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Biomedical subjects

A Mimran

Publications and source records attributed to A Mimran.

At least 253 records · Page 14Linked to original sources
PubMed1975

Effect of a competitive angiotensin antagonist on the renal haemodynamic changes induced by inhibition of prostaglandin synthesis in rats.

1. Inhibition of prostaglandin synthesis by indomethacin induced an increase in blood pressure which did not occur when rats were bilaterally nephrectomized. 2. The blood pressure effect was related to the state of sodium balance and thus to the activity of the renin--angiotensin system. 3. Indomethacin induced a decrease in renal blood flow. 4. Angiotensin receptor blockade with Sar1-Ala8-angiotensin II blunted the blood pressure effect and prevented the renal haemodynamic changes induced by indomethacin.

Angiotensin II↗
PubMed1972

Persistent ductus venosus without portal hypertension in a young alcoholic man.

The discovery of a large patent ductus venosus resulted from radiological investigations in a 34-year-old man, a chronic alcoholic of low mental status. Splenoportal and inferior caval venograms were performed because of recent exacerbation of the neurological symptoms and electroencephalographic criteria of portacaval encephalopathy. Portal pressure was 8 mm Hg. A liver scan, a laparoscopy, and a liver biopsy were performed. They showed that the gland was atrophic with a microscopic appearance of alcoholic fibrosis, but without any nodular regeneration. The relationship between the fistula, the mental state, and the atrophic liver is discussed. Such a malformation appears to be very uncommon.

Adult↗
PubMedDate not supplied

Albuminuria in normals and essential hypertension.

The prevalence and determinants of urinary albumin excretion rate (AER) were assessed in lean and overweight normotensive subjects (NT) and patients with essential hypertension (EH). In NT and EH, the presence of overweight was associated with a significant exacerbation of AER. In the normotensive population, AER was higher in subjects with a positive family history of hypertension. An important role for smoking was observed in the hypertensive population; in fact, the prevalence of microalbuminuria (MA) was almost twofold in lean hypertensive smokers when compared to nonsmokers. Among other determinants of AER, a major influence of systolic arterial pressure, urinary excretion of urea (an estimate of protein intake), and high-density lipoprotein (HDL) cholesterol (inversely correlated with AER) was observed mainly in lean EH patients. The significance of microalbuminuria is unclear. Is it a marker of cardiovascular risk and/or a predictor of the future development of renal disease in EH?

Adolescent↗
PubMedDate not supplied

The antihypertensive effect of captopril. Evidence for an influence of kinins.

The acute effect of the orally-active converting enzyme inhibitor, captopril, was compared to that of saralasin in 13 patients with various forms of hypertension on ad libitum sodium intake. A significant difference between the effects of the two drugs on mean arterial pressure (MAP) was found (-11 +/- 3 mm Hg with saralasin, -24 +/- 4.5 mm Hg after captopril). This difference was not correlated with control plasma renin activity (PRA). To determine the influence of the endogenous kallikrein-kinin system in the antihypertensive action of captopril, the effect of aprotinin (Apro), an inhibitor of kinin generation, on the MAP level achieved by captopril was assessed in five normal subjects and 15 patients with hypertension on ad libitum sodium intake. In normal subjects, captopril did not alter MAP, nor did Apro have any effect. In six patients with essential hypertension and normal PRA, MAP decreased by 5.5 +/- 2 mm Hg following captopril, and Apro did not modify this level. In nine patients with renovascular hypertension (RVH), MAP fell by 22 +/ 3 mm Hg after captopril administration, and Apro infusion induced a rise in MAP of 13 +/- 1.7 mm Hg. A positive correlation between log control PRA and the effect of aprotinin was obtained ( r = 0.63, p less than 0.005). Apro had no effect in two patients with RVH who experiences a large drop in MAP during salasin. These results suggest that endogenous kinins as well as other substances, the generation of which is inhibited by aprotinin, may participate to the antihypertensive effect of captopril in patients with angiotensin-dependent hypertension. The lack of an aprotinin effect on the MAP level achieved during saralasin infusion suggests that the influence of the kallikrein-kinin system is related to the effect of captopril rather than the fall in arterial pressure resulting from angiotensin blockade.

Aprotinin↗
PubMedDate not supplied

Comparative effect of captopril and nifedipine in normotensive patients with incipient diabetic nephropathy.

In these studies, the effect of a 6-wk treatment by placebo, the calcium-channel blocker nifedipine, or the converting-enzyme inhibitor captopril was assessed in normotensive patients with insulin-dependent diabetes and incipient nephropathy. In response to captopril and nifedipine, arterial pressure decreased slightly and to a similar extent. These drugs resulted in opposite effects on urinary excretion of albumin [i.e., increase in urinary albumin excretion (UAE) by 40% during nifedipine treatment and decrease by 40% during captopril treatment]. No change in UAE was observed in the placebo group. This observation of opposite changes in UAE in the presence of a similar fall in arterial pressure suggests that the effects of captopril and nifedipine on UAE result from some difference in their intrarenal action. The data do not present recommendations for the use or disuse of captopril or nifedipine in such a group of patients and do not allow extrapolation to hypertensive diabetic subjects well controlled by other conventional antihypertensive agents.

Adult↗
PubMedDate not supplied

Microalbuminuria in essential hypertension.

The prevalence of microalbuminuria in patients with essential hypertension ranges between 10 and 25%. The level of albuminuria is highly correlated with arterial pressure and more closely ambulatory arterial pressure. The interaction between albuminuria and arterial pressure is enhanced by overweight and smoking. The renal mechanisms of microalbuminuria are not well elucidated; however, an increase in filtration fraction suggestive of intraglomerular hypertension was observed in patients with hyperfiltration. The significance of microalbuminuria as a marker of cardiovascular risk or hypertensive renal damage needs to be confirmed through long-term follow-up studies. Antihypertensive treatment has variable influence on albuminuria; and angiotensin-converting enzyme inhibitors and to a lesser extent other agents, tend to partially correct this abnormality.

Albuminuria↗
PubMedDate not supplied

Cardioprotective effect of enalapril in renovascular and angiotensin II hypertension.

The influence of chronic treatment with enalapril or losartan (10 or 30 mg/kg/24h, respectively) on cardiac mass was evaluated in one-kidney, one clip (1K-1C) hypertensive rats submitted to sodium restriction 3 weeks after clipping and in rats infused for 10 days with angiotensin II (ANGII: 200 ng/kg/min). In 1K-1C hypertension, cardiac mass and arterial pressure were reduced to a similar extent by enalapril and losartan. In ANGII hypertension, enalapril and losartan blunted the increase in cardiac mass whereas losartan but not enalapril prevented the development of hypertension. The cardioprotective effect of enalapril was attenuated by concomitant blockade of bradykinin receptors (Hoe140: 300 micrograms/kg/24h) in both models. The beneficial influence of enalapril on cardiac mass appears to be independent of its effect on blood pressure and ANGII generation and seems partly mediated by endogenous bradykinin in these high ANGII models of hypertension.

Angiotensin II↗
PubMedDate not supplied

Angiotensin II receptor antagonists and hypertension.

Over recent years, a number of imidazole derivatives that specifically bind to the angiotensin II type 1 receptor, thereafter called sartans, have been developed and made available to the clinician. Whether targeting antihypertensive treatment with such a high specificity within the renin cascade may carry major clinical advantage over inhibiting angiotensin converting-enzyme remains to be demonstrated. In short-term studies, the efficacy of these drugs at reducing blood pressure was similar to that of established comparators, whereas overall side effect profile was comparable to that of placebo.

Angiotensin II↗