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Biomedical subjects

B Waeber

Publications and source records attributed to B Waeber.

At least 361 records · Page 20Linked to original sources
PubMed1984

[Role of vasopressin in reducing the cutaneous blood flow induced by cigarette smoke].

The authors demonstrate that skin vasoconstriction induced by cigarette smoking in normal volunteers is due to a concomitant enhancement of arginine vasopressin release. The skin blood flow reduction after smoking was more pronounced in the subjects reaching the highest levels of arginine vasopressin, and this effect no longer developed after administration of a specific vasopressin antagonist acting at the vascular site.

Adolescent↗
PubMed1984

[Role of bradykinin in hypotension induced by the active factor derived from factor XII].

The active fragment derived from factor XII (factor XIIf) was purified from human plasma and administered intravenously to normotensive conscious rats. Factor XIIf-mediated hypotension was dose-dependent and augmented by pretreatment with captopril, an inhibitor of the angiotensin I- and bradykinin-processing enzyme. In contrast, factor XIIf-induced hypotension was not enhanced by blockade of the renin-angiotensin system by saralasin, a competitive antagonist of angiotensin II at the vascular receptor level. These results suggest that factor XIIf-mediated hypotension is due to the formation of bradykinin.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1984

Deterioration of renal function in hypertensive patients with scleroderma despite blood pressure normalization with captopril.

The orally active angiotensin-converting enzyme inhibitor captopril was administered for up to 11 weeks to three patients with progressive systemic sclerosis presenting with hypertension and plasma creatinine levels of 3.1, 7.2 and 10.4 mg/100 ml. Only one patient had malignant phase hypertension. In this patient a diuretic had to be added to captopril in order to keep blood pressure under control. Despite sustained blood pressure control during captopril administration, renal function deteriorated and hemodialysis treatment had to be started in all patients. Up to that time no substantial improvement in skin lesions was observed. During the period of dialysis, blood pressure was normal in all patients even though administration of captopril was discontinued. All three patients died of respiratory failure while on chronic hemodialysis for 3 to 4 weeks. These observations confirm that angiotensin-converting enzyme inhibition may be helpful in controlling blood pressure of patients with scleroderma. However, in contrast to some earlier reports, they also indicate that converting enzyme inhibition does not always prevent the multivisceral vascular lesions of scleroderma.

Acute Kidney Injury↗
PubMed1984

[Acute renal insufficiency following inhibition of the angiotensin conversion enzyme by various agents].

At a two years' interval, a patient with severe hypertension was treated with captopril and MK 521, two different angiotensin converting enzyme inhibitors. Each time the blood pressure decreased to normal levels after addition of diuretic therapy but the patient developed acute renal failure. On both occasions the interruption of the inhibitors restored renal function very rapidly. In this woman, considered to suffer from essential hypertension on the basis of a normal intravenous pyelogram, arteriography showed bilateral renal-artery stenosis.

Acute Kidney Injury↗
PubMed1984

A potent converting enzyme inhibitor CGS 13928C. Drug profile in normal volunteers.

The converting enzyme inhibitor CGS 13928C was evaluated in 15 healthy male volunteers. First the efficacy of a single oral dose of 0.5, 1, 2 or 5 mg in antagonizing the pressor response to exogenous angiotensin I was tested with continuous monitoring of the blood pressure and heart rate by an intraarterial catheter. CGS 13928C 1, 2 and 5 mg consistently reduced the response to angiotensin within 2 to 3 h and for a period exceeding the 4 h of monitoring. The 2 mg dose was hardly more effective than 1 mg and 5 mg did not further enhance the blockade. Subsequently, plasma renin and converting enzyme activity, angiotensin I, angiotensin II and aldosterone were measured serially before and up to 72 h following oral administration of either 1 mg (n = 7) or 2 mg (n = 8) CGS 13928C. As expected, plasma renin activity and angiotensin I rose, while plasma converting enzyme activity, angiotensin II and aldosterone fell following both doses of the drug. No side-effects occurred. In normal volunteers CGS 13928C is an effective and extremely potent, orally active converting enzyme inhibitor.

Adult↗
PubMed1984

Ambulatory blood pressure recording to identify hypertensive patients who truly need therapy.

