Search PubMed⌕ Search

Biomedical subjects

M Thibonnier

Publications and source records attributed to M Thibonnier.

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

[Role of vasopressin in arterial hypertension].

On isolated arteriole preparations vasopressin behaves as an extremely potent vasoconstrictor. In healthy animals and man its pressor effect is counteracted by several compensatory mechanisms, including stimulation of the baroreceptor reflex with reduction of sympathetic activity, decrease in renin secretion, sodium loss and reduction of vascular response to vasopressor agents. Alterations of these mechanisms unmask the hypertensive effect of vasopressin as shown by several experimental hypertension models in animals. In human pathology vasopressin has been shown to be a good indicator of the severity pf arterial hypertension, but its role in that disease will only be determined when vascular antagonists of vasopressin devoid of paryial agonistic activity become available.

Animals↗
PubMed1982

Suppression of antidiuretic hormone hypersecretion during surgery by extradural anaesthesia.

The concentrations of antidiuretic hormone in plasma and urine were determined in three groups of patients submitted to the same operative procedure. Seven (group I) underwent general anaesthesia with thiopentone, fentanyl and nitrous oxide and received an infusion of isotonic saline solution 5ml min-l. Seven patients (group II) anaesthetized similarly, received isotonic saline solution 15 ml min-1. In group III (five patients) anaesthesia was produced by extradural blockade. Surgery under general anaesthesia induced a significant increase in plasma and urine ADH concentrations which were not modified by the fluid load. Extradural anaesthesia suppressed almost completely the release of ADH during surgery. This effect of extradural anaesthesia could be related to the interruption of conduction along nociceptive neural pathways.

Aged↗
PubMed1982

Antihypertensive effect of diacetolol in essential hypertension.

1 Diacetolol is the N-acetylated metabolite of acebutolol and possesses beta-adrenergic receptor blocking properties. 2 Its antihypertensive action was assessed in accordance with a double-blind randomised cross-over scheme in 17 patients with moderate essential hypertension previously well controlled with acebutolol. 3 Significant reductions in lying mean arterial blood pressure were observed with daily doses of 200 mg (- 9%), 400 mg (- 10%) and 800 mg (- 14%), and were associated with significant decreases in heart rate and plasma renin activity. 4 The diacetolol mean plasma level measured 8 to 10 h after drug ingestion was proportional to the dose (207 +/- 27, 394 +/- 63 and 823 +/- 135 ng/ml for respectively 200, 400 and 800 mg/day).

Acebutolol↗
PubMed1982

Cardiac output distribution during vasopressin infusion or dehydration in conscious dogs.

To better understand the role of arginine vasopressin in cardiovascular regulation, we measured in unanesthetized dogs regional blood flows with radioactive microspheres before and during 1-h vasopressin infusions that increased the vasopressin concentration of plasma by 11 +/- 0.6 pg/ml. Cardiac output measured by an electromagnetic flowmeter decreased by 13%. Blood flows to the skeletal muscle and skin, the areas most affected, decreased by 30.8 and 34.3%, respectively. In the same group of dogs a period of 48-h water restriction increased plasma vasopressin by 6.9 +/- 1.3 pg/ml and reduced cardiac output by 14.4%. Skeletal muscle blood flow decreased by 32.8%, a pattern strikingly similar to that following vasopressin infusion. Obvious differences between vasopressin infusion and dehydration were also noted, in particular in the skin and splanchnic areas. However, the possibility that vasopressin contributed to the cardiovascular adjustments to dehydration must be considered. The use of an antagonist of the vascular effects of vasopressin, [1-deaminopenicillamine, 2-(O-methyl)tyrosine]arginine-vasopressin ([dPTyr(Me)]AVP), did not permit us to clarify this issue, because this analogue given alone exerted pronounced systemic and regional cardiovascular effects that resembled those of vasopressin.

Animals↗
PubMed1982

Acute antihypertensive and hormonal effects of a calcium antagonist in essential hypertension.

In a double-blind versus placebo preliminary study conducted in seven mildly hypertensive patients, the 10-mg capsule form of nifedipine was able to reduce significantly systolic and diastolic blood pressure (-14%) for 3 h. In a single-dose, cross-over study, captopril (1 mg/kg) and nifedipine (20 mg) significantly reduced blood pressure in 12 patients with moderate essential hypertension, but the mean maximum arterial pressure reduction was faster and greater with nifedipine than with captopril (-23 +/- 2% at 37 +/- 15 min and -17 +/- 1% at 86 +/- 25 min, respectively). Nifedipine did not significantly alter the renin angiotensin aldosterone system in supine and upright positions, and the blood pressure drop it induced was not related to the initial level of activation of that system. Associated with the stimulation of the sympathetic nervous system, an increased release of vasopressin was noted during nifedipine administration. Finally, nifedipine, a calcium antagonist, was a potent antihypertensive drug through its vasodilating properties. It provoked specific hormonal alterations, i.e., stimulation of catecholamines and vasopressin release, whereas the renin angiotensin aldosterone system was not significantly altered.

Antihypertensive Agents↗
PubMed1981

[The renin-angiotensin system and its inhibition (author's transl)].

The recent development of several inhibitors of the renin-angiotensin system has perfected our knowledge of the part played by this system in the control of physiological and pathological arterial pressure. Peptides inhibiting angiotensin II, such as Sar1, Ala8 angiotensin II, block the peripheral effects of angiotensin on vascular renal and adrenal receptors. Inhibition of the conversion enzyme, notably with captopril, prevents the formation of angiotensin II from angiotensin I and also results in accumulation of a vasodilator and natriuretic peptide: bradykinin. Finally, it is now possible to inhibit more specifically the reaction of renin with its substrate, angiotensinogen, by using pepstatin or its derivatives, or peptide analogues of the substrate. The use of these inhibitors, especially captopril (so far the most studied), has made it clear that renin plays a part in experimental and human essential hypertension and participates in the control of arterial blood pressure in subjects with normal sodium intake.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1981

Antihypertensive and hormonal effects of single oral doses of captopril and nifedipine in essential hypertension.

