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Biomedical subjects

B Waeber

Publications and source records attributed to B Waeber.

At least 271 records · Page 15Linked to original sources
PubMed1987

Differential blood pressure response to atriopeptin III and sodium nitroprusside in conscious rats with adrenal medullectomy.

This study was undertaken to test whether the presence or absence of a functioning adrenal medulla influences the blood pressure response of conscious normotensive rats to a 30 min infusion of vasodilating agents such as atriopeptin III (1 microgram/min i.v.), a synthetic atrial natriuretic peptide, and sodium nitroprusside (8 micrograms/min i.v.). Rats either had their adrenal medulla removed or were sham-operated 8-10 days before the experimental day. The blood pressure lowering effect of sodium nitroprusside, but not that of atriopeptin III, was enhanced in rats with no adrenal medulla.

Adrenal Medulla↗
PubMed1987

Are some hypertensive patients overtreated? A prospective study of ambulatory blood pressure recording.

Ambulatory blood pressure (BP) was recorded in hypertensive patients whose physicians had been asked to reduce diastolic pressure measured in the office to 90 mm Hg or less. 34 hypertensive patients with a diastolic pressure measured by their physician of 95 mm Hg or more despite antihypertensive therapy had their treatment changed with the aim of achieving this pre-set goal within 3 months. At the beginning and the end of the study, ambulatory BP was monitored during the daytime with a portable non-invasive recorder. The results of the ambulatory recordings were not made available to the physicians until completion of the study. In half the patients the ambulatory diastolic pressure was already 90 mm Hg or less at the start. In these patients, treatment adjustment did not further decrease ambulatory BP. In contrast, patients who initially had an ambulatory diastolic pressure above 90 mm Hg had a significantly decreased ambulatory BP at the end of the study. Intensifying the therapy of hypertensive patients who have a normal ambulatory BP may result in overtreatment without any real gain in BP control.

Adult↗
PubMed1987

Influence of sodium intake on circulating levels of neuropeptide Y.

Neuropeptide Y (NPY) is present in the adrenal medulla, in sympathetic neurons as well as in the circulation. This peptide not only exerts a direct vasoconstrictor effect, but also potentiates the vasoconstriction evoked by norepinephrine and sympathetic nerve stimulation. The vasoconstrictor effect of norepinephrine is also enhanced by salt loading and reduced by salt depletion. The purpose of this study was therefore to assess whether there exists a relationship between dietary sodium intake and the levels of circulating NPY. Uninephrectomized normotensive rats were maintained for 3 weeks either on a low, a regular or a high sodium intake. On the day of the experiment, plasma levels of NPY and catecholamines were measured in the unanesthetized animals. There was no significant difference in plasma norepinephrine and epinephrine levels between the 3 groups of rats. Plasma NPY levels were the lowest (65.4 +/- 8.8 fmol/ml, n-10, Mean +/- SEM) in salt-restricted and the highest (151.2 +/- 25 fmol/ml, n-14, p less than 0.02) in salt-loaded animals. Intermediate values were obtained in rats kept on a regular sodium intake (117.6 +/- 20.1 fmol/ml). These findings are therefore compatible with the hypothesis that sodium balance might to some extent influence blood pressure regulation via changes in circulating NPY levels which in turn modify blood pressure responsiveness.

Animals↗
PubMed1987

[Renal function after administration of angiotensin-converting enzyme inhibitors].

Angiotensin converting enzyme (ACE) inhibitors are widely used today for the management of hypertension and congestive heart failure. These agents inhibit angiotensin II synthesis. In some particular circumstances they may be responsible for deterioration of renal function, e.g. in hypertensive patients with bilateral renal artery stenosis or with stenosis of the artery supplying a single kidney, or in patients with severe congestive heart failure or marked nephroangiosclerosis. In these patients renal perfusion pressure may become too low to maintain adequate glomerular filtration as there remains no angiotensin II to increase the tone of the efferent arteriole. In high risk patients it is therefore recommended that serum creatinine be checked after initiating therapy with an ACE inhibitor.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1987

[Therapeutic strategy in arterial hypertension].

Diuretics and beta-blocking agents have been used for several years as first-step drugs in the treatment of hypertension. There is now growing evidence that calcium channel blockers and angiotensin converting enzyme inhibitors can also be administered as first-line antihypertensive agents. These agents offer attractive features from the hemodynamic and metabolic viewpoint and with regard to side effects. Diuretics, beta-blocking agents, calcium channel blockers and angiotensin converting enzyme inhibitors, administered either alone or in combination, normalize blood pressure in almost all hypertensive patients.

Adrenergic beta-Antagonists↗
PubMed1987

Effect on blood pressure and the renin-angiotensin system of repeated doses of the converting enzyme inhibitor CGS 14824A.

