Cardiovascular reactivity and design in rats with experimental "neurogenic hypertension"

The arterial barorecptors were denervated in 20 normotensive Wistar rats. 2 1/2 months after the operation their cardiovascular responses to "mental stress" were compared to those of matched control rats (NCR). At the time of investigation the blood pressure of the baroreceptor denervated rats (BDR) was increased some 15 per cent above that of the control group. There was, however, no difference in response to "mental stress" between groups, if anything the BDR reponded with less pronounced tachycardia. Two months subsequent to the stress-test the men blood pressure of the BDR was still significantly above normal levels, but the BDR did not exhibit structural cardiovascular adaptation, which has been documented in most types of stable hypertension as a response to the increased mean blood pressure. The results imply that hypertension induced by baroreceptor denervation is not of a stable and persistent type in which case structural changes in the cardiovascular system would have developed within the observation period (approximately 4 months). Emotional stimuli, however, do not seem to contribute to periodic blood pressure increase at the time of measurement, as earlier suggested.     

Cardiovascular reactivity, hostility, and family history of hypertension

This study was conducted to evaluate the relations between cardiovascular reactivity and two types of hostility, namely, overt expression of hostility in contrast to the covert experience of hostility. Diastolic blood pressure reactivity was associated with not overtly expressing hostility. For persons with a parental history of hypertension, systolic blood pressure (SBP) reactivity was associated with low scores on the covert hostility measure of irritability, while for persons without a parental history of hypertension, SBP reactivity was associated with high scores for irritability. The results are discussed in light of research in the area of cardiovascular reactivity and stress-related cardiovascular disease.     

Cardiovascular reactivity and family history of hypertension: a meta-analysis

A regression-based meta-analysis examined the degree to which the effects of a family history of hypertension on cardiovascular reactivity are moderated by the magnitude of cardiovascular responses elicited in challenge/task conditions. Mean change scores for negative family history groups were regressed on mean change scores for positive family history groups. The slopes of separate regression lines obtained for systolic and diastolic blood pressure and heart rate were significantly less than 1.0 and the y-intercepts for these regression lines were significantly greater than zero. This pattern indicates that family history differences in cardiovascular reactivity to stress are greatest in situations that elicit the smallest baseline-stressor change scores in non-family-history groups.     

Cardiovascular and adrenal sensitivity to angiotensin II in essential hypertension

Summary Regulation of aldosterone secretion by sodium chloride is impaired in a group of essential hypertensives: high-salt diet fails to suppress aldosterone in these patients despite low renin values. The mechanism of this impaired regulation of aldosterone has not been clarified so far. We tested the sensitivity of aldosterone secretion and blood pressure to A II in 20 normotensive controls (aged 20–60, MAP 92±3 mm Hg), in ten normotensives with one or two parents with hypertension, and in 21 patients with essential hypertension (aged 17–65, MAP 119±4 mm Hg). After a period of 6 days on high-salt intake (300–320 mEq Na⁺/day), A II (0.1, 0.5, 1.0 and 2.0 ng/kg/min) was infused, each concentration for 30 min. According to aldosterone excretion during sodium loading, patients were divided into group A with complete suppression (n=12, aldosterone excretion 3.6±0.4 µg/day) and in group B with insufficient suppression (n=9, aldosterone excretion 15.5±2.3 µg/day). Despite similarly low plasma renins, rise of serum aldosterone levels during A II infusion was significantly higher in group B patients than in group A patients and normotensive controls. Rise in mean arterial blood pressure, however, brought about by graded A II infusion was similar in both groups of hypertensives and in normotensive controls. The results demonstrate an increased adrenal sensitivity to A II in a subgroup of essential hypertensives only. A similar adrenal hypersensitivity to A II found by others in patients with hyperaldosteronism due to adrenal hyperplasia supports the hypothesis that the same mechanism underlies both disorders.Abbreviations MAP mean arterial blood pressure - A II Angiotensin II Dedicated to Prof. Dr. W. Kaufmann on the occasion of his 60^th birthday     

Sodium chloride as regulator of renal prostaglandin E2 production in patients with essential hypertension

