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Biomedical subjects

F Arzilli

Publications and source records attributed to F Arzilli.

At least 37 records · Page 2Linked to original sources
PubMed1982

Interaction between oxprenolol and indomethacin on blood pressure in essential hypertensive patients.

A double-blind, cross-over study in 16 patients with essential hypertension was carried out, to evaluate any possible interference by indomethacin, a known prostaglandin-synthetase inhibitor, with the antihypertensive effect of oxprenolol, a non-selective beta-adrenoceptor blocking agent. Both indomethacin and oxprenolol, as well as the two drugs combined, inhibited plasma renin activity; no change was found in urinary sodium excretion or body weight. Oxprenolol alone caused a highly significant decrease in the systolic ( - 10.4 mmHg, p less than 0.001), diastolic ( - 7.4 mmHg, p less than 0.001) and mean ( - 7.7 mmHg, p less than 0.01) blood pressures, whereas indomethacin did not influence blood pressure. When the two drugs were given in combination, blood pressure decreased (systolic: - 5.9 mmHg; diastolic: - 4.0 mmHg; mean: - 4.6 mmHg), but the changes induced in blood pressure were reduced by about 50% when compared with those in the oxprenolol alone period. The data show that indomethacin seems to interfere with the antihypertensive effect of oxprenolol, by an action which may be due to the inhibition of prostaglandin synthesis.

Adult↗
PubMed1982

Effects of prostaglandins inhibition on changes in active and inactive renin induced by antihypertensive drugs.

The behaviour of active (AR) and inactive (IR) renin was studied in 48 hypertensive patients (37 with uncomplicated essential hypertension and 11 with reno-vascular hypertension) treated with indomethacin alone or with AR stimulating (bumetanide, tienilic acid, captopril) and inhibiting (atenolol) drugs before and after indomethacin addition. In 10 pts indomethacin (50mg q.i.d./3 days) reduced (p less than 0.05) AR and to a lesser extent IR. In 6 pts bumetanide (1 mg) increased (p less than 0.05) only AR and this effect was abolished by indomethacin. In 6 pts tienilic acid (250 mg) increased (p less than 0.05) only AR and this action was unchanged by indomethacin. In 11 renovascular pts captopril (100mg) increased AR (p less than 0.01) and lesser IR and both these effects were uninfluenced by indomethacin. In 11 essential hypertensive pts captopril (25mg b.i.d./3 days) increased only AR (p less than 0.02), but after 1 year both AR and IR were increased (p less than 0.05) and these effects were abolished by indomethacin. In all the above reported protocols we did never find any inverse correlation between either AR and IR values or their induced changes. These data suggest that prostaglandins stimulate, even if not to a similar extent, both AR and IR and that drugs, which stimulate renin either through or independently of PGs, did not cause any apparent interconversion of plasma IR into AR. In 6 pts atenolol (100 mg daily/6 days) reduced AR (p less than 0.05) and tended to increase IR. Indomethacin addition further decreased AR and reduced IR (both p less than 0.05 vs atenolol alone): however the proportion (% of total) of IR was still reduced. These findings suggest that beta 1-adrenoreceptors blockade exerts a divergent effect on active and inactive renin and that this action is not influenced by PGs synthesis inhibition.

Adult↗
PubMed1980

Influence of indomethacin on the natriuretic and renin-stimulating effect of bumetanide in essential hypertension.

The effect of bumetanide on absolute and fractional sodium excretion, creatinine clearance, and plasma renin activity (PRA) was studied in eight patients with essential hypertension before and after indomethacin. After bumetanide, urinary sodium excretion increased only in the first 4 hr, creatinine clearance only in the first 2 hr, and PRA rose progressively. After indomethacin, bumetanide caused a smaller increase in urinary sodium excretion, decreased creatinine clearance, and caused a small early and late PRA rise. Prostaglandin inhibition and indomethacin did not, per se, affect the tubular natriuretic mechanism but they abolished both early vascular and sustained PRA-stimulating effects of bumetanide.

Adult↗
PubMed1980

Influence of age and sodium intake on plasma renin activity of normal subjects.

