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Biomedical subjects

R Pedrinelli

Publications and source records attributed to R Pedrinelli.

At least 127 records · Page 7Linked to original sources
PubMed1984

Dose-response relationship of prizidilol hydrochloride (SK&F 92657): a comparison between acute and chronic effects in patients with essential hypertension.

Three different doses (50, 100 and 200 mg) of prizidilol hydrochloride (SK&F 92657), a novel antihypertensive agent with vasodilating and beta-adrenoreceptor blocking properties, were given to three (n = 5) groups of essential hypertensive patients in order to evaluate hypotensive dose-response relationship of the drug and its beta-adrenoreceptor blocking properties. Irrespective of the dose given, acute administration of prizidilol did not effectively decrease blood pressure; however after one-week of treatment prizidilol was effective in reducing blood pressure at both the 100 and the 200 mg b.i.d. schedules. At these doses the drug decreased resting heart rate and plasma renin activity for the first 4-6 h after both acute and steady-state dosing. Similarly postdynamic exercise tachycardia was reduced to a significant extent by the drug; after acute administration this effect lasted 2 h with the lowest dose and 4 h with the highest one. After chronic administration this effect lasted up to 10 h for both the 100 and 200 mg doses. These data indicate that: chronic prizidilol treatment can achieve a satisfactory control of blood pressure in patients with mild-moderate essential hypertension; when prizidilol is administered chronically in hypertensive patients, an equally effective control of blood pressure can be obtained with either a 200 mg b.i.d. or a 100 mg b.i.d. schedule; prizidilol possesses beta-adrenoceptor blocking properties in man which can contribute to its pharmacodynamic activity.

Acetylation↗
PubMed1982

Humoral and hemodynamic effects of increasing doses of captopril in patients with essential hypertension.

To compare the hemodynamic and humoral effects of increasing doses of captopril, blood pressure, heart rate, plasma renin activity, plasma aldosterone and angiotensin-converting enzyme activity were measured in 10 patients with mild uncomplicated essential hypertension before and after captopril given in an increasing dose of 25, 50 and 100 mg twice a day, with each dose given for 3 days. The maximal decrease in blood pressure, which was predicted both by basal plasma renin activity values and by the hypotensive response to the first dose, was found after the lowest (25 mg) dose; this effect was detectable for 12 hours independently of the dose administered. Similarly, plasma renin activity was already maximally increased and plasma aldosterone maximally decreased at the lowest dose, while angiotensin-converting enzyme activity showed a dose-dependent inhibition. These data suggest that (1) neither the magnitude nor the duration of the hypotensive effect nor the resin-stimulating and aldosterone-inhibiting actions of captopril are enhanced by drug doses above 25 mg (at least up to 100 mg), and (2) there was no apparent correlation between the degree of angiotensin-converting enzyme inhibition with increasing doses of captopril and the hypotensive effects of the drug.

Adult↗
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

The effect of oxprenolol and indomethacin on renin and aldosterone of normal subjects during low sodium diet.

To study the mechanisms underlying renin and aldosterone increase during low sodium diet, eight normal subjects were studied during normal sodium diet (5 g of NaCl per day) for 5 days, after 4 days of low sodium diet, and, on continuing low sodium diet, after randomized treatment with oxprenolol (100 mg), indomethacin (200 mg) and oxprenolol + indomethacin (100 + 200 mg) each given for 24 h with a 48 h interval between each treatment. Renin (PRA) increased significantly after low sodium diet and the increase was inversely related to urinary sodium excretion. Both oxprenolol and indomethacin significantly reduced PRA to values similar to those during normal sodium intake, while the combination of the two drugs showed a net additive effect on PRA. PRA decrements after either oxprenolol or indomethacin were significantly related to PRA values after low sodium diet while no correlation was present between PRA values after oxprenolol and indomethacin. Aldosterone excretion showed a trend similar to that of PRA, being related to PRA on normal and low sodium diet, and to a lesser extent after drug treatment. These studies suggest that both the sympathetic nervous system and prostaglandins may play a permissive role in the regulation of renin and aldosterone of normal subjects on low sodium diet.

Adolescent↗
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↗
PubMed1982

The renin-angiotensin-aldosterone system and blood pressure during oxprenolol treatment in hypertensive patients pretreated with diuretics.

The interrelationship between PRA, urinary aldosterone excretion, and blood pressure was studied in 11 patients with essential hypertension while receiving a diuretic (1st week) and subsequently a diuretic + oxprenolol (2nd week). The diuretic reduced blood pressure and body weight but increased PRA and aldosterone. Oxprenolol reduced PRA on the 1st day but to a lesser extent on the 7th day. Blood pressure was decreased 1 day after oxprenolol administration, but to a greater extent on the 7th day. Blood pressure decrements were independent of renin suppression, but directly correlated to aldosterone changes. These data suggest that the hypotensive effect of oxprenolol in patients receiving diuretic treatment is independent of its suppression of renin. Aldosterone suppression may instead contribute to the hypotensive effect of the drug.

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↗
PubMed1980

The effect of clonidine on renin and aldosterone of hypertensive patients.

UNLABELLED: The behaviour of blood pressure, sodium balance, plasma potassium, urinary and plasma aldosterone, plasma cortisol, growth hormone, 17 OH ketogenic steroids were studied in 20 mild hypertensive in-patients (10 with low and 10 with normal PRA) before, 1 day and 5 days after clonidine. Blood pressure was significantly decreased by clonidine while PRA was as a mean unchanged. No correlation was found between blood pressure changes and either basal PRA or aldosterone values or PRA and aldosterone changes after clonidine. Urinary aldosterone was significantly decreased by clonidine and aldosterone changes were unrelated to those parameters (PRA, plasma potassium, sodium balance, ACTH) which are known to influence aldosterone secretion, while GH showed a small increment the first day but was unchanged the fifth day. Plasma aldosterone was not significantly changed by clonidine but its changes showed an inverse correlation to urinary aldosterone changes. CONCLUSIONS: In our normal and low renin patients the antihypertensive action of clonidine is neither predicted by basal PRA and urinary aldosterone values nor explained by their changes. The opposite effect of clonidine on urinary aldosterone and plasma aldosterone may point to a decrease of metabolic clearance rate of the hormone exerted by the drug.

Adult↗
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↗
PubMedDate not supplied

Mediation of renin release in essential hypertension by alpha-adrenoreceptors.

We studied the role of alpha-adrenoceptors in controlling renin release by infusing increasing doses of phentolamine into six patients with essential hypertension. Furthermore, in order to evaluate the relative importance of alpha 1- and alpha 2-adrenoceptors, phentolamine infusion was repeated in the same patients after pretreatment with prazosin, a selective alpha 1-blocking agent, and oxprenolol, a nonselective beta-blocker. After placebo, phentolamine infusion did not change mean blood pressure or heart rate and increased plasma renin activity (PRA) in a dose-dependent fashion. This finding suggests that the drug acts directly on the intrarenal renin producing apparatus and seems to confirm the inhibitory role of alpha-adrenoceptors in the control of renin release. After prazosin and oxprenolol pretreatment, PRA was respectively increased and decreased but it was unmodified by phentolamine infusion. This latter finding may indicate that both alpha 1- and alpha 2-adrenoceptors are involved in renin release or that alpha-adrenoceptors cannot be clearly differentiated into alpha 1- and alpha 2-subtypes.

Adult↗