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Biomedical subjects

H Witzgall

Publications and source records attributed to H Witzgall.

At least 37 records · Page 2Linked to original sources
PubMed1982

Rapid increase of mineralocorticoids after furosemide in low-renin essential hypertension: evidence for 18-hydroxycorticosterone to be a better marker than aldosterone.

The response of plasma renin activity (PRA), plasma aldosterone, 18-hydroxycorticosterone (18-OH-B), 18-hydroxydeoxycorticosterone (18-OH-DOC) and corticosterone to furosemide were compared in 20 normal control subjects, 16 patients with normal-renin essential hypertension (NREH) and 12 patients with low-renin essential hypertension (LREH). Analyses were performed before medication, and 15 min (supine) and 120 min (active orthostasis) after IV administration of 40 mg furosemide. In normotensive subjects PRA increased 15 min after administration of furosemide from 0.8 +/- 0.4 ng AI/ml . h (SD) to 3.4 +/- 1.4 (P less than 0.01), plasma aldosterone from 109 +/- 28 pg/ml to 139 +/- 40 (less than 0.01) and 18-OH-B from 199 +/- 90 to 279 +/- 85 (P less than 0.01). In patients with NREH, PRA increased significantly less (P less than 0.01) and no significant increase of plasma aldosterone or 18-OH-B was found. PRA of patients with LREH (0.2 +/- 0.1 ng AI/ml . h) remained practically unchanged 15 min after furosemide administration, but in contrast to NREH aldosterone increased from 111 +/- 37 to 160 +/- 66 (P less than 0.05) and 18-OH-B from 162 +/- 101 to 261 +/- 71 pg/ml (P less than 0.01). The relative increase in plasma 18-OH-B was significantly greater in patients with LREH than in patients with NREH. The plasma levels of aldosterone and 18-OH-B 120 min after furosemide administration were significantly higher in normotensive subjects than in either hypertensive group (P less than 0.01). Corticosterone and 18-OH-DOC levels were the same in all investigated groups and increased significantly (P less than 0.01) only at 120 min after furosemide erone and 18-OH-B 120 min after furosemide administration were significantly higher in normotensive subjects than in either hypertensive group (P less than 0.01). Corticosterone and 18-OH-DOC levels were the same in all investigated groups and increased significantly (P less than 0.01) only at 120 min after furosemide erone and 18-OH-B 120 min after furosemide administration were significantly higher in normotensive subjects than in either hypertensive group (P less than 0.01). Corticosterone and 18-OH-DOC levels were the same in all investigated groups and increased significantly (P less than 0.01) only at 120 min after furosemide administration combined with active orthostasis. In summary, our results support the concept that sensitivity of the mineralocorticoid-producing cells is enhanced in patients with LREH. Postfurosemide 18-OH-B seems to be a better marker of this phenomenon than aldosterone.

18-Hydroxycorticosterone↗
PubMed1982

Arachidonic acid metabolites, hypertension and arteriosclerosis.

The level of arterial blood pressure is set by complete interactions of several mechanisms which influence both blood flow in and resistance of the vascular system. An imbalance favouring elevation of vascular resistance or extracellular volume will result in hypertension. Such alterations may include increased activity of the sympathetic nervous system, of the renin-angiotensin system, or excessive secretion of mineralocorticoids. Of equal importance may be a reduced activity of blood pressure-lowering factors such as prostaglandins and the kallikrein-kinin system. This paper describes the possible significance of prostaglandins in the pathophysiology of hypertension and in degenerative vascular disease, based on their involvement in the control of vascular resistance, renal regulation of extracellular volume and platelet-vessel wall interactions. An abnormality in the biosyn-thesis of certain prostaglandin endoperoxide metabolites may lead to hypertension even without an increase in the activity of the classic blood-pressure-elevating systems. The contribution of prostaglandins for the development of hypertension and degenerative vascular disease may be based on an inherent abnormality of the prostaglandin system, as well as on the effects of major risk factors such as dietary intake of sodium and fat on prostaglandin synthesis. Specific blockade or stimulation of distinct biosynthetic pathways leading to antagonistically acting prostaglandins and nutritional manipulation of precursor fatty acids should lead to a better understanding of the pathomechanisms involved and may offer new strategies for therapy or prevention of these cardiovascular disorders.

Arachidonic Acids↗
PubMed1982

Acute haemodynamic and hormonal effects of captopril are diminished by indomethacin.

