[Silent myocardial ischemia].
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Angina Pectoris↗
Biomedical subjects
K Boehringer
Publications and source records attributed to K Boehringer.
Disturbed noradrenergic blood pressure control in normotensive members of hypertensive families.
The possible influence of a family history of hypertension on some variables of adrenergic blood pressure regulation was assessed. Blood pressure, heart rate, plasma renin activity, adrenaline and noradrenaline concentrations, and plasma or urinary electrolyte estimations did not differ significantly between two groups of normotensive subjects matched for age and sex with and without a family history of hypertension. Compared with subjects without a family history, however, an appreciably decreased pressor dose of infused noradrenaline, a distinct shift to the left in the relation between noradrenaline induced changes in mean arterial pressure and concomitant plasma noradrenaline concentrations, and an enhanced pressor response to given increases in plasma noradrenaline concentrations occurred in the group with a family history. These findings suggest that an imbalance between cardiovascular noradrenaline responsiveness and circulating noradrenaline is a common familial disturbance which could possibly predispose to the development of essential hypertension.
Adult↗
Relationship between plasma aldosterone and angiotensin II before and after noradrenergic inhibition in normal subjects and patients with mild essential hypertension.
The responsiveness of plasma aldosterone to the infusion of angiotensin II at dose rates of 2, 4, and 10 ng/kg X min was assessed in 11 normal subjects and 13 patients with mild essential hypertension before and after 4 weeks of treatment with the sympatholytic agent debrisoquine. Debrisoquine treatment caused a significant (P less than 0.01) decrease in circulating norepinephrine (-45%), but did not modify plasma levels of angiotensin II, renin, aldosterone, or epinephrine or the metabolism of sodium or potassium. In normal subjects, debrisoquine caused a significant shift to the left (P less than 0.05) of the correlation relating plasma aldosterone to plasma angiotensin II levels. In patients with essential hypertension, the aldosterone-angiotensin II interrelationship was not modified. These findings suggest that the sympathetic nervous system exerts an inhibitory influence on aldosterone responsiveness to angiotensin II in normal man, and that this physiological interaction is impaired in patients with essential hypertension.
Adult↗
Acute effects of combined vasodilation and beta-adrenoceptor blockade with prizidilol on renal function.
1 The effects of a single oral dose of 600 mg of prizidilol on renal function were studied 5 to 6 h after dosing in six normal subjects and eight patients with essential hypertension. 2 Mean arterial blood pressure was reduced to 92% of the control value in normal subjects and to 75% in hypertensive patients. Heart rate increased slightly. 3 In normal subjects, effective renal plasma flow was increased to 107% of control values while glomerular filtration rate (83%), filtration fraction (79%), sodium (84%) and potassium (50%) clearances were significantly decreased. 4 In hypertensive subjects, effective renal plasma flow was increased to 120% of control values, while glomerular filtration rate (67%), filtration fraction (57%), sodium (27%) and potassium (72%) clearances were significantly decreased. 5 Plasma noradrenaline increased significantly in normal subjects (150%) and in patients (173%). Plasma renin activity, aldosterone and epinephrine levels did not change consistently. 6 The results indicate that the acute effects of prizidilol on blood pressure and renal function are more marked in hypertensive than in normotensive subjects. Prizidilol increases renal plasma flow like hydralazine and depresses glomerular filtration rate and fractional sodium excretion like endralazine. In addition to the fall in arterial pressure, efferent vasodilation and/or a specific effect on the glomerular ultrafiltration coefficient Kf may account for the striking decrease in filtration fraction.
Adrenergic beta-Antagonists↗
Serum lipoproteins in patients with mild renal disease treated with the diuretic muzolimine.