In a single-dose crossover study Captopril (SQ 14225), 1 mg/kg body weight, and Nifedipine (Bay a 1040) 20 mg were administered orally to 12 hospitalized patients with essential hypertension (Stage 1 or 2, W.H.O.). Both drugs significantly reduced blood pressure, but each dose acted differently: the mean maximum arterial pressure reduction was faster and greater with Nifedipine than with Captopril: -23 +/- 2% at 37 +/- 15 min and -17 +/- 1% at 86 +/- 25 min, respectively. Captopril inhibited angiotensin II and aldosterone production, but did not accelerate heart rate or stimulate vasopressin release. Nifedipine stimulated vasopressin release and increased heart rate, but the renin angiotensin aldosterone system was not significantly affected. The blood pressure reduction was related to the initial level of activation of the renin angiotensin system only for Captopril. The blood pressure reduction induced by one drug was not related to that produced by the other in the same patient.

Administration, Oral↗
PubMed1981

Reduction of plasma and urinary vasopressin during treatment of severe hypertension by captopril.

Plasma concentrations and urinary excretion rate of vasopressin (VP) were examined in ten cases of severe hypertension before and during short-term treatment by Captopril (SQ 14225). Before Captopril, plasma and urinary VP were high (respectively 5.24 pmol/l and 68 pmol/day) and positively correlated to plasma renin activity (PRA) and plasma aldosterone (PA). The decline in blood pressure (mean -15%) after Captopril was correlated not only to initial PRA and PA values, but also to plasma (r = 0.89; P less than 0.001) and urinary (r = 0.78; P less than 0.01) VP values. The initial dose of Captopril (1 mg/kg) induced a rapid decrease in blood pressure whereas plasma VP did not rise and aldosterone decreased. At the eighth day of Captopril treatment (mean daily dose 6 +/- 1.5 mg/kg) the drop in blood pressure (-12%) and in aldosterone persisted together with a significant reduction in plasma (1.18 pmol/l; P less than 0.01) and urinary (25 pmol/day; P less than 0.01) VP. It is suggested that these sustained simultaneous reductions in the rates of secretion of vasopressin and aldosterone are both elements of the antihypertensive effect of Captopril.

Adolescent↗
PubMed1980

[Application of the saralasin test to the treatment of malignant or accelerated arterial hypertension (author's transl)].

A test using saralasin, an antagonist of angiotensin II, was carried out in 9 patients with malignant or accelerated arterial hypertension, and the initial treatment was modified according to the results: if the fall in mean arterial blood pressure was greater than 10 p. cent, beta-blockers or alpha-beta blockers were prescribed alone; if not, diuretics were used concomitantly. Blood pressure response correlated with plasma renin activity and aldosterone, and the reduction in mean arterial blood pressure after 24 hours' treatment correlated with that observed with saralasin. In longer term saralasin has no predictive value with regard to the course of the hypertensive disease or the results of future treatments.

Adult↗
PubMed1980

[Variations of the renin aldosterone system in Cushing's disease (author's transl)].

The renin aldosterone system was studied in 5 cases of Cushing's disease (bilateral benign hyperplasia) without medication. For a daily sodium intake of 120 mmol plasma angiotensinogen was abnormally increased, plasma renin activity (PRA) remained normal, but without significant diurnal variation. Plasma aldosterone (PA) was normal and its circadian rhythm was maintained. One hour active orthostatism and low sodium diet (20 mmol of sodium during 4 days) induced a normal PRA increase but an insufficient PA response. Positive significant correlations were found between PRA and PA and between plasma angiotensinogen and plasma cortisol. The mechanisms underlying this functional hypoaldosteronism were discussed.

Adult↗
PubMed1980

Antihypertensive effect of fractionated sublingual administration of nifedipine in moderate essential hypertension.

The magnitude and duration of the antihypertensive effect of nifedipine were studied in 7 cases of moderate essential hypertension. In a double-blind crossover study, nifedipine 10 mg or a placebo were administered sublingually 4 times a day for 2 days, and the results were compared. Each dose of nifedipine reduced systolic and diastolic blood pressure by 14% both in the supine and upright positions. The antihypertensive action lasted for about 3 h and it was not cumulative. The reduction in blood pressure was associated with a temporary increase in heart rate. Administration of nifedipine 10 mg did not significantly raise plasma renin activity or plasma aldosterone. The drug was well tolerated and no side effects were detected.

Administration, Oral↗
PubMed1980

Comparative trial of labetalol and acebutolol, alone or associated with dihydralazine, in treatment of essential hypertension.

1 Labetalol, an alpha- and beta- adrenoceptor blocking drug, was compared with acebutolol, alone or associated with dihydralazine in forty patients with moderate essential hypertension. 2 Labetalol (400--800 mg daily) seemed to have a slightly higher potency than acebutolol alone (400--800 mg daily). 3 Labetalol (1200--1600 mg daily) had the same potency as the combination of acebutolol (400--800 mg daily) and dihydralazine (50--100 mg daily). 4 Contrarily to acebutolol, the drop in blood pressure with labetalol was not correlated with initial plasma renin activity. 5 Labetalol side effects were minor and did not lead to drug withdrawal.

Acebutolol↗