Supine and upright plasma renin activity (PRA) were measured i 104 normal subjects (age range 13-74 years, 71 males and 33 females) on a constant diet of normal potassium (60-80 mEq/day) and of varying but constant, sodium content (range 10-260 mEq/day). Both supine and upright PRA values were inversely related to the 24-hour urinary sodium excretion, while only upright PRA values showed a significant inverse correlation with age. Through a multiple regression analysis it was shown that age increased the significance of the PRA/sodium relationship by about 10%. Besides posture, two other factors seem to influence the PRA-age relationship: the age range and the sodium intake. In fact, the PRA-age relationship was not detectable either when subjects below 20 and above 50 were excluded, or when sodium intake was increased above 140 mEq/day. These data can explain the contrasting reports on the age influence on renin secretion. The relationship between PRA and urinary sodium confirms the dependance of PRA on the state of sodium balance. Age significantly influences the PRA/sodium relationship of normal subjects on normal or low sodium intake and in the upright position. Therefore, the decline of PRA with age may be explained by the decrease either of renin storage or of sympathetic nervous system activity on renin release.

Adolescent↗
PubMed1979

Effect of increasing doses of labetalol on blood pressure, plasma renin activity and aldosterone in hypertensive patients.

1. Four different doses of labetalol (150, 300, 600 and 900 mg/day) were given for 1 week to each of four groups of patients with essential hypertension (six patients for each group). 2. Labetalol decreased mean blood pressure and heart rate to the same extent on the first and the seventh days of treatment. Only standing blood pressure showed a dose-dependent inhibition both in the supine and upright position. 3. Labetalol exerted a net inhibitory effect on plasma renin activity, which was related to basal renin values and was already maximal at the lowest doses. This effect was well maintained in the supine position. This effect was well maintained in the supine position, although during standing it tended to be less evident with increasing doses. 4. Urinary aldosterone was decreased in a dose-dependent fashion and its changes were largely independent fashion and its changes were largely independent of plasma renin activity. 5. Neither basal values nor changes of renin and aldosterone were related to the hypotensive effect of labetalol. 6. During labetalol treatment urinary sodium excretion fell for 2-3 days and then returned to basal values. The retentive effect of labetalol on sodium was directly related to the decrease of blood pressure, and the successive sodium escape might be explained either by the observed increase of plasma volume (indirectly measured by packed cell volume) or by aldosterone inhibition.

Adult↗
PubMed1978

The effect of indomethacin on plasma renin activity and urinary aldosterone of patients with essential hypertension.

The effect of indomethacin on plasma renin activity (PRA), urinary aldosterone, 17 OH ketogenic steroids and plasma cortisol was studied in twenty-three patients with essential hypertension and compared in eleven patients to oxprenolol effect by 2 x 2 factorial trial. Indomethacin decreased PRA and urinary aldosterone: its effect was maintained when the drug was given for three days and it was related to basal PRA and aldosterone values. Therefore in patients with low PRA (renin-sodium index) PRA and aldosterone were unchanged, while they decreased in the normal high PRA group. Aldosterone changes were related to those of PRA, while 17 OH ketogenic steroids and plasma cortisol were unchanged. Both indomethacin and oxprenolol decreased PRA, but no interaction or additive effect was found between the two drugs. The present data indicate that indomethacin can decrease both PRA and aldosterone to an extent which is related to basal values and that aldosterone changes are mainly explained by those of PRA. The PRA unresponsiveness to indomethacin found in low renin patients may suggest renal prostaglandin deficiency. Finally the lack of interaction or of additive effect between indomethacin and oxprenolol may be explained by postulating either that the two drugs act on a common pathway or that an additive effect on PRA cannot be detected renin being maximally suppressed by full renal beta-receptors blockade.

17-Ketosteroids↗
PubMed1978

Plasma renin activity in renal veins of renovascular patients.

PRA was simultaneously measured in both renal veins and in a peripheral vein of patients with essential (6) and renovascular (37) hypertension. In renovascular patients suppression or renin secretion from the contralateral kidney was always observed: otherwise in patients with essential hypertension both kidneys contribute to peripheral PRA. The suppression of renin secretion from the ischemic kidney either by nephrectomy or by revascularization, joins with normalization either of peripheral PRA or of blood pressure. This finding points to the role of the renin-angiotensin system in the genesis of human renovascular hypertension.

Adolescent↗
PubMed1977

The effect of beta-adrenergic blockade on patterns of urinary sodium excretion, blood pressure and plasma renin activity in patients with essential and renovascular hypertension.

