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Biomedical subjects

P Milliez

Publications and source records attributed to P Milliez.

At least 19 recordsLinked to original sources
PubMed1982

Effects of captopril on prostaglandin and natriuresis in patients with essential hypertension.

The antihypertensive, renal and hormonal effects of captopril were studied in 10 patients with essential hypertension. Captopril significantly decreased arterial blood pressure with a concomitant increase in glomerular filtration rate, natriuresis and kaliuresis and a significant selective increase in urinary (renal) prostaglandin E2; other plasma and urinary prostaglandin (F2 alpha, 6-keto-prostaglandin F1 alpha; thromboxane B2) were not significantly changed. The urinary prostaglandin E2 increase was observed even in patients with pretreatment subnormal prostaglandin E2 excretion. Increases in urinary prostaglandin E2 were significantly positively correlated with increases in urinary sodium concentration. It is concluded that the antihypertensive effect of captopril is mediated, at least partially, by prostaglandin E2 release from renal and extrarenal tissues. Captopril enhances natriuresis at a lower perfusion pressure.

Blood Pressure↗
PubMed1982

The role of expansion, of prostaglandins and catecholamines in the development of acute renal failure.

A single injection either of isotonic or hypertonic saline solutions protected rats against acute renal failure (ARF) induced with glycerol. This protection was accompanied by increased urinary prostaglandin E (PGE) concentration. On the contrary, a single s.c. injection either of hypotonic saline or isotonic glucose solution, which did not increase urinary PGE concentration, or depletion of the endogenous catecholamines, using reserpine, did not protect the animals against acute renal failure.

Acute Kidney Injury↗
PubMed1982

[Urinary thromboxane B2 in hypertensive patients].

UNLABELLED: Thromboxane A2 (TxA2) is a vasoconstrictor synthetized by the kidney. Its role in hypertension is unknown. We measured urinary TxB2 (the metabolite of renal TxA2) by radioimmunoassay and studied renal functions in 15 borderline, 15 sustained essential hypertensive patients and 12 age-matched normotensive subjects (6 young and 6 older adults). Results were as follows: Normotensive subjects: Mean arterial blood pressure (MBP) 97 +/- 2 mmHg, urinary TxB2 (UTxB2V) 159 +/- 12 pg/min, glomerular filtration rate (GFR) 120 +/- 8 ml/min, sodium excretion (UNaV) 73 +/- 9 mueq/min. Hypertensive patients: MBP 115 +/- 2 mmHg (p less than 0,001 vs controls), UTxB2V 298 +/- 24 pg/min (p less than 0,005), GFR 128 +/- 6 ml/min, UNaV 51 +/- 4 mueq/min (p less than 0.02). There was a positive significant correlation between UTxB2V and GFR (p less than 0,005) and between UTxB2V and UNaV (p less than 0,005) in hypertensive but not in normotensive subjects. There was no correlation between GFR and UNaV in either group. CONCLUSION: 1. Urinary (i.e. renal) TxB2 is significantly elevated in hypertensive patients; 2. TxA2 may be a mediator of pressure natriuresis.

Adolescent↗
PubMed1981

[Demonstration of renal arteries by tomography during intravenous urography (author's transl)].

A new method to demonstrate the renal arteries is presented. It consists of taking with a Synchroplan apparatus simultaneous tomographic sections during the aortic and arterial stage of intravenous urography (IVU). Direct visualization of the vessels avoids the false negative results of IVU alone in investigations of renovascular lesions, such as bilateral stenosis of the renal artery, stenoses with few functional disorders, aneurysms and associated arterial and urinary lesions. Lesions of the infra-renal portion of the aorta and of the splanchnic arteries are also visualized. In a series of 37 patients investigated for renovascular hypertension, the new method proved more sensitive, more specific and of higher predictive value than conventional IVU. In another series of 19 patients who had undergone revascularization of the kidneys, the authors were able to obtain good visualization of the new vascular system and to establish correlations between morphological features and the effects of hypertension. The method therefore appears to be valuable in detecting renovascular lesions in arterial hypertension, monitoring renal artery lesions and following up patients with surgical revascularization.

Humans↗
PubMed1981

[Effectiveness of captopril in severe hypertension (author's transl)].