Summary The effect of dietary sodium intake (5 days' low salt, 4 days' high salt) on 24-h urinary prostaglandin E₂ (PGE₂) and prostaglandin F₂ (PGF₂) excretion, blood pressure (BP), and plasma renin activity (PRA) was evaluated in 16 patients with essential hypertension. Sodium restriction significantly increased urinary PGE₂ excretion (p<0.05) from 151±76 to 328±94 ng/24 h, while high salt intake reduced renal PGE₂ production to 114±41 ng/24 h (p<0.05). There was a moderate but not significant increase in urinary PGF₂ excretion on the low salt regimen, which was reversed under high salt diet. Systolic and diastolic blood pressure fell from 162±11 to 145±10 mm Hg, i.e., 102±6 to 90±9 mm Hg on low sodium intake (35 mEq/day) and returned to levels close to control after 4 days on a high salt diet (250 mEq/day). Under low salt conditions, PRA increased significantly (p<0.001) from 0.83±0.33 to 2.82±1.12 ng AI/ml/h and fell to 0.45±0.31 ng AI/ml/h on high salt regimen (p<0.001).The results demonstrate that dietary sodium chloride intake modulates renal PGE₂ production in patients with essential hypertension. The depressed PGE₂ production under high salt conditions may play a role in regulation of renal vascular resistance and influence sustainment of chronic hypertensive disease.Supported by Deutsche Forschungsgemeinschaft     

Cardiovascular reactivity in a simulated job interview: The role of gender role self-concept

This study investigated the relation of gender role self-concept (G-SC) to cardiovascular and emotional reactions to an ecologically relevant stressor in a sample of graduating male and female university students. Thirty-seven men and 37 women completed the Personal Attribute Questionnaire and worked on four tasks designed to reflect common features of a job interview. Blood pressure and heart rate were measured at baseline, during, and after each task; subjective stress was measured at baseline and after each task. Subjective and objective stress scores were averaged across tasks and analyzed by sex and G-SC (i.e., instrumentality, expressiveness). Results indicated that women as a group demonstrated greater emotional reactivity, but did not differ in their physiological reactions when compared to men. Regardless of sex, participants' instrumentality scores contributed significantly to the variation in subjective stress response: those scoring high on instrumentality reported less stress, but evidenced greater blood pressure reactivity than those scoring low on instrumentality. These results suggest that gender roles, particularly an instrumental self-concept, may play an important role in both subjective and objective reactions to an ecologically relevant stressor.     

Ventilatory responses in patients with essential hypertension.

We investigated the ventilatory responses to hypoxia and hypercapnia in patients with essential hypertension (HT) as compared with healthy subjects (NV). Further, to evaluate the contribution of the peripheral chemoreceptors to ventilatory response, we used a withdrawal test. Hypoxic ventilatory drive (HVR) was measured as the parameter A denoting the shape of VI (inspiratory minute ventilation)-PETO2 (end-tidal PO2) curve which was calculated by the empirical equation: VI = V0 + A/(PETO2-32). Hypercapnic ventilatory drive (HCVR) was measured as the parameter S denoting the shape of the VI-PETCO2 (end-tidal PCO2) relation which was calculated by the empirical equation: VI = S(PETCO2-B). There were no significant differences in the parameters of HVR and HCVR between NV and HT. A positive correlation between A/BSA and S/BSA was found to be significant in NV (r = 0.873, p less than 0.05). Conversely, there was no significant correlation between A/BSA and S/BSA (r = 0.547) in HT. On the other hand, the withdrawal responses (delta VI/BSA and % delta VI:delta VI/VI x 100%) were obtained from the magnitude of depression in ventilation caused by two breaths of O2 in hypoxic hypercapnia. In the withdrawal responses, delta VI/BSA and % delta VI in HT were significantly higher than those in NV. A/BSA significantly correlated with delta VI/BSA (NV, r = 0.684, p less than 0.05; HT, r = 0.648, p less than 0.05) in both NV and HT. However, delta VI/BSA in HT tended to be higher than that in NV, under the same value of A/BSA. These results suggested that the peripheral chemoreceptor activity was augmented in HT.     

Dynamics of reactivity of mesenteric microvessels in rats with experimental renal and hormonal hypertension

Reactivity of mesenteric arterioles 10–30 in diameter to application of histamine (100–500 g) adrenalin, and noradrenalin (1–10 g) was studied in rats with experimental renal and hormonal hypertension. The sensitivity of the microvessels to the vasoactive substances was shown to vary with the stage of development of experimental hypertension.Laboratory of General Pathophysiology and Experimental Therapy, Institute of General Pathology and Pathological Physiology, Academy of Medical Sciences of the USSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR A. M. Chernukh.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 81, No. 2, pp. 150–152, February, 1976.     

