Search PubMed⌕ Search

Biomedical subjects

G J Wenting

Publications and source records attributed to G J Wenting.

At least 73 records · Page 4Linked to original sources
PubMed1982

Treatment of hypertension with ketanserin, a new selective 5-HT2 receptor antagonist.

The new selective 5-HT2 receptor blocking agent ketanserin was given in a dose of 10 mg intravenously to 12 patients with essential hypertension. It caused a distinct fall in supine systemic arterial, right atrial, pulmonary artery, and pulmonary capillary "wedge" pressures. Cardiac output, renal blood flow, and glomerular filtration rate showed no persistent changes. Thus 5-HT2 receptor blockade caused dilatation of both resistance and capacitance vessels and of the renal vascular bed. Heart rate and plasma concentrations of renin and noradrenaline rose after ketanserin. These data suggest that 5-HT may have a role in maintaining high blood pressure.

Adult↗
PubMed1982

Recurrence of hypertension in primary aldosteronism after discontinuation of spironolactone. Time course of changes in cardiac output and body fluid volumes.

Hemodynamic mechanisms underlying the hypertensive action of long-standing sodium overload were studied in ten subjects with aldosterone-producing adenoma. Arterial pressure was 129+/-4/91+/-4 mm Hg (mean+/-SEM) during spironolactone treatment, 177+/-5/114+/-3 mm Hg six weeks after the drug had been stopped, and 136+/-4/94+/-3 mm Hg two months after operation. In the six weeks following cessation of spironolactone, cardiac output, stroke volume, blood volume and sodium space were determined at weekly intervals. In each subject the biochemical syndrome of aldosterone-excess had been fully developed in two weeks. The hemodynamic changes in that period were also uniform. Mean arterial pressure in week 2 was increased by 20+/-3% with parallel increments of cardiac output and stroke volume of 22+/-5 and 30+/-6%. Blood volume and sodium space were increased by 11+/-2 and 29+/-4%. The patterns in weeks 2-6 were not uniform. In five subjects (age 33-49 yr) the hypertension was maintained through increased cardiac output; in week 6 it was 34+/-7% above its initial value, and stroke volume and blood volume were 37+/-4 and 16+/-4% above control. In the remaining five subjects (age 50-60 yr) cardiac output, stroke volume and blood volume returned to their initial values, and total peripheral resistance in week 6 was 36+/-13% above control. Sodium space remained expanded in both groups. The measurements after surgery confirmed the existence of the high-flow and high-resistance patterns; there was a decrease in cardiac output in the former group of subjects and a decrease in resistance in the latter. Apparently, increased resistance is not a direct consequence of increased flow. The observed age-related differences in hemodynamic patterns of sodium overload bear some resemblance to essential hypertension where a high-flow state of long duration may precede the ultimate phase of low vascular capacitance and high resistance.

Aldosterone↗
PubMed1981

Haemodynamic profile of captopril treatment in various forms of hypertension.

The effects of captopril 450 mg/day for 4 weeks on blood pressure, heart rate, cardiac output and extracellular fluid volume were compared in severe, often drug-resistant hypertension (n = 23), mild to moderate hypertension associated with renal artery stenosis (n = 10) and mild to moderate essential hypertension (n = 20). Plasma renin in the three groups was 52 +/- 19, 58 +/- 17 and 20 +/- 4 microU/ml (mean +/- SEM), respectively. Blood pressure fell by 18 +/- 4%, 21 +/- 2% and 18 +/- 1%. The pressure drop was mainly due to a fall in peripheral vascular resistance. Addition of the diuretic hydrochlorothiazide (25-100 mg/day) caused a further fall in resistance. Despite the vasodilator effect of captopril, reflex cardiostimulation and reactive fluid retention were not observed. In severe hypertension, captopril alone was more effective in lowering blood pressure than combined diuretic-betablocker-vasodilator therapy. Moreover, cardiac output in these patients was higher and resistance was lower after captopril than during combined treatment. Thus, captopril was capable of normalising the abnormal haemodynamic state in patients with essential hypertension, and in hypertension associated with renal artery stenosis. Despite marked differences in pre-treatment plasma renin, the effects of captopril on systemic haemodynamics were similar in all the patients.

Adult↗
PubMed1980

Captopril affects blood pressure equally in renovascular and essential hypertension and in the fluid-depleted anephric state.

