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Biomedical subjects

R Kolloch

Publications and source records attributed to R Kolloch.

At least 73 records · Page 4Linked to original sources
PubMed1979

Increased catecholamine excretion after labetalol therapy: a spurious effect of drug metabolites.

Patients with essential hypertension were treated for four weeks with the alpha- and beta-adreno-receptor blocking agent labetalol. Urinary excretion of total catecholamines, metanephrine plus normetanephrine and vanillylmandelic acid was measured with various methods before and during treatment. An unidentified substance interfering with the fluorimetric method for catecholamines and the photometric assay for metanephrines caused falsely high values of those substances. Using appropriate methodology no changes of total catecholamines, metanephrine plus normetanephrine and vanillylmandelic acid excretion were found after labetalol therapy. Our findings are important in preventing errors in the diagnosis of pheochromocytoma as well as in the evaluation of the effects of labetalol on the sympathetic nervous system in man.

Catecholamines↗
PubMed1979

Increased plasma and urinary normetanephrine in young patients with primary hypertension.

1. Normetanephrine was measured in small samples of plasma and urine of hypertensive patients and normal volunteers (age 20-60 years) by a specific radioenzymatic assay with bovine adrenal phenylethanolamine N-methyltransferase and tritiated S-adenosylmethionine. 2. Noradrenaline was measured simultaneously in plasma and urine. 3. Plasma normetanephrine and noradrenaline concentrations varied in direct proportion to activation or suppression of sympathetic nerve function. 4. Both plasma and urinary normetanephrine concentrations were elevated in patients with phaeochromocytoma. 5. Plasma normetanephrine concentrations were related to plasma noradrenaline concentrations of hypertensive subjects. 6. Plasma normetanephrine and noradrenaline concentrations and urinary normetanephrine excretion rates were increased in some young patients with primary hypertension, suggesting that sympathetic nerve hyperactivity is a pathogenic factor in these patients.

Adrenal Glands↗
PubMed1978

[Effect of a chronic alpha adrenergic receptor blockade on basal secretion of renin in essential hypertension].

To investigate the effect of chronic alpha-adrenergic receptor blockade on renin release, plasma renin activity (PRA) was determined overnight at short intervals in 9 patients with essential hypertension before and after 7 days medication with phenoxybenzamine (20 mg orally/day). Inhibition of basal (supine) renin secretion in response to alpha-adrenergic receptor blockade was more apparent in patients with elevated PRA (n = 3) than in those with normal PRA. On the other hand, patients with low PRA (n = 2) even showed an increase in renin release. In addition, night-day variations with secretory episodes in PRA were blunted during drug administration. It is suggested that alpha-adrenergic receptor blockade inhibits renin secretion distal to its blockade of specific adrenergic receptors. However, the increase in renin release during phenoxybenzamine observed in patients with low PRA indicates that the responsiveness of renin secretion to stimulatory effects (most probably induced by the lowered blood pressure in our patients) remained intact during alpha-adrenergic receptor blockade.

Adrenergic alpha-Antagonists↗
PubMed1978

Enhanced hypothalamic noradrenaline biosynthesis in Goldblatt I renovascular hypertension.

1. Hypertension was induced in rats by renal artery clip with the contralateral kidney removed (Goldblatt I) or left intact (Goldblatt II). 2. Plasma noradrenaline was increased 62% in the Goldblatt I animals after 3 weeks. 3. Hypothalamic tyrosine hydroxylase and dopamine beta-hydroxylase activities, and the concentration of noradrenaline were increased in the Goldblatt I animals after 3 weeks. 4. Enhanced hypothalamic noradrenaline synthesis may be a pathogenic factor in Goldblatt I renovascular hypertension.

Animals↗
PubMed1977

[Aldosterone and renin in liver cirrhosis with ascites].

Supine plasma aldosterone and plasma renin activity were determined in patients with cirrhosis of the liver and ascites (n = 10). Most of the patients initially showed an increase in plasma aldosterone and plasma renin activity. However, values within the normal range were observed (plasma aldosterone, n = 3; plasma renin activity, n = 4). In the ascitic fluid renin activity could not be detected, whereas aldosterone concentrations correlated significantly with the respective plasma levels (r = 0.8, p less than 0.01). During therapy with spironolactone alone (n =2) or in combination with furosemide (n = 4), diuresis and natriuresis showed no correlation with changes in plasma aldosterone and/or plasma renin activity. Our results suggest that other factors than renin and aldosterone secretion may be important in the formation of ascites in patients with cirrhosis of the liver. In addition, the inverse correlation between mean arterial blood pressure and plasma renin activity (r = -0.65, p less than 0.05) found in our patients supports the assumption that the increase in renin secretion is probably induced by changes in (renal) hemodynamics.