Fifteen patients with severe essential or renal hypertension were treated with captopril. In thirteen, a single oral dose of 1 mg/kg produced a mean fall of 20.7 +/- 16.42 mmHg (18%) in mean arterial pressure (MAP) without concomitant increase in heart rate. The fall was significant at 20 minutes and maximum at 90 minutes on average. It correlated closely with the initial plasma renin activity (PRA) (r = 0.96) and with the increase in PRA under treatment (r = 0.75). After an 8-day treatment with captopril alone in increasing dosage (mean: 453 +/- 140 mg/day), the fall in MAP still was 20.3% and correlated with that observed with a single dose. Blood pressure returned to normal levels (MAP Less Than 110 mmHg) in seven of these patients. Twelve patients were treated for a mean period of 36 days and all had normal blood pressure at the end of that period. However, seven had required addition of frusemide to the treatment. A moderate increase in serum creatinine was observed in 7 cases, but there were no other adverse reactions. Captopril alone or combined with diuretics proved to be a very effective drug for the treatment of hypertension, particularly in patients with high initial PRA.

Adolescent↗
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

Investigation of the mechanism of action of prostaglandin synthesis inhibitors on renin and aldosterone secretion and sodium excretion.

Mean blood pressure (MBP) was found to be lower, while renal plasma flow (RPF), glomerular filtration rats (GFR), sodium excretion rate (U(Na)V), potassium excretion rate (U(k)V) and urinary prostaglandin E (PGE) concentration were higher in 15 normotensive subjects (15NS) compared with the values obtained in 15 essential hypertensive patients (15EHP) of the same mean age. After volume expansion of the 15HP with isotonic saline infusion, RPF, U(Na)V, U(k)V, urine volume (UV) and urinary PGE increased significantly while plasma renin activity (PRA) decreased significantly. Urinary aldosterone concentration and MBP decreased also but not significantly. After oral administration of 75 mg of indomethacin, in the same loaded group of 15 EHP, urinary PGE, urinary aldosterone and PRA decreased significantly while RPF, GRF, U(Na)V remained unaltered and MBP increased. When these values obtained in saline loaded and indomethacin treated 15EHP were compared to those obtained in the same group before volume expansion, it was found that RPF, U(NaV, U(k)V and UV were higher after indomethacin-saline administration while MBP, GRF and urinary PGE did not differ significantly and PRA and urinary aldosterone were significantly lower. These findings argue against the suggestion that PGE increases sodium reabsorption at the distal tubule and indicate that the unaltered sodium excretion rate in saline loaded and indomethacin treated unanaesthetized subjects, results from the simultaneous decrease of renomedullary PGE, Renin and aldosterone secretion.

Adult↗
PubMed1981

Takayasu's aortitis with renovascular hypertension: successful complex revascularization.

We report a case of Takayasu's disease in a young Algerian woman with severe renovascular hypertension that failed to respond to medical treatment. There was a general inflammatory syndrome but no important immunological abnormality. Histology showed non-specific aortoarteritis. A left nephrectomy was done, a monofilament knitted polypropylene prosthesis was placed between the thoracic aorta and the aortic bifurcation, and an aorto-reno-mesenteric graft was inserted. The patient was normotensive with no further therapy 2 years later.

Adult↗
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

[Essential arterial hypertension. Effects of labetalol on blood pressure and renin-angiotensin system (author's transl)].

The effects of labetalol, an alpha- and beta-adrenoceptor blocking drug, on blood pressure, heart rate, plasma renin activity (PRA) and plasma aldosterone were studied in 17 adult patients with essential hypertension. Following a total dose of 1 g labetalol administered over a 48-hour period, there was a rapid and significant fall in systolic and diastolic BP averaging 16,5 +/- 7,9%/14,8 +/- 7,5% respectively supine, 18,7 +/- 8,3%/17,8 +/- 7,2% standing and 23,9 +/- 7,1%/16,8 +/- 10,3% after moderate exercise; 24 hours after labetalol was discontinued, the BP had gone up but was still below pretreatment values. Bradycardia remained slight throughout. During treatment a significant decrease in PRA (mean : 45%) was observed in all patients and found to correlate in standing position with changes in standing and post-exercise mean arterial pressure. There was no significant changes in plasma aldosterone. Side-effects were mild and limited to tingling of the scalp in 5 patients. No clinical symptoms of postural hypotension were recorded.

Adult↗