Remission of essential hypertension after renal transplantation

Six patients in whom "essential hypertension" led to nephrosclerosis and kidney failure received kidney transplants from normotensive donors. After an average follow-up of 4.5 years, all were normotensive and had evidence of reversal of hypertensive damage to the heart and retinal vessels. These six patients, all of whom were black, and six control subjects matched for age, sex, and race were admitted to the General Clinical Research Center for 11 days for observation of their blood pressure and their responses to salt deprivation and salt loading. Mean arterial pressure (+/- S.E.M.) among the patients who had previously had essential hypertension was similar to that of the normal controls (92 +/- 1.9 vs. 94 +/- 3.9; P not significant), and both groups had similar responses to salt deprivation and salt loading. Thus, essential hypertension in human beings is shown to be similar to the hypertension seen in spontaneously hypertensive rats in that both can be corrected by transplantation of a kidney from a normotensive donor. This observation supports the concept of the primary of the kidney in causing essential hypertension.     

Abnormal endothelium-dependent vascular relaxation in patients with essential hypertension

BACKGROUND. Endothelium regulates vascular tone by influencing the contractile activity of vascular smooth muscle. This regulatory effect of the endothelium on blood vessels has been shown to be impaired in atherosclerotic arteries in humans and animals and in animal models of hypertension. METHODS. To determine whether patients with essential hypertension have an endothelium-dependent abnormality in vascular relaxation, we studied the response of the forearm vasculature to acetylcholine (an endothelium-dependent vasodilator) and sodium nitroprusside (a direct dilator of smooth muscle) in 18 hypertensive patients (mean age [+/- SD], 50.7 +/- 10 years; 10 men and 8 women) two weeks after the withdrawal of antihypertensive medications and in 18 normal controls (mean age, 49.9 +/- 9; 9 men and 9 women). The drugs were infused at increasing concentrations into the brachial artery, and the response in forearm blood flow was measured by strain-gauge plethysmography. RESULTS. The basal forearm blood flow was similar in the patients and controls (mean +/- SD, 3.4 +/- 1.3 and 3.7 +/- 0.8 ml per minute per 100 ml of forearm tissue, respectively; P not significant). The responses of blood flow and vascular resistance to acetylcholine were significantly reduced in the hypertensive patients (P less than 0.0001); maximal forearm flow was 9.1 +/- 5 ml per minute per 100 ml in the patients and 20.0 +/- 8 ml per minute per 100 ml in the controls (P less than 0.0002). However, there were no significant differences between groups in the responses of blood flow and vascular resistance to sodium nitroprusside. Because the vasodilator effect of acetylcholine might also be due to presynaptic inhibition of the release of norepinephrine by adrenergic nerve terminals, the effect of acetylcholine was assessed during phentolamine-induced alpha-adrenergic blockade. Under these conditions, it was also evident that the responses to acetylcholine were significantly blunted in the hypertensive patients (P less than 0.03). CONCLUSIONS. Endothelium-mediated vasodilation is impaired in patients with essential hypertension. This defect may play an important part in the functional abnormalities of resistance vessels that are observed in hypertensive patients.     

Beta-adrenergic blockade in diuretic-treated patients with essential hypertension.

The influence of beta-adrenergic blockade (160 mg per day of propranolol for four weeks) on plasma renin activity, plasma volume, and arterial pressure was explored in 20 patients with essential hypertension with hyper-reninemia from long-term diuretic therapy. In 15 of these patients renin activity remained elevated (range, 3.1 to 23.0 ng per milliliter). Plasma volume was unchanged in eight, increased in 11 and reduced in one. In 17 subjects mean arterial pressure decreased by more than 10 mm Hg, but these impressive reductions could not be explained by quantitative changes in either renin activity (r equals 0.1) or plasma volume (r equals 0.1). These data suggest that suppression of plasma renin activity by beta-adrenergic blockade is not attainable during diuretic therapy and is not the major factor responsible for the antihypertensive action of propranolol.     

