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Biomedical subjects

R Kolloch

Publications and source records attributed to R Kolloch.

At least 55 records · Page 3Linked to original sources
PubMed1986

Persistent hemodynamic and clinical improvement after captopril in patients with pulmonary hypertension.

Ten patients with primary or secondary pulmonary hypertension who had normal left ventricular function (group I) and nine patients with pulmonary hypertension in response to impaired left ventricular function (group II) were given captopril. At peak effect (1.5 hours after administration) pulmonary vascular resistance fell from 935 to 717 dyn X s X cm-5 in group I and from 554 to 355 dyn X s X cm-5 in group II in association with a decrease in pulmonary arterial pressure by 8 and 12 mmHg, respectively (p less than 0.01). Systemic vascular resistance declined by 26 and 29 per cent, and cardiac index increased by 17 and 20 per cent, respectively (p less than 0.01). On re-catheterization four to 15 months later, seven chronically treated patients (five of group I; two of group II) showed additional reductions in pulmonary vascular resistance (25 per cent) and pulmonary arterial pressure (20 per cent), whereas systemic hemodynamics had almost reached pre-treatment values. All patients reported symptomatic improvement. The hemodynamic changes did not correlate with concomitant alterations in circulating renin or angiotensin II levels. These data suggest that captopril can produce sustained hemodynamic and clinical benefits in patients with pulmonary hypertension of various causes and may be useful for the chronic treatment of this disorder.

Adolescent↗
PubMed1985

Hemodynamic, renal, and hormonal responses to changes in dietary potassium in normotensive and hypertensive man: long-term antihypertensive effect of potassium supplementation in essential hypertension.

The hemodynamic, hormonal, and renal responses to alterations in dietary potassium were studied in normotensive and hypertensive subjects. In a short-term study, nine normotensive and nine hypertensive young men received a normal diet and low potassium, high potassium, and high potassium/low sodium diets for 1 week, each. The long-term effect of potassium supplementation (normal diet plus 96 mmol KC1/d for 8 weeks) was evaluated in 17 patients with essential hypertension. Blood pressure did not change significantly during short-term alterations of potassium intake but decreased during long-term supplementation (from 152.2 +/- 3.5/99.6 +/- 1.9 mm Hg to 137.4 +/- 2.9/89.1 +/- 1.4 mm Hg). High dietary potassium induced a significant but transient natriuresis. Plasma potassium concentration was increased during long- but not during short-term high potassium intake. In contrast to plasma renin activity (PRA) and aldosterone, urinary kallikrein was consistently stimulated during long-term potassium supplementation. The plasma concentrations of adrenaline and noradrenaline were significantly higher in hypertensive than in normotensive subjects and were not markedly altered by the dietary changes. It is concluded that long- but not short-term potassium supplementation lowers blood pressure in patients with essential hypertension. The antihypertensive effect may be mediated by potassium-induced natriuresis, by a stimulation of Na-K-ATPase secondary to increased plasma potassium levels, and/or by a modulation of the renin-angiotensin-aldosterone, kallikrein-kinin, and sympathetic nervous systems.

Adult↗
PubMed1985

Blood pressure, heart rate and A-V conduction responses to nicardipine in hypertensive patients receiving atenolol.

The antihypertensive effect of the combined use of the new calcium channel blocker nicardipine and atenolol was assessed in a double-blind, placebo-controlled trial involving twenty hypertensive patients. Atenolol 100 mg once daily was given to all patients. In addition, either placebo or nicardipine, in increasing doses (5-20 mg three times daily), was allocated randomly to the patients. Compared with placebo, nicardipine had an additional dose-dependent, blood-pressure-lowering effect in the hypertensive patients who had been pretreated with atenolol. An increase in the heart rate was not observed, suggesting that atenolol prevented reflex activation of sympathetic nerve tone caused by the vasodilating properties of nicardipine. The combination of both atenolol and nicardipine was well tolerated by all patients; side effects were minor and did not cause discontinuation of the treatment. No effects on A-V conduction were observed. It is concluded that the combined administration of nicardipine and atenolol is a useful treatment for hypertension that is well accepted by the patients.

Adult↗
PubMed1985

Cyclic Cushing's syndrome combined with cortisol suppressible, dexamethasone non-suppressible ACTH secretion: a new variant of Cushing's syndrome.