Ambulatory blood pressure profiles were obtained with the Remler system, a portable semi-automatic blood pressure recorder, in 245 untreated patients considered by their physician to be hypertensive. The average blood pressures recorded during the usual daily activities of the patients were greater than 140 mmHg for the systolic and greater than 89 mmHg for the diastolic in only 96 (39%) and 107 (44%) of them respectively. Blood pressure monitoring in ambulatory patients appears to be useful for the practitioner to detect those patients who require antihypertensive therapy. Possibly, unnecessary therapy of only seemingly hypertensive patients may be avoided by this technique.

Adolescent↗
PubMed1984

Effect of centrally acting antihypertensive drugs on the renin-angiotensin system and vasopressin.

Such compounds as clonidine, guanabenz and guanfacine, which stimulate central alpha-adrenoceptors, reduce blood pressure predominantly by reducing sympathetic outflow. Notwithstanding, they also tend to reduce renin secretion, aldosterone, and even vasopressin levels. In some clinical settings, inactivation of the renin-angiotensin system may contribute to their antihypertensive effect. In addition, the absence of sodium retention, which appears to be a special feature of guanabenz, may also have a beneficial effect on blood pressure. In contrast, it is unlikely that a decrease in vasopressin secretion has any major influence on blood pressure.

Adrenergic alpha-Agonists↗
PubMed1984

Response of plasma arginine vasopressin levels to rapid changes in altitude.

Plasma arginine vasopressin levels were studied in 15 normal working men exposed at 4-day intervals to a rapid increase or decrease in altitude of 2000 m. Plasma arginine vasopressin levels were significantly lower (P less than 0.001) at the higher altitude though plasma osmolality did not change. It is concluded that the important diuresis known to physiologically occur in response to high altitude may be related to a decrease in antidiuretic hormone release.

Adaptation, Physiological↗
PubMed1984

Does vasopressin sustain blood pressure of normally hydrated healthy volunteers?

The inhibitor of the pressor effect of arginine vasopressin (AVP), d(CH2)5Tyr(Me)AVP, at a dose of 5 micrograms/kg iv was shown in four healthy volunteers to antagonize the blood pressure, heart rate, and skin blood flow response to a lysine vasopressin infusion of 1 mIU X kg-1 X min-1. The inhibition lasted for more than 2 h. When the same dose of the vasopressin antagonist was administered to 10 healthy normally hydrated volunteers with their renin system intact or acutely blocked by 25 mg of captopril po, none of the above parameters changed. It is concluded that circulating vasopressin, even in the face of a blocked renin-angiotensin system, does not actively contribute to maintenance of cardiovascular homeostasis.

Adult↗
PubMed1984

Alpha 1-adrenoceptor blockade in renal hypertensive rats with low and high renin levels.

A total of 75 male Wistar rats with one-kidney, one-clip renal hypertension was maintained on either a regular (RNa) or a low-salt (LNa) diet for 3 wk after clipping. Blood pressure in the unanesthetized rats was equally elevated independent of sodium intake. Plasma renin activity was higher in LNa animals, and blood pressure was renin dependent only in this group, as evidenced by the blood pressure response to 10 mg/kg captopril iv. There was no significant difference in plasma catecholamines between RNa and LNa rats, although in the former the sympathetic nervous system is believed to play a major role in sustaining high blood pressure. The acute intravenous administration of 0.5 mg/kg prazosin did not induce a more pronounced blood pressure fall in the RNa rats. Prazosin enhanced plasma norepinephrine levels similarly in both groups, but epinephrine levels only rose in the LNa animals. Prazosin also markedly stimulated plasma renin activity rendering blood pressure renin dependent even in RNa rats. Thus, using alpha 1-adrenoceptor blockade, it has not been possible to demonstrate that the blood pressure elevation of salt-repleted one-kidney, one-clip renal hypertensive rats is due to an enhanced sympathetic nerve activity. Data obtained with sympatholytic agents must be interpreted with great caution if renin activity cannot be kept unchanged.

Animals↗
PubMed1984

Skin blood flow reduction induced by cigarette smoking: role of vasopressin.