1. The haemodynamic effects of 100 mg of captopril in renovascular hypertension (n = 11), essential hypertension (n = 12) and the anephric state (n = 7) were compared. Brachial artery pressure was measured in all patients, and changes in right atrial pressure, pulmonary artery pressure, pulmonary capillary wedge pressure and cardiac output were followed in renovascular and essential hypertension. Nephrectomized patients were studied before and after fluid withdrawal by ultrafiltration. 2. The pretreatment concentration of active renin in plasma was 100 +/- 24 mu-units/ml (mean +/- SEM) in renovascular hypertension, and 24 +/- 4 mu-units/ml in essential hypertension. In nephrectomized patients pretreatment renin was 1.7 +/- 0.3 mu-units/ml, and renin was unresponsive to withdrawal of 1.8 +/- 0.21 of body fluid. 3. The effects of captopril were maximal after 60-90 min. Mean arterial pressure after 90 min was lowered by 19 +/- 4% in renovascular hypertension, by 17 +/- 4% in essential hypertension and by 16 +/- 3% in fluid-depleted nephrectomized patients. These changes were not significantly different despite the marked differences in renin. Captopril had no effect on arterial pressure in the fluid-replete anephric state. 4. The effects of captopril on cardiac filling pressures and cardiac output in renovascular and essential hypertension were also not different. 5. It is concluded that the antihypertensive action of captopril may be largely independent of circulating renin.

Adult↗
PubMed1979

Evidence for activation of circulating inactive renin by the human kidney.

1. In eight patients with essential hypertension (EHT) and six patients with renovascular hypertension (RVHT) peripheral venous enzymatically active and inactive renin values were followed after acute stimulation of renin release by the vasodilating agent diazoxide (300 mg intravenously). Active renin rose during the first hour after diazoxide and remained high during the following 15 h, but inactive renin fell during the first hour and rose thereafter. Peripheral venous active and inactive renin were not different from arterial values both before and after diazoxide. 2. Sixteen patients with EHT received propranolol, 80 mg, four times a day. Six of them had a first injection of diazoxide the day before propranolol was started and a second one after 10--14 days of propranolol treatment. Peripheral vein active renin was lowered by propranolol, but inactive renin was raised. Both the diazoxide-induced rapid rise of active renin and the fall of inactive renin observed in untreated patients were absent during treatment with propranolol. 3. In four patients with EHT and seven patients with RVHT renal vein sampling was performed before and 30 min after diazoxide. Increased release of active renin from kidneys that were not markedly contracted was associated with a fall of the renal vein to peripheral vein ratio of inactive renin to a value less than one. 4. It is concluded that under certain circumstances stimulated release of active renin is associated with removal of inactive renin from the circulation by the kidney. This may in fact be due to intrarenal transformation of circulating inactive renin into its active counterpart. The findings suggest that a beta-adrenoreceptor might be involved in this activation process.

Diazoxide↗
PubMed1978

Renal release of active and inactive renin in essential and renovascular hypertension.

1. Active and acid-activable inactive renin were measured in renal venous and arterial plasma of 18 patients with essential hypertension (EHT) and 19 patients with renovascular hypertension (RVHT). In seven patients with EHT and in 11 patients with RVHT measurements were made before and 25-35 min after an intravenous injection of 300 mg of diazoxide. 2. Under basal conditions the renal vein to artery ratios for active and inactive renin in EHT ranged from 0.71 to 1.96 and from 0.68 to 1.44 respectively. In 14 patients with RVHT the renal vein to artery ratio for active renin on the affected side was above the range found in EHT and in six of them the renal vein to artery ratio for inactive renin was also elevated. 3. The diazoxide-induced release of active renin from kidneys, which had a stenotic artery but were not seriously contracted, was associated with a fall of the renal vein to artery ratio for inactive renin to a value below 1.00. 4. The results indicate that changes in the release of active and inactive renin do not always run in parallel. The findings are compatible with the hypothesis that circulating inactive renin can be activated in the kidney.

Diazoxide↗
PubMed1978

Sympathetic and parasympathetic components of reflex cardiostimulation during vasodilator treatment of hypertension.

1. Haemodynamic responses to diazoxide (300 mg intravenously) were studied in 15 hypertensive patients before and after chronic beta-adrenoreceptor blockade by 320 mg of propranolol daily. After diazoxide alone, mean arterial pressure and total peripheral resistance were lowered by 24 +/- 3 and 35 +/- 5% (mean +/- SEM) respectively. Cardiac output and heart rate rose by 25 +/- 9 and 21 +/- 3%. During beta-adrenoreceptor blockade, the percentage changes of mean arterial pressure, heart rate, cardiac output and total peripheral resistance after vasodilatation were not significantly different from those after diazoxide alone. 2. Atropine, 0.04 mg/kg body weight, was given to 12 hypertensive patients chronically treated with beta-adrenoreceptor blockade, before acute vasodilatation by diazoxide. Diazoxide caused no increase in heart rate after combined beta-adrenoreceptor and parasympathetic blockade. However, cardiac output rose by 14 +/- 5%. 3. We conclude that withdrawal of parasympathetic tone is an important determinant of circulatory homeostasis after acute vasodilatation during beta-adrenoreceptor blockade.

Adrenergic beta-Antagonists↗