Patients with renal functional impairment are prone to develop hypertension and hyperlipidemia, and both abnormalities tend to occur already at an early stage of kidney disease. In 18 patients with mild renal disease (glomerular filtration rate 65 +/- 5 ml/min) and hypertension (mean blood pressure 126 +/- 4 mm Hg), the effect of six weeks of treatment with the loop-diuretic muzolimine on serum lipoproteins was assessed. Compared to placebo values, the diuretic significantly increased serum low-density lipoprotein cholesterol (LDL-C) and apoprotein B (+ 18 and 11%, respectively, P less than 0.005) in 13 men or postmenopausal women, but not in 5 premenopausal women. Serum high-density lipoprotein cholesterol (HDL-C), and total triglycerides or lipoprotein triglyceride fractions were not consistently changed in both subgroups. Thus, the ratio LDL-C/HDL-C was increased from 3.2 +/- 0.3 to 3.9 +/- 0.3 (P less than 0.05) in the men or postmenopausal women, while no such tendency occurred in the premenopausal women (4.1 +/- 0.6 to 3.7 +/- 0.6). Changes in serum LDL-C were not associated with hemoconcentration or alterations in carbohydrate metabolism and were not related to variations in serum potassium or blood pressure. Increased serum levels of the atherogenic LDL-C fraction during diuretic treatment in men or postmenopausal women with renal disease may represent a potentially undesirable effect, particularly since such patients may tend to have hyperlipidemia in the untreated state.
Female↗
Acute effects of prizidilol on blood pressure, heart rate, catecholamines, renin and aldosterone in essential hypertension.
Prizidilol is a new antihypertensive agent reported to possess combined precapillary vasodilator and betareceptor-blocking properties. To clarify the profile of the acute effects of prizidilol in man, a variable dose study was performed in 8 patients with benign essential hypertension. Blood pressure, heart rate, plasma renin activity, aldosterone, plasma and urinary catecholamines and electrolytes were determined at short intervals before and up to 23 h after oral administration of placebo and prizidilol 150, 300 and 600 mg. The 4 studies were performed at weekly intervals according to a Latin square design. Prizidilol produced dose-dependent decreases in supine and upright blood pressure, with an initial change after about 2 h and maximal effects from 4 to 8 h after drug ingestion. Following a high dose of prizidilol, supine mean blood pressure (average 128 mmHg prior to treatment) was normalised (less than 107 mmHg) from 3 to 7 h and was still below predose level 23 h after ingestion. The only reported side effects were postural dizziness in 2 cases (corresponding to a fall in systolic upright blood pressure to less than 95 mmHg) and headache in one case. A biphasic variation in heart rate and plasma renin activity, with an early drop and a subsequent tendency to a slight rise, was observed after an intermediate or high dose of prizidilol. Plasma norepinephrine levels were increased by a high dose of prizidilol, while plasma epinephrine, aldosterone and plasma and urinary electrolytes were not consistently changed. Prizidilol in a a single oral dose appeared to be a potent antihypertensive agent. The profile of heart rate and plasma renin point to early dominance of beta-blockade followed by appearance of the concomitant vasodilator properties of prizidiol.
Adrenergic beta-Antagonists↗
Comparative evaluation of the new vasodilator carprazidil and minoxidil in the treatment of moderate to severe hypertension.
The efficacy and side effects of the new vasodilator carprazidil and the established vasodilator minoxidil were compared in 18 hypertensive patients inadequately controlled by 2 to 4 conventional drugs; the latter included diuretics, beta-blockers and/or sympatholytics and, in half the cases, vasodilators, such as hydralazine, diazoxide or the postsynaptic alpha-blocker prazosin. The vasodilators were withdrawn and, using a crossover design all patients received carprazidil (mean final dose 88 mg) and minoxidil (20 mg) for an average period of 5 to 6 months. The effects of the 2 agents appeared to be qualitatively and quantitatively similar. Both tended to cause sodium retention and an increase in heart rate, which required an increased dose of diuretic in one third of the cases or of a beta-blocker in a quarter. With this approach mean body weight and blood volume were not altered in the established phase of carprazidil or minoxidil treatment; heart rate and plasma norepinephrine tended to be only minimally increased, plasma renin was slightly increased, and plasma aldosterone and epinephrine were largely unchanged. Supine and upright blood pressure were reduced from initial values of 189/113 and 167/ 113 mm Hg, to 149/95 and 138/95 mm Hg (-18 and - 17%), respectively, during carprazidil, and to 154/95 and 141/96 mm Hg (-17 and - 15%) during minoxidil therapy. Hypertrichosis occurred with both agents in almost all patients, and limits their more prolonged use in females. No adverse side effects on haematological parameters, liver or renal function were observed, nor was antinuclear antibody detected. It is concluded that carprazidil and minoxidil are equivalent vasodilator agents in the treatment of severe hypertension, particularly in males.
Adult↗
Studies on aldosterone responsiveness to angiotensin II during clinical variations in calcium metabolism in normal man.