A new, orally active angiotensin converting enzyme (ACE) inhibitor, CGS 14824A, was evaluated in 12 healthy male volunteers. Two groups each of 6 volunteers were given 5 or 10 mg once daily p.o. for 8 days. Four hours after the first and the last morning doses, plasma angiotensin II, aldosterone and plasma converting enzyme activity had fallen, while blood angiotensin I and plasma renin activity had risen. Throughout the study, more than 90% inhibition of ACE was found immediately before giving either the 5 or 10 mg dose and 50% blockade was still present 72 h following the last dose. Based on the determination of ACE, there was no evidence of drug accumulation. No significant change in blood pressure or heart rate was observed during the course of the study. CGS 14824A was an effective, orally active, long-lasting and well tolerated converting enzyme inhibitor.

Adult↗
PubMed1987

Effect of indomethacin and propranolol on the blood pressure and renin response to atriopeptin III in conscious rats.

The effect of prostaglandin synthesis inhibition and of beta-adrenoceptor blockade on the blood pressure and renin response to the synthetic atrial natriuretic peptide atriopeptin III was assessed in unanesthetized normotensive rats. This peptide was infused i.v. for 30 min at a rate of 1 microgram/min in rats pretreated either with indomethacin (5 mg i.v.) or propranolol (1 mg i.v.). The blood pressure reducing effect of atriopeptin III was attenuated neither by indomethacin nor by propranolol. Atriopeptin III per se did not modify plasma renin activity. Both the administration of indomethacin and of propranolol had a suppressing effect on renin release during atriopeptin III infusion. These data suggest that the vasodilating properties of atrial natriuretic peptides do not depend in the conscious normotensive rats on the production of prostaglandins. They also provide evidence that during infusion of such peptides, both prostaglandins and beta-adrenergic mechanisms are still involved in the regulation of renin secretion.

Animals↗
PubMed1987

Pharmacokinetics of synthetic atrial natriuretic peptides in normal men.

The kinetics of atrial natriuretic peptides (ANP) and the kinetic profile of their effect on blood pressure and renal hemodynamic and electrolyte excretion were investigated in 20 salt-loaded healthy volunteers during and after constant rate infusion. At steady state, mean plasma concentrations of ANP were measured at 210, 430, and 2990 pg/ml and mean systemic clearance was 2.6, 2.5, and 1.7 L/min for ANP infusion rates of 0.5, 1, and 5 micrograms/min, respectively, which corresponds to the clearance rate of other vasoactive peptide hormones. The apparent volume of distribution averaged 17 L and the mean half-life was 4.5 minutes. ANP induced dose-related effects on systemic and renal hemodynamic, as well as urinary electrolyte excretion, albeit with a time lag between onset and full effect.

Adult↗
PubMed1987

Site of the action of a synthetic atrial natriuretic peptide evaluated in humans.

The renal site of the natriuretic effect of human, atrial natriuretic peptide (hANP) was studied using clearance techniques in eight salt-loaded normal volunteers undergoing maximal water diuresis. Lithium was used as a marker of proximal sodium reabsorption. According to a two-way, single blind, crossover design, hANP (Met12-(3-28)-eicosahexapeptide, (2 micrograms/min) or its vehicle (Ve) were infused for two hours, followed by a two-hour recovery period. Blood pressure, heart rate and insulin clearance remained unchanged. During hANP infusion, the filtration fraction increased slightly from 19.6 to 24.3% (P less than 0.001), fractional water excretion rose transiently at the beginning of the infusion. Fractional excretion of sodium increased markedly from 2.2% to 7.4% (P less than 0.001) but remained unchanged with Ve. ANP increased fractional excretion of lithium slightly from 46 to 58% (P less than 0.01), while it remained stable at 47% during Ve. The distal tubular rejection fraction of sodium calculated from sodium and lithium clearances rose markedly from 4.7 to 13% (P less than 0.001) and returned to 6.2% at the end of the recovery period. Thus, under salt loading and water diuresis conditions, hANP infusion did not alter GFR, but reduced proximal reabsorption of sodium, and markedly enhanced the fraction of sodium escaping distal tubular reabsorption, suggesting that hANP-induced natriuresis is due, for an important part, to inhibition of sodium reabsorption in the distal nephron.

Adult↗
PubMed1987

Lack of angiotensin I accumulation after converting enzyme blockade by enalapril or lisinopril in man.

In nine normal volunteers, a series of five venous blood samples was obtained before and up to 24 h after converting enzyme inhibition by a single oral dose of enalapril or lisinopril. Plasma renin activity and blood angiotensin I were measured. A close linear relationship was found between the increase in plasma renin activity and the increase in blood angiotensin I. The linear correlation between plasma renin activity and blood angiotensin I remained after converting enzyme inhibition. Thus, the rise in angiotensin I after inhibition of the conversion of angiotensin I to angiotensin II is due to an enhanced release of renin rather than to accumulation of angiotensin I.

