extreme diastolic blood pressure percentiles in the population. Human TH promoter haplotype/reporter plasmids were transfected into chromaffin cells. Forty-nine single nucleotide polymorphisms (SNPs) and one tetranucleotide repeat were discovered, but coding region polymorphism did not account for common phenotypic variation. A block of linkage disequilibrium spanned four common variants in the proximal promoter. Catecholamine secretory traits were significantly heritable, as were stress-induced blood pressure changes. In the TH promoter, significant associations were found for urinary catecholamine excretion, as well as blood pressure response to stress. TH promoter haplotype #2 (TGGG) showed pleiotropy, increasing both norepinephrine excretion and blood pressure during stress. In hypertension, a case-control study (1266 subjects, 53% women) established the effect of C-824T in determination of blood pressure. We conclude that human catecholamine secretory traits are heritable, displaying joint genetic determination (pleiotropy) with autonomic activity and finally with blood pressure in the population. Catecholamine secretion is influenced by genetic variation in the adrenergic pathway encoding catecholamine synthesis, especially at the classically rate-limiting step, TH. The results suggest novel pathophysiological links between a key adrenergic locus, catecholamine metabolism, and blood pressure, and suggest new strategies to approach the mechanism, diagnosis, and treatment of systemic hypertension.

Common genetic variants in the chromogranin A promoter alter autonomic activity and blood pressure

Chromogranin A (CHGA) is stored and released from the same secretory vesicles that contain catecholamines in chromaffin cells and noradrenergic neurons. We had previously identified common genetic variants at the CHGA locus in several human populations. Here we focus on whether inter-individual variants in the promoter region are of physiological significance. A common haplotype, CGATA (Hap-B), blunted the blood pressure response to cold stress and the effect exhibited molecular heterosis with the greatest blood pressure change found in Hap-A/Hap-B heterozygotes. Homozygosity for three minor alleles with peak effects within the haplotype predicted lower stress-induced blood pressure changes. The G-462A variant predicted resting blood pressure in the population with higher pressures occurring in heterozygotes (heterosis). Using cells transfected with CHGA promoter-luciferase reporter constructs, the Hap-B haplotype had decreased luciferase expression compared to the TTGTC (Hap-A) haplotype under both basal conditions and after activation by pre-ganglionic stimuli. The G-462A variant altered a COUP-TF transcriptional control motif. The two alleles in transfected promoters differed in basal activity and in the responses to COUP-II-TF transactivation and to retinoic acid. In vitro findings of molecular heterosis were also noted with the transfected CHGA promoter wherein the diploid combination of the two G-462A alleles gave rise to higher luciferase expression than either allele in isolation. Our results suggest that common genetic variants in the CHGA promoter may regulate heritable changes in blood pressure.

Tyrosine Hydroxylase, the Rate-Limiting Enzyme in Catecholamine Biosynthesis

Tyrosine hydroxylase (TH) is the rate-limiting enzyme in catecholamine biosynthesis. Does common genetic variation at human TH alter autonomic activity and predispose to cardiovascular disease? We undertook systematic polymorphism discovery at the TH locus and then tested variants for contributions to sympathetic function and blood pressure. We resequenced 80 ethnically diverse individuals across the TH locus. One hundred seventy-two twin pairs were evaluated for sympathetic traits, including catecholamine production, reflex control of the circulation, and environmental (cold) stress responses. To evaluate hypertension, we genotyped subjects selected from the most extreme diastolic blood pressure percentiles in the population. Human TH promoter haplotype/reporter plasmids were transfected into chromaffin cells. Forty-nine single-nucleotide polymorphisms were discovered, but coding region polymorphism did not account for common phenotypic variation. A block of linkage disequilibrium spanned 4 common variants in the proximal promoter. Catecholamine secretory traits were significantly heritable (h2), as were stress-induced blood pressure changes. In the TH promoter, significant associations were found for urinary catecholamine excretion and for blood pressure response to stress. TH promoter haplotype 2 (TGGG) showed pleiotropy, increasing both norepinephrine excretion and blood pressure during stress. Coalescent simulations suggest that TH haplotype 2 likely arose approximately 380,000 years ago. In hypertension, 2 independent case-control studies (1266 subjects with 53% women and 927 subjects with 24% women) replicated the effect of C-824T in the determination of blood pressure. We conclude that human catecholamine secretory traits are heritable, displaying joint genetic determination (pleiotropy) with autonomic activity and finally with blood pressure in the population. Catecholamine secretion is influenced by genetic variation in the adrenergic pathway encoding catecholamine synthesis, especially at the classically rate-limiting step, TH. The results suggest novel pathophysiological links between a key adrenergic locus, catecholamine metabolism, and blood pressure and suggest new strategies to approach the mechanism, diagnosis, and treatment of systemic hypertension.

