PubMed Health⌕ Search

Biomedical subjects

A Distler

Publications and source records attributed to A Distler.

At least 217 records · Page 12Linked to original sources
PubMed1978

Plasma noradrenaline and the pressor action of exogenous noradrenaline in normotensive subjects and patients with essential hypertension.

1. An inverse relationship was found between plasma noradrenaline and reactivity to exogenous noradrenaline in normotensive subjects. 2. The relationship between plasma noradrenaline and reactivity was distrubed in age-matched patients with essential hypertension. 3. A multiple-regression analysis showed a highly significant correlation between adrenergic activity and reactivity to noradrenaline and the mean arterial blood pressure level (r = 0.91). The results suggest that adrenergic activity and pressor response to noradrenaline combined are important determinants of arterial blood pressure. 4. An inverse relationship could also be demonstrated between plasma renin activity and reactivity to exogenous angiotensin II. No difference was observed between normotensive and hypertensive subjects.

Adult↗
PubMed1978

Antihypertensive effect of N-amidino-2-(2,6-dichlorophenyl) acetamide hydrochloride. A double-blind cross-over trial versus clonidine.

Sixteen patients with essential hypertension were treated with N-Amidino-2-(2,6-dichlorophenyl) acetamide hydrochloride (BS 100--141) and clonidine for five weeks each in a double-blind cross-over trial. Dosage ranged from 2 to 6 mg BS 100--141 and from 0.3 to 0.9 mg clonidine daily in two or three divided doses. Both compounds caused a significant and comparable fall in blood pressure. Patients whose blood pressure was not reduced to normal levels by 2 to 3 mg BS 100--141 daily did not respond better to an increase in the dose. Dry mouth and constipation occurred about equally frequently with both agents, but sedation and orthostatic circulatory effects were considerably more frequent with clonidine. Rebound hypertension likewise occurred in five patients following clonidine withdrawal as opposed to no patient after BS 100-141.

Adolescent↗
PubMed1977

[Hemodynamic effects of sar1-ala8-angiotensin in patients with renovascular hypertension (author's transl)].

In 7 hypertensive patients with renal artery stenosis and in 1 patient with hypertension and unilateral pyelonephritic nephrophthisi the influence of the angiotensin II antagonist, saralasin on systemic hemodynamics was studied. In the patients with normal renin infusion of saralasin produced an increase in total peripheral resistance, in patients with elevated renin a decrease in peripheral resistance was observed. In 3 patients who had extremely high renin levels while under sodium saralasin produced a dangerous drop in blood pressure concomitant with a marked decrease in cardiac output and in central venous pressure, heart rate remained unchanged or increased just slightly. The findings suggest that in patients with high plasma renin peripheral resistance, venous tone, venous retrun, and cardiac output are to a large extent controlled by circulating angiotensin II.

Adult↗
PubMed1977

[Sympathetic responsiveness and antihypertensive effect of beta-receptor blockade in essential hypertension: the effect of atenolol (author's transl)].

Plasmin noradrenaline concentration after bicycle exercise (200 W for 2 min), compared with base line concentration, was used as an index of sympathetic responsiveness in patients with essential hypertension. Atenolol (JCI 66082, a "cardioselective" beta-blocker) was given in a daily dose of 200 mg to 16 patients for five weeks. This caused a decrease in supine blood pressure of 37/23 and, on standing, of 36/25 mm Hg compared with the placebo period. There was a significant correlation between the ratio of the increase in plasma noradrenaline concentration on exercise over its base line concentration and the subsequent fall in mean arterial pressure (r=0.840; P less than 0.001). There was a less significant correlation between plasma renin concentration and subsequent decrease in mean arterial pressure (r=0.542; P less than 0.05). Administrations of atenolol caused a rise in plasma noradrenaline both on lying and after exercise (P less than 0.0125), and a fall in plasma renin concentration (P less than 0.01). The results suggest that the antihypertensive effect of atenolol is related to the responsiveness of the sympathetic nervous sytem. Adrenergic activity is apparently an important determinant of blood pressure response to beta-blockade.

Adrenergic beta-Antagonists↗
PubMed1977

Low renin hypertension.

Low renin hypertension probably does not represent a clinical entity. In many patients with low renin hypertension blood pressure is normalized by treatment with diuretics only; in these patients a (genetic?) sensitivity to salt might play a predominant role in the pathogenesis of hypertension and renin suppression. In another group of patients renin suppression appears to be secondary to the hypertensive process. This is indicated by the observation that prevalence of low renin hypertension increases with age and that it is more frequent in advanced stages of hypertension. Also a diminished sympathetic tone might play a part in the renin unresponsiveness. Finally, although no positive evidence was found, the possibility cannot be excluded that, at least in some cases, a mineralocorticoid other than aldosterone is involved. Neither in normotensive subjects nor in hypertensive patients, both with normal and with low plasma renin was a correlation between plasma renin concentration and plasma aldosterone concentration following stimulation by upright posture found. More detailed studies will be necessary to clarify the relationship between the renin-angiotensin system and aldosterone secretion during upright posture, in particular in patients with low renin hypertension.