The effect of vasopressin released by cigarette smoking on blood pressure (BP), heart rate (HR), and skin blood flow (SBF) was investigated in 12 normotensive habitual smokers. At a 1-wk interval, each subject smoked within 10 min two cigarettes before and after intravenous injection of either the specific vascular vasopressin antagonist d(CH2)5Tyr(Me)AVP (5 micrograms/kg) or its vehicle administered in double-blind fashion. SBF was assessed with a laser Doppler flowmeter. Smoking increased plasma vasopressin (P less than 0.01). In six subjects subsequently treated with the antagonist, plasma vasopressin rose to greater than 10 pg/ml and SBF fell by 18.2 +/- 4.8%. This SBF reduction was prevented by the vasopressin antagonist. In contrast, the vehicle had no effect. In the 24 studies taken together, there was a significant correlation (r = -0.60, P less than 0.01) between the SBF decrease during the first smoking period and the plasma vasopressin levels measured afterwards. The BP and HR rise caused by smoking was not modified by the antagonist. Thus it appears that the decrease in SBF induced by smoking is due to enhanced vasopressin secretion.

Adolescent↗
PubMed1984

Renin and the complications of acute myocardial infarction.

To determine whether plasma renin activity in addition to catecholamines could be used as risk indicators, these parameters were measured in 19 patients with acute myocardial infarction. During the course of hospitalization, five patients developed ventricular fibrillation and three, cardiogenic shock. On admission, heart rate, plasma norepinephrine, epinephrine, and renin levels of these eight patients were significantly higher than those of the other patients with uncomplicated course. Peak creatine kinase MB activity was positively related to initial plasma renin activity (r = 0.62, p less than 0.01). Thus, the patients with the highest sympathetic activity following an acute myocardial infarction also had the highest plasma renin levels. They seem particularly prone to develop large infarcts and life-threatening complications.

Acute Disease↗
PubMed1984

Skin blood flow and cigarette smoking: the role of vasopressin.

In a study carried-out in double-blind fashion it was possible to demonstrate that skin vasoconstriction induced by cigarette smoking in normal volunteers is due to a concomitant enhancement of arginine vasopressin release. The skin blood flow reduction occurring after smoking was indeed more pronounced in the subjects reaching the highest levels of arginine vasopressin and this effect was curtailed by the administration of a specific vasopressin antagonist acting at the vascular site.

Adolescent↗
PubMed1984

Measurement of low angiotensin concentrations after ethanol and Dowex extraction procedures.

Current radioimmunoassays do not demonstrate total absence of angiotensin II during converting enzyme inhibition. To assess the meaning of plasma angiotensin II determinations during converting enzyme inhibition, plasma angiotensin I and II levels of normotensive humans during maximal converting enzyme inhibition by single oral doses of CGS 13945, MK 421, or MK 521 were compared with those of anephric rats (18 hr after nephrectomy) after intravenous administration of MK 422 (1 mg/kg). Prior to radioimmunoassay, plasma was extracted with Dowex for angiotensin II and blood extracted with ethanol for angiotensin I. During converting enzyme inhibition, in the 20 normotensive subjects plasma angiotensin II was 6.3 +/- 2.3 pg/ml (mean +/- S.D.) and blood angiotensin I was 65 +/- 59 pg/ml. In the nephrectomized rats, plasma angiotensin II was 8.9 +/- 2.3 pg/ml without converting enzyme inhibitor (n = 15) and 7.6 +/- 2.8 with MK 422 (n = 14), and blood angiotensin I was 9.8 +/- 2.4 pg/ml and 8.2 +/- 0.7, respectively. Dowex extraction of Tris buffer containing no angiotensin II provided blank values ranging from 5.0 to 7.8 pg/ml (n = 5). Thus plasma angiotensin II of normotensive humans treated with converting enzyme inhibitors fell to blank levels even in the presence of markedly elevated plasma angiotensin I. Angiotensin II concentrations in anephric rats with or without converting enzyme inhibition were the same. We therefore conclude that plasma levels of angiotensin II below 8 pg/ml measured after Dowex extraction probably reflect complete converting enzyme inhibition and virtual absence of angiotensin II generation.

Adult↗