Aldosterone↗
PubMed1977

[Raised plasma-prolactin levels in essential hypertension: index of reduced hypothalamic dopaminergic activity (author's transl)].

Serial measurements of plasma-prolactin concentration (HPr) and plasma-renin activity (PRA) at 30-min intervals were made in 19 male patients with essential hypertension and in 8 normotensive subjects. HPr was markedly higher in the hypertensive patients than in the normotensive controls. Patients with reduced plasma-renin activity and only slightly elevated HPr-levels showed lower urinary sodium excretion, but a more pronouced 24-h natriuretic response to i.v. furosemide than patients with normal renin and very high HPr-levels. Six patients were treated with the dopaminergic agonist bromocriptine. The drug induced a significant blood pressure reduction in five patients and normalised pressure in two patients. The data do not indicate a role for prolactin in sustaining hypertension via renal salt retaining mechanisms. It is suggested that the raised HPr-levels represent an index of altered central nervous function, characterized by reduced hypothalamic activity. The blood pressure-lowering effect of the dopaminergic agonist bromocriptine fits with the hypothesis that reduced hypothalamic dopaminergic activity might be a factor in the pathogenesis of essential hypertension.

Adult↗
PubMed1977

Hyperprolactinaemia and antihypertensive effect of bromocriptine in essential hypertension. Identification of abnormal central dopamine control.

Plasma-prolactin concentration was up to four times higher in male patients with essential hypertension than in normotensive controls. Oral administration of bromocriptine, a dopaminergic agonist, suppressed plasma-prolactin and lowered arterial pressure. It is proposed that in the hypertensive patients the raised prolactin levels reflect a defect in central dopamine control which is normalised by bromocriptine. The antihypertensive effect of bromocriptine suggests that the dopaminergic system is involved in blood-pressure regulation and that reduced central dopaminergic activity may be a factor in the maintenance of essential hypertension.

Adult↗
PubMed1976

Renin, aldosterone and arterial pressure responses to acute beta-adrenergic receptor blockage in hypertensive patients.

The effect of acute (intravenous) beta-adrenergic blockade with propranolol or pindolol on arterial pressure (BP), plasma renin activity (PRA), and plasma concentration of aldosterone (PA) was evaluated in 20 essential hypertensive men. BP, PRA and PA were determined during continuous recumbency over-night (8 p.m. to 6 a.m.) every 30 min. Two groups of patients were observed. Patients of group 1 exhibited a characteristic day-night rhythm of PRA with low values before midnight and large increases early in the morning. Conversely, no rhythm and very low PRA values were observed in patients of group II. BP was higher in group II than in group I. In group I following intravenous propranolol or pindolol, BP fell within minutes and levels as well as rhythms of PRA were converted to those of group II without treatment. In group II day-night profiles of PRA and BP remained unchanged. Rhythm and concentration of PA in the two groups were not influenced by either drug. In 4 patients of group I infusion of angiotensin II inhibitor did not lower BP. The observations suggest that in the two groups dissimilarities in rhythms of PRA as well as in BP responses to beta-blockade may reflect differences in neuro-adrenergic tone.

Adult↗
PubMed1976

Acute and long-term studies of the mechanisms of action of beta-blocking drugs in lowering blood pressure.