Attenuated adrenocortical and blood pressure responses to psychological stress in ad libitum and abstinent smokers

Chronic smoking may alter physiological systems involved in the stress response. This study was designed to examine the effects of ad libitum smoking and abstinence on adrenocortical and cardiovascular responses to acute psychological stress in dependent cigarette smokers. We evaluated differences among abstinent smokers, smokers who continued to smoke at their normal rate, and nonsmokers in salivary cortisol concentrations, systolic and diastolic blood pressure (BP), heart rate (HR), and mood reports. Measurements were obtained during rest and in response to acute psychological stress (public speaking) in one session (stress session) and during continuous rest in a control session. Thirty-eight smokers (21 women) and 32 nonsmokers (18 women) participated. Smokers were assigned to either abstain from smoking the night prior to and the day of each session, or to continue smoking at their normal rate before each session. All groups showed significant stress-induced changes in BP and HR. Smokers, regardless of their assigned condition, showed attenuated systolic BP responses to the public-speaking stressor when compared to nonsmokers. While resting cortisol levels were greater among smokers than nonsmokers, no cortisol response to the acute stressor was demonstrated in either ad libitum or abstinent smokers. These results indicate that chronic smoking diminishes adrenocortical and cardiovascular responses to stress, and that short-term abstinence does not correct these alterations.

Effects of angiotensins on day-night fluctuations and stress-induced changes in blood pressure.

In this study we evaluated by telemetry the effects of ANG II and ANG-(1-7) infusion on the circadian rhythms of blood pressure (BP) and heart rate (HR) and on the cardiovascular adjustment resulting from restraint stress in rats. ANG II or ANG-(1-7) or vehicle were infused subcutaneously for 7 days. Restraint stress was carried out before, during, and after infusion at 7-day intervals. Parallel with an increase in MAP, ANG II infusion produced an inversion of MAP circadian rhythm with a significant MAP acrophase inversion. It also produced bradycardia during the first 3 days of infusion. Thereafter, HR progressively increased, reaching values similar to or above those of the control period at the end of the infusion period. HR circadian variation was not changed by ANG II infusion. Strikingly, ANG II significantly attenuated the increase in MAP induced by restraint stress without altering the HR response. ANG-(1-7) infusion produced a slight but significant decrease in MAP restricted to the daytime period. No significant changes in the MAP acrophase were observed. In addition, ANG-(1-7) infusion produced a small but significant sustained bradycardia. ANG-(1-7) did not change cardiovascular responses to restraint stress. These data indicate that ANG II can influence the activity of brain areas involved in the determination of stress-induced or circadian-dependent variations of blood pressure without changing HR fluctuations. A significant modulatory influence of ANG-(1-7) on basal MAP and HR is also suggested.

Effects of chronic treatment with (+)-nicotine on the stress-induced hypertension and downregulation of central nicotinic receptors in rats Comparative study with (−)-nicotine

The effects of chronic treatment with (+)-nicotine on the immobilization stress-induced changes in blood pressure, body weight, and [ 3H]cytisine binding to brain nicotinic receptors were examined in rats and were compared with those of (−)-nicotine. Immobilization stress (2 hr/day −1, for 2 weeks) induced a moderate elevation of blood pressure, loss of body weight gain, and downregulation of [ 3H]cytisine binding sites in cerebral cortex and midbrain. Chronic treatment with (+)- or (−)-nicotine inhibited the stress-induced hypertension but did not suppress the inhibition of body weight gain by stress. Body weight before stress load was also reduced by (−)-nicotine but not (+)-nicotine treatment. Treatment with each isomer increased the maximum number of [ 3H]cytisine binding sites (B max) of brain stem, cerebral cortex, and hippocampus. The B max in midbrain was also increased by (+)-nicotine but not by (−)-nicotine. Stress-induced downregulation in cerebral cortex was inhibited by both isomers. These results suggest that (+)- and (−)-nicotine cause various effects, including anti-stress effect, on the central nervous system in rats, which are slightly different between the isomers.

Effects of propranolol and atenolol on immobilization stress-induced hypertension and down-regulation of central β-adrenoceptors in rats

Effects of chronic treatment with propranolol or atenolol on stress-induced changes in blood pressure, body weight and cerebral β-adrenoceptors in rats were examined and compared with the effects of chronic treatment with prazosin. Immobilization stress (2 h daily for 2 weeks) induced a moderate elevation of blood pressure, loss of body weight gain and downregulation of cerebral β-adrenoceptors, but produced no changes in the cerebral α 1-adrenoceptors. Chronic administration of propranolol (5 or 50 mg · kg −1), atenolol (5 or 50 mg · kg −1) or prazosin (2 or 20 mg · kg −1) inhibited stress-induced hypertension but did not affect loss of body weight gain. Propranolol increased the density of cerebral β-adrenoceptors by 77% and reduced the downregulation induced by stress. Atenolol also increased the density of cerebral β-adrenoceptors by 34% and abolished the stress-induced downregulation in cerebral β-adrenoceptor density. In contrast, prazosin had no effect on the cerebral β-adrenoceptors in nonstressed or stressed rats. These results suggest that the antihypertensive action of propranolol and atenolol may be partly associated with the inhibition of stress-activated central β-adrenoceptor transmission.