1. Angiotensin II was infused at stepwise increasing dose rates (2, 4 and 10 pmol min-1 kg-1) in 12 normal subjects. Infusions were performed in the presence of normocalcaemia, mild hypercalcemia induced by concomitant calcium gluconate infusion, and after 2 weeks of treatment with nifedipine. 2. Pre-infusion plasma levels of angiotensin II, renin or aldosterone were not altered by acute mild hypercalcaemia or administration of nifedipine. The angiotensin II-induced increases in plasma aldosterone were also similar under the three study conditions. 3. Variations in calcium metabolism occurring under clinical conditions appear to play a minor role in modulating the angiotensin II-dependent pathway of aldosterone regulation in normal man.
Adult↗
Effects of diuretics alone or in combination with beta-adrenoceptor blockers on serum lipoproteins.
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Adrenergic beta-Antagonists↗
Menopause-dependent plasma lipoprotein alterations in diuretic-treated women.
The effects of chlorthalidone, 100 mg/d given for 6 weeks, on serum lipids and lipoproteins were assessed in 22 premenopausal and 18 postmenopausal women. In the latter, chlorthalidone significantly increased total serum cholesterol (13%, p less than 0.001), low-density-lipoprotein (LDL) cholesterol (21%, p less than 0.001) and apoprotein B (16%, p less than 0.05). In contrast, these values were not altered in the premenopausal group. Levels of LDL cholesterol, high-density-lipoprotein cholesterol, total and very-low-density triglycerides, apoproteins A1 and A2, and plasma volume, plasma glucose, insulin, epinephrine, estradiol, and free fatty acids were unchanged in both groups. Chlorthalidone-induced changes in levels of LDL cholesterol did not correlate significantly with variations in blood pressure, plasma potassium, uric acid, renin, aldosterone, or norepinephrine levels. These findings indicate that the thiazide-like diuretic chlorthalidone increases serum LDL cholesterol in postmenopausal but not in premenopausal women.
Adult↗
Effects of acute mild hypercalcemia or of the calcium antagonist nifedipine on cardiovascular responsiveness to norepinephrine or angiotensin II in normal humans.
Pressor doses of infused norepinephrine (NE) (mean pressure, +20 mm Hg) or angiotensin II (AII) (diastolic pressure, +20 mm Hg) and corresponding blood levels of NE or AII were assessed in 12 young normal subjects under basal conditions (study A), during slow calcium infusion (0.034 mg/kg/min) started 60 min previously (study C), and following 2 weeks of treatment with the Ca antagonist nifedipine, 50 mg/day (study D). Control values of blood pressure, 24-h urinary sodium, plasma NE, epinephrine, AII, and renin activity did not differ among the three studies. Plasma Ca was higher during study C than during studies A and D [10.7 +/- 0.8 (+/- SD) versus 9.1 +/- 0.3 mg/dl; p less than 0.01]. Plasma NE or AII levels obtained during NE or AII infusion as well as the pressor doses of AII were not modified by concomitant Ca infusion or following nifedipine. However, compared with basal conditions, the NE pressor dose tended to be decreased slightly during Ca infusion (106 +/- 71 versus 77 +/- 38 ng/kg/min; difference not significant) and was increased markedly following nifedipine (178 +/- 87 ng/kg/min; p less than 0.05). A control infusion of Ca alone (study B) during 120 min did not modify blood pressure or plasma renin and NE levels. Our observations suggest that in normal humans, inhibition of cellular Ca transport may predominantly affect the noradrenergic control mechanism, whereas angiotensinogenic cardiovascular regulation may be less dependent.
Adult↗
[The effect of hydrochlorothiazide/amiloride alone or in combination with alpha-methyldopa on serum lipoproteins].
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Adult↗
Pressor factors and cardiovascular pressor responsiveness in lean and overweight normal or hypertensive subjects.