1. The acute haemodynamic and hormonal effects of 100 mg of captopril (SQ 14.225) orally were tested in twelve healthy men in the sodium replete state before and after indomethacin pretreatment. 2. Without indomethacin, mean arterial blood pressure was reduced at 30 and 60 min after captopril (P less than 0.02). Heart rate did not change during the whole experiment. Although plasma renin activity (PRA) increased (P less than 0.002), plasma and urinary aldosterone and plasma 18-hydroxycorticosterone (18-OH-B) decreased after captopril (P less than 0.02). Prostaglandin (PG) E2, sodium and potassium excretion rates remained constant after captopril. 3. Under indomethacin pretreatment, the fall in mean arterial blood pressure was less than without indomethacin at 30 and 60 min after captopril (P less than 0.05). Heart rate was constantly lower than without indomethacin during the whole experiment (P less than 0.05). Indomethacin pretreatment decreased basal PGE2 excretion (P less than 0.02) and baseline PRA as well as the increase in PRA after captopril (P less than 0.05). Control mineralocorticoid levels were significantly lower than without indomethacin. In indomethacin-pretreated subjects, aldosterone did not further decrease after captopril, and 18-OH-B fell only slightly. 4. Without indomethacin pretreatment a significant, positive correlation was found between PRA values before captopril and the maximum decrease of mean arterial blood pressure after captopril. Under indomethacin pretreatment this correlation was no longer demonstrable. The results suggest that prostaglandins may contribute to the haemodynamic and hormonal actions of captopril.

18-Hydroxycorticosterone↗
PubMed1981

A simultaneous radioimmunoassay for aldosterone and its precursors: human plasma levels following the inhibition of converting enzyme, before and after blockade of prostaglandin biosynthesis.

Plasma aldosterone, 18-hydroxycorticosterone, corticosterone, 18-hydroxydeoxycorticosterone, and deoxycorticosterone were determined in 15 healthy male volunteers (34 +/- 2 years) following the inhibition of converting enzyme with captopril (SQ 14.225), either with or without indomethacin pretreatment. These studies were performed with the aid of a radioimmunological method for the simultaneous determination of the steroids from 1.0 ml of plasma. The procedure involves one extraction and one chromatographic step. Highly sensitive and specific rabbit antisera were raised for all steroids. Precision and accuracy are shown to be equivalent to those of single steroid radioimmunoassays. Without indomethacin pretreatment a constant and significant fall in aldosterone and 18-hydroxycorticosterone plasma levels was obtained after captopril. 18-Hydroxydeoxycorticosterone and corticosterone did not change after inhibition of converting enzyme. Under indomethacin pretreatment all basal steroid levels were significantly reduced. After captopril, aldosterone did not change and 18-hydroxycorticosterone showed a smaller decrease than without indomethacin. 18-Hydroxydeoxycorticosterone and corticosterone increased significantly 1 1/2 hour after captopril. We conclude that indomethacin significantly reduces basal mineralocorticoid production of adrenal zona glomerulosa and fasciculata. Furthermore, the effect of captopril on aldosterone and 18-hydroxycorticosterone is abolished or diminished by inhibition of prostaglandin biosynthesis, but indomethacin does not prevent an augmented secretion of 18-hydroxydeoxycorticosterone and corticosterone.

18-Hydroxycorticosterone↗
PubMed1980

Paper chromatographic systems for the separation of aldosterone, 18-hydroxycorticosterone, 18-hydroxydeoxycorticosterone, corticosterone and deoxycorticosterone.

Regulation of aldosterone (Aldo) biosynthesis is still open to controversy. The direct sites of action of the known stimulants (e.g., potassium, angiotensin II, adrenocorticotropin) on the different enzymes involved in the biochemical pathway of Aldo are not yet clearly defined. We have developed a radioimmunoassay for the determination of Aldo, 18-hydroxycorticosterone (18OH-B), 18-hydroxydeoxycorticosterone (18OH-DOC), corticosterone (B) and deoxycorticosterone (DOC) in plasma. The aim was to evaluate a single chromatographic system for the separation of these five mineralocorticoids before radioimmunoassay.

18-Hydroxycorticosterone↗
PubMed1980

Relief from malignant hypertension by treatment with captopril in a patient on maintenance hemodialysis.

A patient with end-stage renal disease due to malignant hypertension is described. Hypertension was resistant to hemodialysis. The orally active inhibitor of angiotensin-converting enzyme captopril (SQ 14.255; 2-D-methyl-3-mercaptopropanoyl-L-protein) dramatically lowered the elevated blood pressure both under ambulatory and dialysis conditions. No side effects were observed after 6 months' treatment. The effect of captopril could be described as a "biochemical nephrectomy".

Adult↗
PubMed1979

Aldosterone 18-glucuronide excretion determined with and without chromatography in human hypertensives.