拘束ストレスによるラット脳内β-アドレナリン受容体の変動と高血圧

Effects of chronic treatment with propranolol or atenolol on stress-induced changes in blood pressure and cerebral β-adrenoceptors were examined in rats. Immobilization stress (2 h daily for 2 weeks) induced a moderate elevation of blood pressure and downregulation of cerebral β-adrenoceptors. Chronic administration of propranolol (5 mg•kg-1) or atenolol (5 mg•kg-1) inhibited stress-induced hypertension. Propranolol and atenolol increased the density of cerebral β-adrenoceptors and inhibited the downregulation induced by stress. These results suggest that the antihypertensive action of propranolol and atenolol may be partly associated with the inhibition of stress-activated central β-adrenoceptor transmission.

Anger suppression: its relationship to beta-adrenergic receptor sensitivity and stress-induced changes in blood pressure.

While studies from diverse fields of research suggest a relationship between problems expressing anger and cardiovascular illness, few studies have provided a potential pathophysiological link of such a relationship. Forty-five males were classified according to one of three anger expression categories: those who did not suppress their anger (N = 13), those who partially suppressed their anger (N = 19), and those who definitely suppressed their anger (N = 13). For each, we determined lymphocyte beta-adrenergic receptor function and blood pressure responsiveness to a standardized mathematics stressor. Those subjects who routinely suppressed their expression of anger had increased beta-adrenergic receptor sensitivity (P = 0.01) (isoproterenol-stimulated cyclic AMP production) and a greater systolic blood pressure response to the stressor (P = 0.001). Anger suppression was unrelated to the subject's age, weight, or socioeconomic status. These findings may be germane to prior clinical and epidemiologic observations relating anger expression and cardiovascular illness.

Does antihypertensive monotherapy attenuate stress-induced changes in blood pressure?

Does antihypertensive monotherapy attenuate stress-induced changes in blood pressure?

Stress and Alcohol Interaction: An Update of Human Research

The literature on alcohol and stress in human subjects carried out since 1981 is reviewed. The review covers selected aspects of the interaction of alcohol and stress. (1) Most of the review focuses on the role of stress on alcohol ingestion. Retrospective research based on data from the Health and Nutrition Examination Survey indicated an increase in alcohol consumption with anxiety in certain groups of, as yet not well characterized, individuals. For example, although still insufficiently documented, stress does not appear to play a significant role in alcohol ingestion by women and the elderly. By contrast, stress does appear to play a role in the control of alcohol ingestion by adolescents. Prospective studies employing questionnaire-interview formats generally support an effect of stress on alcohol ingestion. However, studies employing male college aged social drinkers did not find a correlation between levels of stress and ingestion of alcohol. Alcoholics also differ in the reasons for drinking alcohol, but generally ingest alcohol to lessen anxiety/stress. It is clear that the Tension Reduction Hypothesis as originally postulated is no longer adequate. Many new models based on an interaction of alcohol and stress have been proposed to explain the control of alcohol consumption. Considering the multidimensionality of factors that appear to contribute to the control of alcohol ingestion, it is unlikely that a single model could possibly be relevant to alcohol ingestion under all conditions. More likely different models may be relevant to alcohol consumption under specific conditions, or for specific populations. (2) Alcohol has been reported to decrease anxiety in agoraphobics. The self-medication by agoraphobics may contribute significantly to their alcohol abuse. (3) Alcohol has also been reported to decrease tremor of the hands in stressed subjects as well as in patients with essential tremor. (4) Although a number of studies have employed electrodermal activity in studies aimed at the interaction of alcohol and stress, the results have been rather inconsistent. (5) The controversy on the purported beneficial effect of alcohol on the cardiovascular system persists. A number of studies have shown a J- or U-shaped relationship between alcohol ingestion and incidence of coronary heart disease. Alcohol may also influence stress-induced changes in blood pressure. Although a number of studies have demonstrated lower blood pressure in individuals ingesting less than two drinks per day compared with abstainers or heavy alcohol imbibers, the evidence is not conclusive. (6) It is not clear whether the interaction of alcohol and stress involves alterations in plasma catecholamines.(ABSTRACT TRUNCATED AT 250 WORDS)

Does antihypertensive monotherapy attenuate stress-induced changes in blood pressure?

Abellán, José; Garcia-Sánchez, Francísco A.; Menárguez, Fernando H.; Martínez-Selva, José M.; Navarro, Norberto; Saavedra, Teresa Author Information

Effect of diuretics and calcium antagonists on circulatory parameters and plasma catecholamines during mental stress.

In a model of mental stress the influence of nifedipine and hydrochlorothiazide on stress-induced changes in blood pressure, heart rate, and plasma catecholamines was studied in normal persons. The drugs were used to investigate whether substances with antihypertensive but no particular sympatholytic properties were capable of suppressing emotionally induced stress reactions. In all subjects blood pressure and heart rate increased significantly during mental stress, and this effect was not inhibited either by nifedipine or hydrochlorothiazide. In the hydrochlorothiazide group plasma noradrenaline levels were significantly higher than in controls in the resting state and during the stress reaction, whereas in the nifedipine group no difference was observed. It is concluded that nifedipine or hydrochlorothiazide do not inhibit emotional stress reactions in normotensive persons.