A 55 year old woman with an unusual form of Cushing's disease was studied. During several periods (periods lasting up to 84 days) evidence of cortisol hypersecretion with cycles occurring every 6 days was found. Suppression of plasma cortisol through orally administered dexamethasone (up to 32 mg per day) could not be achieved either during periods of cyclic cortisol hypersecretion or during apparent remission with normal cortisol secretion. Marked suppression of plasma ACTH was measured in response to an iv infusion of 50 mg cortisol over a period of 55 min whereas a similar test with 2 mg dexamethasone (iv bolus) did not suppress ACTH secretion. Transsphenoidal exploration of the sella revealed a tumour surrounding the anterior pituitary. Examination of the pituitary showed a few tiny tumour structures embedded in normal tissue which could not be removed, when the tumour was resected selectively under preservation of normal appearing tissue. Post-operatively, clinical and chemical remission (normal response to 1 mg dexamethasone) was observed for about 4 months. Thereafter, cortisol hypersecretion occurred again necessitating bilateral adrenalectomy. Our results are compatible with the assumption that normal hypothalamic-pituitary-adrenal suppressibility with cortisol, but not with dexamethasone, was caused by the loss of feedback receptors for dexamethasone in the presence of cortisol receptors in the cells which secrete ACTH or CRF. The combination of cyclic hypercortisolism with dexamethasone non-suppressible Cushing's syndrome has not been reported before and thus represents a new variant of Cushing's syndrome.

Adrenocorticotropic Hormone↗
PubMed1985

Dissociation between kallikrein and aldosterone in Cushing's disease with periodic hormonogenesis.

It has been suggested that the renal kallikrein-kinin system is dependent on mineralocorticoid activity. This hypothesis was studied in a patient with cyclic Cushing's syndrome combined with cortisol suppressible, dexamethasone non-suppressible ACTH secretion. The 24-h urinary excretions of sodium, potassium, cortisol, active and inactive kallikrein, aldosterone, and prostaglandin E2 (PGE2) were studied during normal and excessive cortisol secretion and after bilateral adrenalectomy. Kallikrein, PGE2 and potassium rose during cortisol overproduction while aldosterone and sodium decreased. Kallikrein, PGE2 and potassium were positively related to cortisol excretion, whereas urinary aldosterone and sodium showed a negative relationship to cortisol. Kallikrein was inversely related to aldosterone. Excretion of inactive kallikrein followed closely the changes of active kallikrein. During cortisol excess, as in our patient, the mineralocorticoid activity of cortisol will exceed that of aldosterone. This suggests that the alterations in kallikrein, aldosterone and PGE2 during cortisol excess in the present study were due to the mineralocorticoid potency of the steroid.

Adrenalectomy↗
PubMed1985

The influence of food intake on pharmacodynamics and plasma concentration of captopril.

The influence of food intake on the acute haemodynamic and humoral effects of captopril has been investigated. Eighteen patients with mild-to-moderate essential hypertension (diastolic blood pressure 95-115 mmHg) were treated in a randomized crossover study with a single oral dose of 25 mg captopril after 2 weeks of placebo. They were randomized to receive captopril either 1 h before or together with a standardized breakfast. Blood pressure, heart rate and plasma concentrations of angiotensin converting enzyme (ACE), angiotensin II (ANG II) and captopril were measured before and every 30 min up to 4 h after drug administration. Angiotensin converting enzyme was significantly more suppressed and plasma concentrations of captopril were significantly higher when the drug was given in the fasting patients. However, there was no significant difference in blood pressure reduction whether captopril was administered in the fasting patients or together with food. The results indicate that the antihypertensive efficacy of captopril is not markedly affected when the drug is administered with food.

Adult↗
PubMed1984

Effect of denervation on the leucine-enkephalin content of the adrenal gland of spontaneously hypertensive rats (SHRSP).

Enkephalins are known to inhibit the release of catecholamines from sympathetic nerve endings. Thus a difference in their turnover rate between SHRSP and normotensive rats (WKY) could contribute to the altered sympathetic activity in SHRSP. One week after denervation which inhibits release of leucine-enkephalin (L-ENK), but not synthesis and processing of the L-ENK precursor, L-ENK increased with the same relative extent in both strains of rats, starting from a lower basal concentration in 7 weeks old SHRSP. In adult rats there was no difference between SHRSP and WKY before and after denervation respectively. It is concluded that the lower content of L-ENK in young SHRSP is caused by an increased release.

Adrenal Glands↗
PubMed1983

Converting enzyme activity and essential hypertension.

Serum ACE-activity was studied in 27 young patients with uncomplicated essential hypertension. The possible importance of an increase in ACE for the pathogenesis of essential hypertension was evaluated by comparing the ACE levels to PRA, the plasma concentrations of angiotensin II and to the blood pressure lowering effect of captopril. Mean ACE-activity was slightly but significantly elevated in the hypertensive patients when compared to 28 normotensive control subjects. ACE-activity was not correlated to PRA, angiotensin II or the decrease in blood pressure following captopril. It is concluded that the increase in ACE-activity in essential hypertension is not of pathophysiological or clinical significance.

Administration, Oral↗
PubMed1982

Interactions of diuretics with the renal kallikrein-kinin and prostaglandin systems.