The effects of beta-adrenergic blockade, using oxprenolol, were studied in plasma renin activity, urinary sodium excretion and blood pressure in ten normal subjects and in 120 patients with essential and renovascular hypertension. Blood pressure was reduced by oxprenolol administration. The hypotensive action of the drug was independent of either the basal plasma renin activity or of the plasma renin activity response. Oxprenolol decreased plasma renin activity in normal subjects and in patients with essential hypertension with normal or high basal plasma renin activity. Patients with low plasma renin activity may show a lack of response to the beta-blockade. In patients with renovascular disease the response of plasma renin activity to oxprenolol was not a discriminant factor between patients cured or not cured by surgery. Some renovascular patients were unresponsive to beta-blockade with oxprenolol.

Adolescent↗
PubMed1977

Relationship between juxtaglomerular apparatus and plasma renin activity in human reno-vascular hypertension.

Juxtaglomerular cell count (JGCC) and juxtaglomerular activity (JA) on the fragments of the ischemic kidney and plasma renin activity (PRA) in peripheral venous blood were studied in 26 renovascular patients. In 11 cases PRA was also measured in renal venous blood. JGCC and JA values were always above normal range and both were significantly related to the PRA values in peripheral venous blood, while only JA was related to the PRA values in renal venous blood. These data indicate that in human renovascular hypertension the juxtaglomerular apparatus is hyperplastic and hypergranulated: the correlation between its morphological appearance and PRA seems to indicate that the renin-angiotensin system may be in some way involved in the genesis of hypertension.

Adolescent↗
PubMed1976

Clinical significance of plasma renin activity in human renovascular hypertension.

1. Plasma renin activity (PRA) in peripheral venous blood of patients with renovascular hypertension was found to be high (thirty-five), normal (twenty-one) and low (three). Twenty-one patients with high PRA were cured or improved after successful surgery, as were eight of eleven with normal PRA and one with a low PRA. After surgery high PRA values became normal or low. 2. A beta-receptor-blocking agent (oxprenolol) decreased PRA in twenty-eight patients (responders) and it either did not modify or increased PRA in the other fifteen (non-responders). All fourteen non-responders were cured by surgery, as were thirteen out of fifteen responders; ten non-responders became responders after surgery. Oxprenolol suppressed renin secretion of both kidneys of two patients with essential hypertension, and it either decreased (six) or did not modify (four) renin secretion from the ischaemic kidney. 3. PRA measurement in renal veins of twenty-six patients with renovascular hypertension showed that only the ischaemic kidney contributes to the peripheral PRA, renin secretion being suppressed in the contralateral kidney. The suppression of renin secretion from the ischaemic kidney produced either by nephrectomy (nine) or by aortorenal by-pass (six) normalized blood pressure. 4. Peripheral PRA values are of poor diagnostic significance and PRA unresponsiveness to a beta-receptor-blocking drug and the suppression of renin secretion from the ischaemic kidney are characteristic findings of renovascular hypertension curable by appropriate surgery.

Adolescent↗
PubMed1975

Postural changes of plasma renin activity after renal transplantation.

1. Postural changes of plasma renin activity (PRA) before and after the administration of a beta-blocking agent (oxprenolol) were studied in nine patients with renal homotransplantation and in ten normal subjects. 2. In normal subjects PRA always increased during upright posture without any correlation with postural changes in mean arterial pressure. Oxprenolol reduced the postural increase of PRA. 3. A postural increase of PRA could be detected as early as 20--25 days after renal transplantation, and appeared with increasing frequency as time elapsed. 4. There was a significant inverse correlation (r = -0.794, P less than 0.001) between the postural changes of PRA and those of mean arterial pressure. 5. These results suggest that in patients with renal homotransplantation the postural increase of PRA can only partly be due to circulating catecholamines or the sympathetic nervous system and may be explained by inverse changes in the mean arterial pressure.

Adolescent↗
PubMed1975

[Renin and aldosterone].

The radioimmunological dosages of renin and of aldosterone are used nowadays in clinical practice for research purposes only. The measurement of activity of plasma renin may be considered a significant indication of the concentration of the enzime in plasma and, indirectly, of its secretion. Several factors take a part in the regulation of renin secretion (mean arterial pressure, introduction of sodium and potassium, the sympathetic nervous system, ADH and concentration of angiotensin II in plasma). In pathological conditions such factors may cause alteration of the renin-angiotensin II system, thus determining hyperreninisms and hyporeninisms, whether associated with arterial hypertension or not. Several factors take a part on aldosterone secretion too (ACTH, sodiaemia, potassiaemia, renin-angiotensin II system). In pathological conditions the alteration of the regulation system may lead to hyperaldosteronism or to hypoaldosteronism of primary or secondary type. A survey of recent research on the physiopathology of the renin-aldosterone system is also given.

Aldosterone↗