24 h-urine excretion of aldosterone-18-glucuronide was determined with and without preceding paper chromatography in patients with essential hypertension (n = 50). Radioimmunoassay was performed with a highly specific antibody against aldosterone. Urine specimens determined without chromatography gave significantly higher values than aliquots which were estimated at the same time with chromatography. A highly significant correlation was found between the two methods (r = 0.91, p less than 0.0001). Without chromatography, mean over estimation in samples with concentrations in the low and middle range was on average 32 and 24% respectively, whereas aldosterone concentrations in the upper range showed a 14% over estimation. The RIA procedure for aldosterone without chromatography as here described is suitable for hypertension screening programmes to exclude known forms of primary hyperaldosteronism in which elevated aldosterone excretion rates have to be differentiated from values lying within the normal range.

Aldosterone↗
PubMed1978

[Treatment of essential hypertension with a combination of propranolol, spironolactone-thiabutazide and dihydralazine (author's transl)].

In 61 out-patients with essential hypertension, grade I or II, propranolol was administered alone in increasing doses (3 x 40 mg/d or 3 x 80 mg/d) or, if there was insufficient response, with a double or triple combination consisting additionally of spironolactone (50 mg/d)-thiabutazide (5 mg/d) and dihydralazine (3 x 25 mg/d). This treatment schedule achieved normal pressures in 51 patients, in 22 on 40 mg, in 7 on 80 mg propranolol, in 16 after the addition of the diuretic, and in 6 with the triple combination. Four patients had to be excluded from the study because they developed either marked bradycardia or anxiety states or paraesthesias after propranolol (3 x 40 mg/d). On chronic beta-adrenergic blockade the serum potassium level increased slightly, but remained within normal limits. The initial value of plasma-renin activity was highest in the group of those who responded to the propranolol treatment.

Anxiety↗
PubMed1978

[Pathogenetic, pathophysiological and biochemical aspects of essential hypertension (author's transl)].

Hereditary and environmental factors are involved in the pathogenesis of essential hypertension. Obesity, salt intake and stress are predominant among the environmental influences. Autonomous nervous dysfunction, increased contractility of vascular smooth muscle cells and impaired renal handling of sodium are major abnormalities in essential hypertension. At present it cannot be decided if alterations in the activities of systemic or renal hormonal systems reflect primary defects or adaptive changes in the regulation of blood pressure. In any case the kidney is regarded to have a key position in the long term increase of blood pressure in essential hypertension. Recent studies in essential hypertensive patients suggest that renin release decreases as renal vascular resistance increases. Studies from our laboratory have shown that renal prostaglandins are intrinsic to the renin release mechanism from the kidney. Additionally, there is evidence that renal prostaglandin synthesis is disturbed in essential hypertension, either primarily or secondarily, leading to unresponsive renin secretion. Further studies on the interrelationships of other hormonal systems and on hormone-receptor interactions in the vascular wall are necessary to delineate more precisely the mechanisms which are operative in the pathogenesis and manifestation of essential hypertension.

Adrenal Cortex Hormones↗
PubMed1977

[Behaviour of plasma renin activity during long-term treatment with propranolol (author's transl)].

17 patients (40 +/- 9 years) with essential hypertension were included in the study. A monotherapy of 120, 160 or 240 mg propranolol per day was administered orally according to the antihypertensive effect. Four weeks after treatment, blood pressure and heart rate showed a statistically significant decrease and remained unchanged over a period of six months. Plasma renin activity decreased significantly from 5.7 +/- 6.3 ng/ml/h at the beginning of the study to 1.8 +/- 1.3 ng/ml/h after 4 weeks. 5 months later however plasma renin activity increased again to 5.0 +/- 0.9 ng/ml/h. The difference was statistically significant. From 17 patients 7 (41%) had lower levels of plasma renin activity after 6 months treatment when compared with pretreatment values. In only 3 patients (18%) was plasma renin activity lower after 6 months than after four weeks. We conclude that the increase in plasma renin activity is a reactive mechanism to the reduced blood pressure under long-term conditions. The decrease of plasma renin activity in short-term treatment of essential hypertension is not a mechanism responsible for the antihypertensive effect of propranolol during long-term treatment.

Adult↗
PubMed1976

[The influence of saralasine on blood pressure and renal function in Bartter's syndrome and decompensated hepatic cirrhosis (author's transl)].

Infusion of the angiotensin-II-antagonist saralasine led in one patient with Bartter's syndrome and one patient with decompensated hepatic cirrhosis, both of whom had a markedly raised plasma renin activity, to a fall in systolic and diastolic blood pressure. The results indicate that in normotensive patients a raised angiotensin II concentration in blood is haemodynamically important for the level of blood pressure if plasma renin activity is raised. In normotensives with normal plasma renin activity saralasine in the usual dosage (4.2 mug/kg-min) does not influence the blood pressure.

Adult↗