The renal kallikrein-kinin system may participate in the diuretic, natriuretic and antihypertensive effect of diuretics. This possibility was investigated by studying the influence of hydrochlorothiazide on blood pressure and urinary kallikrein excretion in patients with essential hypertension. Furthermore, the effect of kallikrein-blockade and prostaglandin-synthesis inhibition on the acute furosemide-induced changes of diuresis, natriuresis, GFR and renal plasma flow were studied in normotensive subjects. Thiazide treatment normalized the reduced kallikrein excretion of the hypertensive patients. The fall in mean arterial blood pressure was significantly correlated with the increase in urinary kallikrein excretion. In the normotensive subjects aprotinin-induced kallikrein inhibition failed to alter the acute response to furosemide, whereas indomethacin attenuated the diuretic and natriuretic effect of furosemide. The combination of indomethacin and aprotinin had a greater suppressive effect on plasma renin activity than indomethacin alone, suggesting a participation of kallikrein in renin release. An increase in the activity of the renal kallikrein-kinin system may contribute to the long-term antihypertensive effect of thiazide diuretics but it does not seem to be involved in the acute renal responses to furosemide.

Adult↗
PubMed1982

Long-term efficacy of angiotensin-converting-enzyme inhibition with captopril in mild-to-moderate essential hypertension.

1 Thirty-one patients with mild-to-moderate essential hypertension were treated with captopril for 30 months. 2 Captopril effectively lowered raised blood pressure in hypertensive patients with high, low, and normal renin concentrations. There was no significant change in heart rates. Captopril alone normalised blood pressure (diastolic pressure below 95 mm Hg) in 11 patients. In the other patients the addition of hydrochlorothiazide produced a further hypotensive effect. Blood pressure control could be maintained without any signs of tachyphylaxis. 3 Plasma concentrations of aldosterone and angiotensin II were significantly lower after 30 months of therapy than pretreatment values whether captopril was associated with diuretics or not. No relevant symptomatic or biochemical adverse reactions were observed. 4 These data establish the long-term potential of captopril for outpatient therapy in mild-to-moderate forms of essential hypertension.

Adult↗
PubMed1981

Evidence for participation of kinins in the antihypertensive effect of converting enzyme inhibition.

In low- and normal- renin hypertensive patients, but not in high-renin patients, the acute antihypertensive response to the angiotensin-converting enzyme (ACE) inhibitor captopril was completely blocked by aprotinin-induced kallikrein inhibition. Blood pressure reduction with long-term ACE inhibition could be overcome only in part by aprotinin. It is proposed that in low- and normal-renin hypertension the vasodepressor effect of acute ACE inhibition is mainly due to kinin accumulation. Conversely, in high-renin patients a fall in angiotensin II concentration accounts for the hypotensive response to captopril. From the pressor effect of aprotinin in chronically captopril treated patients it appears that kinins are also involved in the blood pressure reduction with long-term ACE inhibition. The finding that ACE inhibition and kallikrein blockade produced predictable and opposite effects on blood pressure suggests broad participation of changes in depressor kinin production in the control of vascular tone in essential hypertension.

Adult↗
PubMed1980

A radioenzymatic assay for free and conjugated normetanephrine and octopamine excretion in man.

A radioenzymatic method for the measurement of free and conjugated normetanephrine (NMN) and octopamine (OCT) is described for human urine. The assay is based on the conversion of NMN or OCT to radiolabeled metanephrine (MN) or synephrine (SYN) by phenylethanolamine-N-methyl transferase (PNMT), using tritium-labeled S-adenosyl-methionine [3H]SAM as methyl donor. Thin-layer chromatographic separation yields an assay of high specificity. The sensitivity of the assay is 5 and 2.5 pg of NMN or OCT, respectively. The normal value of free and conjugated NMN was found to be 23 +/- 13 and 102 +/- 49 ng/mg creatinine. Four patients with pheochromocytoma had highly increased levels of free and conjugated NMN. The urinary excretions of free and total octopamine were 5.7 +/- 2.8 and 34.8 +/- 16.6 ng/mg of creatinine, respectively, in normal patients.

Adult↗
PubMed1980

Decreased urinary kallikrein activity and elevated blood pressure normalized by orally applied kallikrein in essential hypertension.

Urinary kallikrein excretion was significantly lower in patients with essential hypertension (0.48 +/- 0.05 EU/24 h) than in normotensive controls (1.26 +/- 0.14 EU/24 h). Oral administration of hog pancreatic kallikrein normalized decreased urinary kallikrein and reduced arterial pressure. The treatment-induced rise in urinary kallikrein was due to an enhanced release of endogenous enzyme, as was determined by radioimmunoassay. It is proposed that in the hypertensive patients the low urinary kallikrein excretion reflects a defect in renal kallikrein formation which is normalized by oral kallikrein. The hypotensive action of oral kallikrein as well as its stimulating effects on renal kallikrein release suggest that the kallikrein-kinin system is involved in blood pressure regulation and that impaired renal kallikrein activity may be a factor in the maintenance of essential hypertension.

Adult↗