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Biomedical subjects

R Fagard

Publications and source records attributed to R Fagard.

At least 433 records · Page 24Linked to original sources
PubMed1981

Active and inactive renin in dog plasma before and after bilateral nephrectomy.

No significant amounts of inactive renin could be demonstrated by in vivo treatment (acidification or cryotreatment) of dog plasma obtained before and after bilateral nephrectomy. After bilateral nephrectomy, total and active renin were cleared from the plasma following similar disappearance curves, and dropped to half of their initial value within 30 min.

Animals↗
PubMed1981

Role of various vasodepressor systems in the acute hypotensive effect of captopril in man.

The acute hypotensive effect of captopril 25 mg was investigated in 26 hypertensive patients (11 with essential and 15 with renal arterial disease). Intra-arterial blood pressure was recorded continuously and arterial blood was sampled for renin, angiotensin I and II, aldosterone, kininase II, catecholamines and prostaglandins. Captopril led to an increase in plasma renin activity, active and total plasma renin concentration and angiotensin I, a decrease in plasma kininase II activity, angiotensin II, aldosterone, prostaglandins E2 and F2 alpha and no change in plasma (nor) adrenaline, dopamine and inactive renin concentration. The hypotensive effect of captopril was related to the changes in plasma angiotensin II level and inversely to the changes in prostaglandin E2; the correlation coefficients were low, respectively 0.61 and -0.44. It is likely that the acute hypotensive effect of captopril to some extent is related to changes in plasma angiotensin II and in prostaglandins E2 and F2 alpha. There is no evidence for a role of the adrenergic systems in the hypotensive response.

Adult↗
PubMed1981

The hypotensive effect of propranolol in captopril-treated patients does not involve the plasma renin--angiotensin--aldosterone system.

1. With a double-blind cross-over protocol, 20 hypertensive captopril-treated patients were studied by adding in a variable sequence a placebo and propranolol (80 mg three times a day) to their captopril regimen (200 mg three times a day), during periods each lasting 1 month. During captopril--placebo treatment their diastolic blood pressure remained elevated between 90 and 114 mmHg. 2. The additional administration of propranolol produced a significant hypotensive effect, but no alterations of the plasma angiotensin II and aldosterone concentrations and of the urinary aldosterone excretion occurred. The present data indicate that in captopril-treated patients the hypotensive effect of propranolol is achieved independently of changes in the plasma angiotensin II and aldosterone concentration. 3. The additional administration of propranolol also produced an increase in the serum potassium levels in the absence of any change in plasma aldosterone concentration or in the urinary aldosterone excretion.

Captopril↗
PubMed1981

Relationship between phosphorylation and activity of heme-regulated eukaryotic initiation factor 2 alpha kinase.

In heme-deficient reticulocytes and their lysates, a heme-regulated inhibitor of protein synthesis is activated; this inhibitor is a cyclic AMP-independent protein kinase that specifically phosphorylates the alpha subunit of the eukaryotic initiation factor 2 (eIF-2 alpha). Heme regulates this kinase by inhibiting its activation and activity. The purified heme-regulated kinase (HRI) undergoes autophosphorylation; at least 3 mol of phosphate can be incorporated per HRI subunit (Mr 80,000). The phosphorylation of HRI, its eIF-2 alpha kinase activity, and its ability to inhibit protein synthesis are diminished by hemin (5 microM) and increased by N-ethylmaleimide (MalNEt). Treatment of MalNEt-activated HRI with hemin reduces its autophosphorylation and its ability to inhibit protein synthesis . These findings demonstrate a correlation of the phosphorylation of HRI, its eIF-2 alpha kinase activity, and its inhibition of protein synthesis. The mechanism of hemin regulation of HRI activity was studied by examining the binding of hemin to purified HRI. Significant binding was demonstrable by difference spectroscopy which revealed a pronounced shift in the absorption spectrum of hemin with the appearance of a peak at 418 nm, a shift similar to that observed with proteins known to bind hemin. These findings are consistent with a direct effect of hemin on HRI.

Animals↗
PubMed1981

Effect of chronic diuretic treatment on the plasma renin-angiotensin-aldosterone system in essential hypertension.

1 Chronic treatment with a constant dose of hydrochlorothiazide or tienilic acid increases plasma renin activity (PRA) acutely to reach a maximum within the first week. 2 During chronic diuretic therapy from 1 month to 1 year, PRA remained elevated at a rather constant level, though this was somewhat lower than the maximum level reached after 1 week. 3 A significant (P less than 0.01) correlation (r = 0.74) between changes in plasma angiotensin II and renin activity provoked by chronic treatment for 3 months with hydrochlorothiazide and tienilic acid was found. 4 The increase in plasma aldosterone during chronic treatment with hydrochlorothiazide and tienilic acid (1000 mg) is related (r = 0.68; P less than 0.01) to the rise in plasma angiotensin II.

Adult↗
PubMed1981

Salt and blood pressure in Belgium.

Blood pressure, pulse rate, body weight, and height were measured on two occasions in the inhabitants of a random 10% sample of households in a Belgian village. Twenty-four-hour urinary excretion of creatinine, sodium, and potassium was also determined. In subjects over the age of 19 there was a significant correlation for both systolic and diastolic pressure with age and body weight and, in women, also with pulse rate. After adjusting for these three variables, the systolic blood pressure in men was negatively correlated with the daily urinary potassium excretion, and the diastolic blood pressure in women negatively with the urinary sodium: creatinine ratio. The present data, obtained within one society, do not support a role for dietary sodium in the distribution of blood pressure within this population. Comparison of the present results with data from other countries does not refute the salt-genetic hypothesis but suggests also that a high potassium intake may lower blood pressure.

Adult↗
PubMed1981

Rise in plasma concentration of aldosterone during long-term angiotensin II suppression.

The plasma concentration of aldosterone was followed in seven hypertensive patients before and during long-term angiotensin II suppression with the orally active angiotensin-I-converting-enzyme inhibitor, captopril. The plasma concentration of aldosterone decreased initially from 74 to 21 pg/ml (P less than 0.05) after 1 month of administration of captopril. Thereafter the plasma concentration of aldosterone began to rise and after 1 year reached a level of 165 pg/ml. During long-term captopril therapy the plasma renin activity remained increased and the plasma angiotensin II concentration suppressed. The mechanism responsible for the late rise of the plasma concentration of aldosterone during long-term angiotensin II suppression with captopril remains to be elucidated. A sizeable and lasting hypotensive effect was observed in all patients.

Adult↗
PubMed1980

Dose response in captopril therapy of hypertension.

Dose-response curves of blood pressure and of the biochemical components of the renin-angiotensin-aldosterone system were determined during long-term treatment with captopril in 21 hypertensive patients. Captopril was given in biweekly, doubling doses starting with 25 mg 3 times a day until control of blood pressure was achieved or a total daily dosage of 600 mg was reached. Recumbent and standing systolic and diastolic blood pressure fell on 75 mg captopril daily. Increasing the captopril dose did not induce further significant hypotensive effects. The pretreatment level of plasma renin activity (PRA) was a poor predictor of the hypotensive effect of captopril. The rises in PRA and plasma angiotensin I level (PA I) and the decrease in plasma angiotensin II level (PA II) and plasma aldosterone level (PAC) provide biochemical evidence for angiotensin-converting enzyme (ACE) inhibition in vivo. These effects were present on daily doses of 75 to 150 mg captopril.

Adult↗