Several blood-pressure-regulating factors including exchangeable sodium, blood volume, plasma renin, aldosterone, norepinephrine (NE), and epinephrine (E) levels, urinary catecholamine excretion rates, and cardiovascular responsiveness to infused NE and angiotensin II (AII) were compared among age-matched subgroups of normal subjects (15 with normal weight, 15 with overweight) and patients with essential hypertension (15 with either normal weight, overweight, or obesity). Exchangeable sodium, blood volume, plasma and urinary sodium and potassium, plasma renin, aldosterone and epinephrine levels, and NE or E excretion rates did not differ significantly among the five subgroups. Minimal differences included a slightly higher heart rate in overweight patients than in overweight normal subjects (p less than 0.01) and a tendency for a higher plasma NE in overweight than in normal weight patients. Plasma NE obtained immediately before NE infusion as well as the plasma clearance of NE did not differ among the five subgroups except, however, for a somewhat low NE clearance in obese patients. The NE pressor dose tended to be lower in normal-weight hypertensive than in normal-weight normotensive subjects. No alteration was apparent in overweight or obese hypertensive patients. Pressor responses to AII were similar in the different subgroups. These findings suggest that overweight does not confer a unique aberration in the body sodium-volume state, circulating renin, aldosterone or catecholamines, or cardiovascular responses to NE or AII which result in hypertension.
Adult↗
Calcium and blood pressure regulation in normal and hypertensive subjects.
To elucidate the mechanisms involved in calcium-mediated blood pressure (BP) control, plasma norepinephrine (NE), epinephrine, renin activity, and angiotensin II (AII) levels and the cardiovascular pressor responsiveness to NE and AII were assessed before and during acute mild hypercalcemia or short-term calcium (Ca) inhibition with nifedipine in 20 normal and five borderline hypertensive subjects. In normal subjects, systolic BP and plasma NE and epinephrine concentrations were increased significantly (p less than 0.05) during an acute rise in serum Ca of 3.1 mg/dl (intermediate rate Ca infusion, 0.05 mg/kg/min for 3 hours), but not following an increase of 1 mg/dl (low rate Ca infusion, 0.034 mg/kg/min for 2 hours). In the borderline hypertensive group, low-rate Ca infusion elevating serum Ca by 1 mg/dl was associated with a slight increase in systolic BP (p less than 0.05) and plasma catecholamines. In both groups, the pressor responses to infused NE and AII, and plasma renin and AII levels, were unchanged during mild to moderate hypercalcemia. Nifedipine given for 2 weeks (average dose, 48 mg/d) reduced BP significantly (p less than 0.05) in the borderline hypertensive subjects only and NE pressor responses in both groups (p less than 0.025), but had no significant effect on plasma catecholamines, renin, or AII levels. These findings suggest that the adrenergic BP control mechanism may be more dependent on clinical variations in calcium metabolism than the angiotensin BP regulatory mechanism. Acute hypercalcemia may increase BP at least in part by causing an increase in adrenergic activity without an equivalent decrease in cardiovascular reactivity. Calcium inhibition with nifedipine may modify noradrenergic BP control by lowering the NE pressor reactivity without causing an equivalent increase in adrenergic activity.
Adult↗
Cardiovascular counterregulation during sympathetic inhibition in normal subjects and patients with mild hypertension.
The influence of agents that inhibit sympathetic nerve activity on cardiovascular responsiveness as related to major pressor factors has been unclear. Therefore, these components were evaluated in 11 normal subjects and 13 patients with mild essential hypertension before and after 4 weeks of sympathetic neuron blockade with the agent debrisoquine. In these normal and mildly hypertensive subjects, sympathetic neuron blockade caused approximately similar decreases in urinary and supine or upright plasma norepinephrine (NE) levels (average changes in the two groups, -41% and -45%, respectively; p less than 0.05 to less than 0.005), the chronotropic dose of isoproterenol (-45% and -38%), and the NE pressor dose (-47% and -51%, p less than 0.01), while the relationship between NE-induced changes in blood pressure and concomitant plasma NE concentrations was displaced to the left (p less than 0.01). Supine heart rate was also lowered (-10% and -8%, p less than 0.05). Compared to the orthostatic variations during placebo conditions, mild postural decreases in blood pressure were apparent in both the normal and hypertensive groups (-8% and -7.5%). However, supine blood pressure was unchanged following debrisoquine treatment. Other parameters were also not consistently changed, such as total blood volume, exchangeable body sodium, urinary electrolytes, plasma epinephrine, renin, and angiotensin II (AII) levels, the pressor dose of infused AII, and the relationship between AII-induced changes in blood pressure and plasma AII measured before and during AII infusion. These findings demonstrate that the reduction in sympathetic outflow during sympathetic neuron blockade may elicit a hyperresponsiveness of alpha- and beta-adrenergic receptors that is equal in normal subjects and patients with mild essential hypertension.
Adult↗