Adrenal Cortex↗
PubMed1976

[Studies on the pH-dependence, inhibition and reactivation of angiotension II-amide splitting enzymes in human erythrocytes (author's transl)].

Aminopeptidase activity of three fractions of human erythrocytes (membranes free of hemoglobin; hemolysate free of membranes; enzyme protein fraction made free of hemoglobin by DEAE-cellulose) was measured by a NADH dependent optical test using asparaginyl1-angiotension II-amide as substrate. 1. From the enzyme protein fraction 6 subfractions were obtained by (NH4)2SO4 precipitation. By measuring enzyme kinetics at three different pH-values (pH 5,0; 7,0; 8,0) with and without addition of the effectors Na2EDTA and Ca++ the existence of 6 different enzymes could be demonstrated. 2. The aminopeptidase activity of the hemolysate made free of membranes could be inhibited by diisopropylfluorphosphate and p-chloromercuribenzoate at three different pH-values (pH 5,0; 6,5; 7,0; 8,0 and 6,5; 7,0; 8,0 respectively). 3. A reduction of enzymatic activity of 20% was found after incubation at 37degreesC for two hours.

Calcium↗
PubMed1976

[Diurnal profiles of plasma aldosterone, cortisol, renin, angiotensinogen and angiotensinases in normal subjects (author's transl)].

Plasma cortisol and renin were estimated in 1 h intervals, plasma aldosterone, angiotensinogen and angiotensinases in 3 h intervals over periods of 24 h in six normal volunteers (age 20-26) under control conditions and subsequently under suppression of ACTH release by dexamethasone. Highest cortisol levels were found around 7 a.m., minimum levels between 9 p.m. and 1 a.m. Dexamethasone reduced cortisol to constantly low concentrations. Aldosterone was highest around 4 a.m. under control conditions and under dexamethasone, and showed lowest concentrations between 4 and 10 p.m. There were no significant differences between mean aldosterone concentrations at corresponding time points of the control and the dexamethasone period. Similar to aldosterone, renen showed peak values around 4 a.m. All mean values at corresponding time points between 7 a.m. and 11 p.m. and the 24 hour mean values of each subject were significantly increased under the influence of dexamethasone. No evidence could be achieved for the existence of circadian rhythms of angiotensinogen and angiotensinases. Dexamethasone did not cause significant changes of these parameters.

Adrenocorticotropic Hormone↗
PubMed1975

[Circulatory reflexes in primary aldosteronism (author's transl)].

1. In 7 patients with hypertension, aldosteronism, and low plasma renin (6 patients with a solitary adrenal adenoma, 1 patient with bilateral adrenal hyperplasia) circulatory reflexes (Valsalva's maneuver, head-up tilt and cold pressure test) were examined. Furthermore, the reactivity to the pressor action of tyramine and norepinephrine was determined. For comparison 10 patients with essential hypertension were studied. 2. In 4 of the 7 patients with primary aldosteronism no overshoot following Valsalva's maneuver could be observed. Compared to the patients with essential hypertension the mean overshoot in the patients with primary aldosteronism was significantly reduced. The decrease in blood pressure during head-up tilt was significantly more pronounced in the patients with primary aldosteronism. However, both groups did not differ in their reaction to the cold pressure test. In the patients with primary aldosteronism responsiveness to tyramine was significantly reduced compared to the patients with essential hypertension. No significant difference was observed in the reactivity to norepinephrine between both groups studied. 3. The results point towards a disturbance of the sympathetic nervous system in patients with primary aldosteronism.

Adult↗
PubMed1975

[Metabolism of angiotensin II during angiotensin infusion and following sodium depletion].

1. Angiotensin II (A II) and angiotensin (3--8)-hexapeptide (H) were measured by radioimmunoassay in arterial and venous plasma before and during infusion of angiotensin II-amide in five normotensive subjects, both in sodium-replete and sodium-depleted states. The separation of the oligopeptides was performed by thin layer chromatography. 2. Before sodium-depletion the mean ratio of arterial to venous A II was 1.14+/-0.11:1, corresponding to an A II-extraction of approximately 12% during a single forearm passage. Infusion of A II-amide increased extraction of A II. The mean ratio of arterial to venous A II increased to 1.68+/-0.3:1, corresponding to an extraction of approximately 39% when 8 ng-min-1-kg-1 were infused. 3. Sodium depletion increased arterial and venous concentrations of A II and H. During infusion of angiotensin II-amide the arterial and venous concentrations of A II and H increased approximately parallel to the concentrations before sodium depletion. The extraction of A II did not differ significantly in both states. 4. The augmented extraction extraction of A II observed during infusion of angiotensin II-amide suggest an overproportional increase of the metabolism of A II under the latter condition. Sodium depletion, however, does not appear to cause a percent change in A II metabolism.

Adult↗