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Biomedical subjects

A Salvetti

Publications and source records attributed to A Salvetti.

At least 199 records · Page 11Linked to original sources
PubMed1988

Humoral effects of metoclopramide and domperidone in normal subjects and in hypertensive patients.

To evaluate whether, in humans, metoclopramide (MCP), a DA2 antagonist which readily crosses the brain-blood barrier, can stimulate plasma aldosterone (ALD) through hypophyseal-adrenal axis activation in addition to its direct adrenal antidopaminergic activity, we have investigated the effects of MCP and domperidone (DMP), a specific antagonist of peripheral DA2 receptors, on plasma ALD, adrenocorticotropin (ACTH), cortisol and prolactin (PRL) in 15 subjects. Ten controls and 5 uncomplicated essential hypertensive patients, in whom the dopaminergic tone is hypothesized to be reduced, received, according to a single-blind randomized procedure, MCP (10 mg iv) or DMP (10 mg iv) and, after an interval of at least 1 week, the reverse treatment. MCP and DMP similarly increased PRL (p less than 0.001), while only MCP significantly increased plasma ALD (p less than 0.01), ACTH (p less than 0.02) and cortisol (p less than 0.02) both in normotensives and in hypertensives, without any difference between them. These data confirm that, in spite of similar DA2 antagonistic potency of the two drugs, only MCP is able to increase plasma ALD. Since MCP significantly increased also ACTH levels we cannot exclude an involvement of this hormone on MCP-induced ALD release. Finally, the similar PRL and ALD response in normotensives and hypertensives does not support the hypothesis of a reduced dopaminergic system activity in essential hypertensives.

Adrenocorticotropic Hormone↗
PubMed1988

The combination of a low-Na/high-K salt with metoprolol in the treatment of mild-moderate hypertension. A multicenter study.

To extend our previous findings that a low-Na/high-K salt (S) reduces BP in hospitalized patients, a multicenter study was performed. After a placebo period during which patients were informed by written instruction how to avoid only foods with a high Na content, 143 out-patients (84 males and 59 females, mean age 50.7 years, range 28-69) with DBP greater than or equal to 95 mm Hg randomly received for 4 weeks either metoprolol (M) 200 mg SR qd (67 patients), or S, 2 g bid to add to foods (76 patients). At the end of this period patients with DBP still greater than 90 mm Hg combined the two treatments for a further 4 weeks. Mean blood pressure (mm Hg), HR (bpm), 24-hrs urinary Na and K excretion were measured fortnightly. In comparison to pretreatment values MBP was significantly (P less than 0.01) reduced by both treatments, although to a greater extent in the M group already at the second week, without any further decrement thereafter. In the S group MBP decreased by 4.4 mm Hg and 27/76 patients were responders (DBP less than or equal to 90 mm Hg), while in the M group it was reduced by 9.0 mm Hg and 28/67 patients were responders. In the S group urinary Na excretion was significantly (P less than 0.01) lower than in the M group, and this difference was present until the end of period 1.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Long-term humoral and hemodynamic effects of celiprolol.

To evaluate the humoral and hemodynamic (both systemic and renal) effects of chronic treatment with celiprolol, six out-patients with mild to moderate uncomplicated essential hypertension received placebo for 1 month and celiprolol (400 mg qid) for 6 months. At the end of placebo and of the first and sixth month of treatment, blood pressure (BP), heart rate (HR), renal plasma flow (RPF), glomerular filtration rate (GFR), plasma renin activity (PRA), aldosterone (ALD) and noradrenaline (NA), urinary enzymes (NAG: N-acetyl-beta glucosaminidase, AAP: alanine aminopeptidase) were measured. Compared to placebo, celiprolol significantly and steadily reduced BP and HR. However, although the systemic hemodynamic effect was constant during the whole period of the study, the reduction of renovascular resistance and of plasma noradrenaline, detectable at the first month of therapy, disappeared at the sixth month. However, PRA, plasma aldosterone, GFR, and urinary enzymes did not change. These findings suggest that the antihypertensive effect of celiprolol is well maintained over the 6-month period; the drug did not exert any adverse effect on the kidney, and chronic celiprolol treatment does not influence renal hemodynamics.