Efficiency and safety of ACE-inhibiting imidapril in patients with essential hypertension

In a survey including 2224 patients with essential hypertension we investigated efficacy and tolerability of the new ACE-inhibitor Imidapril. Mean blood pressure at baseline was 172 +/- 19/98 +/- 10 mmHg. Treatment with Imidapril 5-20 mg once daily caused a decrease in BP by 21 +/- 17/11 +/- 10 mmHg (p < 0.01/0.01). Systolic BP was reduced by > 15 mmHg in 71% diastolic BP by > 10 mmHg in 64% of patients. 29% of patients achieved the treatment goal of a blood pressure < or = 140/90 within an average of 26 days. Imidapril decreased pulse-pressure (one of the most important risk markers in hypertension) by 18% (74 +/- 17 to 61 +/- 11 mmHg, p < 0.01). ACE-inhibitor related adverse effects (cough, vertigo, headache, pruritus, tachycardia, orthostatic dysregulation or nausea) were observed in 38 patients (< 2%). Efficacy of treatment was graded by the physician in charge of the patient care by means of a questionnaire. Gradings were excellent or good in 96% of patients, moderate in 3% and poor in < 1%. In summary, the effects of Imidapril on blood pressure were comparable to those of other ACE-inhibitors. However, the frequency of adverse effects was low and similar to that of angiotensin-II-antagonists.     

Cardiovascular reactivity and mental stress-induced myocardial ischemia in patients with coronary artery disease

This report evaluates the relationships of hemodynamic reactivity and determinants of myocardial oxygen demand to myocardial ischemia during mental stress in coronary artery disease patients. Thirty-nine patients and 12 controls were studied by radionuclide ventriculography during three mental tasks (arithmetic, Stroop task, and simulated public speaking). Patients were subdivided into three groups based on the severity of ischemic wall motion responses to the mental stressors. Results revealed that systolic blood pressure (SBP) levels during the mental tasks and SBP reactivity (increases) to stress were highest for the severely ischemic group, lowest for controls, with the mild-moderate ischemic and nonischemic patients in between. Severely ischemic patients started out with lower double product (heart rate x SBP) levels, and reached higher levels during the Stroop and speech tasks. There were no reliable group effects for diastolic blood pressure, heart rate, or left ventricular end-diastolic volumes. Among severely ischemic patients, the most potent task in eliciting ischemia (the speech) was associated with higher cardiovascular levels and elicited greater heart rate, double product, and ventricular volume responses. The present data indicate a relationship between cardiovascular levels and reactivity and the magnitude of ischemia induced by mental stress.     

Effects of education and relaxation training with essential hypertension patients

Thirty subjects with essential hypertension were assigned randomly to either a no treatment control, education, or education with relaxation training group. Independent blood pressure recordings were collected by medical staff at pretest, posttest, and 8-week follow-up. Results suggest a significant interaction between treatment and time for the dependent physiological measure, systolic blood pressure. During the pretest to follow-up period, the control group averaged a 5.9 mm. Hg. increase, the education with relaxation group an 8.8 mm. Hg. decrease, and the education group a 14.9 mm. Hg. decrease in systolic blood pressure. There was no significant difference in group means for diastolic blood pressure within groups over time. As measured at follow-up, education appeared more effective in reducing systolic blood pressure than education with relaxation training. More than one-third of subjects associated unpleasant side effects with their antihypertensive medication. Almost all treatment subjects rated the education and relaxation as helpful for understanding and managing their hypertension.     

Biofeedback of baroreflex sensitivity in patients with mild essential hypertension

An attempt was made to reduce blood pressure by increasing the baroreflex sensitivity (BRS) via biofeedback. Six patients with mild essential hypertension and 5 normotensive participants were studied during 8 biofeedback sessions. Each session consisted of 5 trials, 5 min each. The first and the last trials served as baselines of heart rate, blood pressure, respiration, and BRS. During the3 middle trials the BRS was calculated online using the sequencing technique. The resulting value was used as a visual analogue feedback signal. Participants were asked to increase BRS. The mean BRS was 8.3 [ms/mmHg] for the hypertensive patients and 12.2 [ms/mmHg] for the normotensive participants. During biofeedback trials as well as across sessions neither the hypertensive nor the normotensive group showed a statistically significant increase of BRS, only heart rate variability increased significantly. Contrary to expectation blood pressure increased in both groups. One hypertensive subject made significant progress during the training by performing valsalva maneuvers. The data show that BRS is reduced in hypertensive subjects. The increase of the heart rate variability could be a sign of the activation of the baroreflex although the BRS itself did not increase. Despite the successful technical and organizational im plementation of this biofeedback approach, it was not effective to systematically reduce blood pressure. A further development in the direction of guiding the patient to use the valsalva breathing pattern and/or a prolonged duration of the biofeedback training might be promising.