[Renin and noradrenaline in wistar rats of various ages].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to H M Brecht.
Explore the source record for details and available documents.
15 patients (4 females, 11 males, 21 to 55-year old) with mild to moderate essential hypertension (EH) were treated with placebo for two weeks and thereafter with increasing doses of prindolol (15 to 38 mg/day in the mean) and kept on a mean maintenance dosage of 32 mg/day for an average of 16 weeks in all. Blood pressure (BP), heart rate und plasma noradrenaline (PNA) concentrations were measured under standardized conditions (supine, standing, walking) at the end of two weeks on placebo and after the experimental treatment period. The results were compared to those of a group of 15 normotensive untreated control subjects (NS): after an average of 16 weeks on prindolol BP fell from 163/113 mm Hg to 129/91 mm Hg in the mean. PNA levels in EH before prindolol were significantly higher than in NS (supine: 272 +/- 22.0 ng/l (mean +/- SEM) vs. 135 +/- 15.1 ng/l, standing: 448 +/- 31.9 ng/l vs. 359 +/- 18.4 ng/l, walking: 388 +/- 22.5 ng/l vs. 234 +/- 22.1 ng/l). In EH chronic administration of prindolol led to a significant decrease in PNA concentrations under all the three test conditions to levels which did not differ significantly any more from those derived from NS. The adrenergic response to upright posture reflected in the percentage increase in PNA was significantly less in EH before prindolol when compared to the percentage increase in NS. On prindolol the adrenergic response was not abolidhed, yet it tended to approach the values found in NS. Before prindolol under resting conditions diastolic BP correlated closely with the corresponding PNA levels (p less than 0.01, r = 0.66, n = 15). This correlation could not be reestablished after prindolol treatment. The decrease in PNA after long-term treatment with prindolol was not correlated to the fall in blood pressure. The decrease in PNA indicates a lower activity of the sympathetic nervous system which may contribute to the antihypertensive effect of prindolol.
1. Plasma noradrenaline was measured in fifty-nine patients with mild to severe essential hypertension and in fifteen normotensive control subjects under basal and orthostatic conditions. 2. In patients with essential hypertension mean plasma noradrenaline concentrations were significantly higher than in control subjects under basal and orthostatic conditions. 3. In patients with essential hypertension basal diastolic blood pressure correlated closely with the corresponding plasma noradrenaline concentrations. 4. Long-term treatment with prindolol of patients with essential hypertension led to a significant fall in diastolic and systolic blood pressure and heart rate and to a significant decrease in plasma noradrenaline concentrations under basal and orthostatic conditions. 5. The adrenergic response to upright posture, reflected by an increase in plasma noradrenaline, was not abolished by prindolol. 6. It is concluded that the anti-hypertensive effect of prindolol in patients with essential hypertension is at least partially mediated by a decrease of sympathetic nervous activity.
1. The effect of long-term treatment with prindolol on blood pressure, total body potassium (Kt), exchangeable sodium (Nae) and plasma renin activity was investigated in twelve patients with essential hypertension. 2. Systolic and diastolic pressures were significantly reduced from 164/112 to 127/90 mmHg under basal conditions. 3. Before treatment Nae in patients with essential hypertension was significantly higher than in normotensive individuals. After an average of 16 weeks on prindolol Nae in patients with essential hypertension was significantly decreased, despite an average increased in body weight of 2 kg in the patients. 4. In contrast to the decrease in Nae, Kt was found to be significantly increased after long-term treatment with prindolol. Kt values of patients before and after prindolol, however, did not differ significantly from the corresponding sex- and age-dependent normal values. 5. Plasma renin activity was slightly diminished under basal and orthostatic conditions; the stimulatory effect orthostatis was not abolished but reduced by prindolol. 6. It is suggested that the changes in sodium balance contribute to the anti-hypertensive effect of prindolol in patients with essential hypertension.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The chronic administration of prindolol in patients with essential hypertension resulted in the following: 1) a significant decrease in blood pressure and heart rate (with only the exception of the unchanged diastolic blood pressure after the stimulus of the seven-minute standing period), 2) a significant decrease of plasma noradrenaline concentrativn at rest and under orthostatic conditions, 3) a significant decrease of PRC at rest and an even more pronounced suppression of PRA after the stimulus of upright posture, 4)a significant decrease in total exchangeable sodium and 5) a concomitant significant increase in total body potassium even with an increase in body weight. These findings are not subject to easy interpretation. In particular, we cannot conclude which of the changed parameters plays the initial role in lowering blood pressure. A working hypothesis might presume that beta blocking agents inhibit central and/or peripheral sympathetic nervous activity. The results reduction in plasma renin concentration would in turn lead to a drop in aldosterone secretion rate indicated by the increase in potassium and decrease in sodiummour data would support such a sequence of events.
Plasma concentrations of noradrenaline (NA), adrenaline (A) and renin (R) were measured in 29 regular haemodialysis patients (RHP) [13 normotensive, 10 hypertensive, 6 binephrectomised] and in 15 healthy control subjects (C) under various physiological conditions: supine-standing-walking. RHP had significant higher plasma levels of noradrenaline and adrenaline in the mean than C. All RHP responded to passive orthostasis with a significant increase in diastolic blood pressure, heart rate and plasma NA. In contrast to C, plasma NA did not drop after two hours of active orthostasis. Hypertensive RHP had significant higher plasma concentrations of R and A than normotensives. It is concluded that the sympathetic nervous system (SNS) plays a minor role in hypertensive blood pressure regulation of RHP. The adequate response to passive orthostasis in RHP with regard to diastolic blood pressure, heart rate and plasma NA indicates and intact function of the SNS under this condition. Hypertension in RHP not controllable by salt and volume depletion can be attributed to elevated levels of R, which in turn may stimulate adrenaline release from the adrenals. The mechanisms responsible for the elevated levels of circulating catecholamines remain unclear: an inhibition of re-uptake, disturbances in enzymatic metabolism or/and abolished renal clearance are suggested.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
A renin-like enzyme is present in brain tissue and is independent of kidney and plasma renin. In the presence of homologous substrate it forms angiotensin. Administration of aldosterone significantly decreases this angiotensinforming enzyme activity, while administration of progesterone markedly enhances it.
Explore the source record for details and available documents.