The antihypertensive effect of intravenous (acute) and oral (long-term) beta-adrenergic blockade with propranolol or pindolol was evaluated in 46 male patients with either borderline (group I; 23 patients) or sustained (group II; 23 patients) essential hypertension. Arterial pressure, plasma renin activity and plasma concentration of aldosterone were determined during continuous recumbency overnight every 30 minutes before and after treatment. Patients of group I exhibited a marked variation of their recumbent plasma renin activity with relatively low values before midnight and large increases early in the morning. In contrast, low plasma renin activity values and only minimal fluctuations in renin were observed in patients of group II. Plasma renin activity had a consistent relationship with blood pressure both after acute (r = 0.79) and long-term (r = 0.4) beta-blockade. In four patients of group I, who had high plasma renin activity and had responded to intravenous propranolol, infusion of angiotensin II inhibitor did not lower pressure. In group I following beta-blockade, day-night profiles of renin were similar to those observed in group II before treatment. Thus in this latter subgroup, low renin profiles might reflect reduced beta-adrenergic activity. Acute as well as long-term beta-blockade consistently eliminated the day-night rhythm of plasma renin activity, but it did not change rhythm of plasma concentration of aldosterone. Plasma concentration of aldosterone was lower in group II but appeared to be inappropriately high relative to renin levels. These observations suggest that in hypertensive patients classified according to blood pressure and recumbent plasma renin activity profiles a significant relationship exists between changes in plasma renin activity and arterial pressure responses. Thus, patients with high renin levels respond better to treatment than patients with low renin levels. We conclude that in the patients studied, sympathetic nervous system activity mainly determined renin levels as well as antihypertensive effectiveness of the beta-blocking drugs.

Administration, Oral↗
PubMed1976

Differential effects of acute and chronic beta-adrenoreceptor blockade on blood pressure and the renin-angiotensin-aldosterone system in essential hypertension.

1. Serial measurements of plasma renin activity (PRA), plasma aldosterone concentration (PA) and blood pressure were performed overnight in patients with borderline (group 1) and sustained essential hypertension (group 2) before and after acute and chronic administration of either propranolol or pindolol. 2. Group 1 patients exhibited a typical rhythm of recumbent PRA with low values before midnight and large increases early in the morning. 3. In contrast, no rhythm and very low PRA values were observed in patients of group 2. Blood pressure was higher in group 2 than in group 1. There was a significant correlation between the hyporeninaemic and hypotensive effect of either acute (r = 0-79) or chronic (r = 0.4) beta-receptor blockade. 4. In group 1, after beta-receptor blockade the day-night profile of renin was similar to that observed in group 2 before treatment. Thus, in this latter subgroup, low-renin profiles might reflect reduced beta-adrenoreceptor activity. 5. Plasma aldosterone was lower in group 2 but appeared to be inappropriately high relative to renin. 6. The data suggest that in hypertensive patients classified according to their blood pressure and recumbent PRA profiles a significant relationship exists between changes in PRA and arterial pressure. Thus patients with high PRA respond better to treatment than patients with low renin. We conclude that in the patients studied sympathetic nervous system activity mainly determined renin values as well as anti-hypertensive effectiveness of the beta-blocking drugs.

Adult↗
PubMed1975

[Effect of chronic beta-adrenergic blockade on blood pressure and release of renin, aldosterone and cortisol in essential hypertension (author's transl)].

Blood pressure (BP), plasma renin activity (PRA) and plasma concentration of aldosterone (PA) and cortisol (PC) were determined in essential hypertensive patients before and after beta-adrenergic blockade with propranolol and prindolol. Serial measurements of PRA, PA and PC at 30 min intervals (8 p.m. to 6 a.m.) were performed in 8 patients. Administration of propranolol (50 mg three times daily) over a period of 4 weeks was followed by a significant reduction in BP, PRA and PA. PC remained unaltered. The pattern of rhythmic secretion of renin was abolished whereas that of aldosterone persisted at a lower level. Prindolol (10 mg three times daily) had a similar effect on BP as propranolol but failed to lower PRA and PA. Rhythmic secretion of renin was also markedly altered with prindolol in the absence of any change in rhythmicity of PA and PC. The hypotensive action of prindolol was not mediated via inhibition of renin release. The dissociation between PRA and PA rhythmicity indicates that during beta-adrenergic blockade diurnal rhythm of aldosterone secretion is not regulated by the renin-angiotensin-system. Rhythmicity of PC was normal, indicating that also ACTH-secretion was unaltered. Thus, under beta-blockade unchanged diurnal rhythm of aldosterone may be due to normal ACTH-secretion.

Adrenergic beta-Antagonists↗
PubMed1975

[Infusion therapy in disorders of the sodium and water balance].

Water depletion, water in excess and sodium depletion are the most important disturbance of sodium-water balance. Water, electrolytes and acid-base balance have always to be considered in their complex correlation because of their various interrdependency. The restoration of balance concerning imput and output is considered as a basic principle of any intravenous therapy.

Acid-Base Equilibrium↗