Adult↗
PubMed1987

Renal effects of converting enzyme inhibition.

Angiotensin-converting enzyme inhibition, by preventing the generation of angiotensin II, has some pronounced effects on renal function. Its actions occur at the vascular, the glomerular, the juxtaglomerular, and also at the tubular medullary level. In clinical medicine, depending on the circumstances of the patients under treatment, converting enzyme inhibitors can interfere with renal hemodynamics and glomerular filtration, with solute excretion by the kidney and other variables of normal renal function. In most circumstances, the effects of converting enzyme inhibition on the kidney are rather beneficial to the patient. However, under some extreme conditions, they may become potentially hazardous. A basic understanding of the physiology of the renin-angiotensin system and of its actions on the kidney makes it possible to understand the impact of the converting enzyme inhibitors, to avoid most of the unwanted effects and to ensure greatest benefit to the patient.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1987

Treatment of hypertension with ACE inhibitors as first step: pharmacologic and clinical considerations.

A stepped-care approach to the treatment of hypertension has been developed to provide some practical guidelines for practicing physicians. Obviously, only drugs that are effective as monotherapy, and that are particularly well tolerated and safe, can be recommended for the use in the first step. In this discussion, evidence is provided in favor of using ACE inhibitors as first-step agents. They are effective in a large fraction of hypertensive patients when given as monotherapy and they are well tolerated even in the presence of associated diseases. They have a favorable hemodynamic profile, induce no tolerance, and can be combined with almost any other drug. They elicit few side effects, many of which are due to inadequate handling of the agents by the physician, and they appear to provide in general a particularly good quality of life to the patient.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1987

Influence of bradykinin on blood pressure regulation of spontaneously hypertensive rats maintained on different sodium intakes.

1. The role of circulating bradykinin in blood pressure regulation was studied in conscious spontaneously hypertensive rats utilizing the competitive antagonist of bradykinin B4162. 2. This antagonist was administered at a bolus dose (400 micrograms i.v.) known to block the hypotensive effect of exogenous bradykinin for at least 2 min. The rats were maintained for 10 days either on a low or a high sodium intake. 3. The antagonist of bradykinin significantly increased blood pressure only in salt-depleted rats. In other rats kept on a low or a high sodium intake, dose-response curves to exogenous bradykinin were established. Dietary sodium had no influence on the blood pressure-lowering effect of bradykinin. 4. These data therefore suggest that circulating bradykinin may be involved in the blood pressure control of spontaneously hypertensive rats when the renin-angiotensin system is stimulated by salt depletion.

Animals↗
PubMed1987

Postpropranolol vasodilation in adrenalectomized glucocorticoid hypertensive rats.

Acute beta-adrenoreceptor blockade results in an enhanced blood pressure-lowering effect in glucocorticoid hypertensive rats in the absence of the adrenals. To evaluate the possible mechanism of this enhanced blood pressure-lowering effect, systemic and regional hemodynamics were determined by the radioactive microsphere technique before and after propranolol administration in bilaterally adrenalectomized (AX) and sham-operated (SH) glucocorticoid hypertensive rats. Propranolol decreased mean blood pressure (BP) and heart rate (HR) to a greater extent in the AX animals. In response to propranolol, cardiac output (CO) decreased equally in both the AX and SH animals. Regional vascular responses to propranolol were similar between the AX and SH animals, except in muscle. In muscle propranolol significantly decreased blood flow and increased resistance in the SH animals. In marked contrast, in the AX animals propranolol significantly increased blood flow and decreased vascular resistance. The results of this study show that in adrenalectomized glucocorticoid hypertensive rats, the enhanced BP lowering effect of acute beta-adrenoreceptor blockade is not mediated by changes in CO. Additionally, in glucocorticoid hypertensive rats acute beta-adrenoreceptor blockade causes selective vasodilation in skeletal muscle.

Adrenalectomy↗
PubMed1987

Angiotensin-converting enzyme inhibitor versus calcium antagonist in the treatment of hypertension.

Sixteen patients with essential hypertension were treated for 2 consecutive 6-week periods with either the angiotensin-converting enzyme (ACE) inhibitor enalapril (20 mg once daily) or the calcium antagonist diltiazem (120 mg twice daily). The sequence of the treatment phases was randomly allocated. Blood pressure decreased from 154/102 +/- 5/2 mm Hg (mean +/- SEM) to 135/96 +/- 4/2 and 140/98 +/- 3/2 mm Hg during treatment with enalapril and diltiazem, respectively. It was impossible in the individual hypertensive patient to predict the long-term blood pressure response to one of the agents studied based on the long-term blood pressure response to the other agent.

Adult↗