Adult↗
PubMed1988

Acute dose-response curve of enalapril in renovascular hypertensives.

We evaluated the acute blood pressure lowering effect of enalapril in terms of dose-response curve and compared this effect with that on humoral parameters. Eleven renovascular patients with acute angiotensin-converting enzyme (ACE) inhibition received (according to a randomized double-blind cross-over design) placebo, 10, 20, and 40 mg of enalapril with a 72-hour interval between each dose. Seated blood pressure and heart rate were measured every hour for 6 hours and then again at the twelfth and twenty-fourth hour, while venous blood samples for plasma renin activity, plasma aldosterone and serum ACE measurements were obtained at the fourth and twenty-fourth hour after receiving the placebo or drug. Blood pressure was significantly reduced by all three doses of enalapril at hour 4, while at hour 24 it was reduced only by the 20- and 40-mg doses. A significant correlation (r = 0.68; P less than 0.001) was found between percentage decrements of mean blood pressure and the log of the doses at hour 4 with a similar (although not significant) trend at hour 24. Plasma renin activity was significantly and to a similar extent increased by the three doses of enalapril at hour 4, while at hour 24 it was significantly increased only by the 40-mg dose. Serum ACE and plasma aldosterone were significantly reduced both at hours 4 and 24 without any difference between doses. No correlation was found between mean blood pressure changes and those of humoral factors.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Ouabain vasoconstricts human forearm arterioles through alpha-adrenergic stimulation.

Studies on the role of endogenous sodium pump inhibitors in hypertension have used ouabain, a Na,K-ATPase inhibitor, as a pharmacological probe to test the effect of direct vascular Na,K-ATPase inhibition in man. Previous work has suggested that there are no alpha-adrenoceptor mediated components in the vasoconstrictor effect of this drug, although several animal and in vitro studies have shown a complex interaction between ouabain and either sympathetic neurotransmission or alpha-adrenergic excitation-contraction coupling mechanisms. To re-examine this issue, we infused ouabain at 7 micrograms/dl per min for 20 min without (saline infusion) or with phentolamine (8.0 micrograms/dl per min for 15 min), an alpha-adrenoceptor blocking agent, in uncomplicated mild to moderate hypertensive patients. The drugs were infused into the brachial artery, and forearm blood flow (by strain-gauge plethysmography), systemic blood pressure and heart rate were measured concomitantly. After local phentolamine pretreatment, ouabain lost its vasoconstrictor effect (n = 5). This result is unlikely to have been related to vasodilation because histamine, a non-alpha-adrenergic vasodilator, infused in another group (n = 5) of patients at rates roughly equieffective to phentolamine (0.05 microgram/dl per min for 15 min) did not modify the vasoconstrictor action of ouabain. Thus alpha-adrenoceptor mediated components caused the forearm vascular effect of ouabain and must be taken into account when using ouabain to study endogenous sodium pump inhibitor(s) in human hypertension.

Adult↗
PubMed1988

Captopril at 50 mg as well as at 100 mg once a day reduces blood pressure for up to 24 h: a double-blind randomized crossover study in mild to moderate hypertensives.

The extent and the duration of the antihypertensive effect of captopril, given once a day at a dose of 50 mg, compared with placebo and with the 100 mg once daily dose was studied in 30 mild or moderate uncomplicated essential hypertensives (mean +/- s.e.m. age 52.0 +/- 1.5 years), who responded (mean blood pressure decrease greater than 10%) to a single oral dose (12.5 mg) of captopril. According to a randomized, double-blind, crossover design, they were given 50 mg captopril four times a day, 100 mg captopril four times a day or matched placebo for 1 month. At the end of each treatment period blood pressure and heart rate were measured every 30 min from 3 h before to 2 h after the last dose. Although the heart rate did not change, mean blood pressure after the 50- and 100-mg doses of captopril was consistently significantly (P less than or equal to 0.05) lower than after placebo. The hypotensive effect peaked at the second hour and was still significant 24 h after dosing without any significant differences between the 50- and the 100-mg doses. These findings indicate that captopril, given chronically once a day at a dose of 50 mg to mild to moderate hypertensive responders, exerts its hypotensive effect up to 24 h and that doubling the dose does not increase either the extent or the duration of its action.

Blood Pressure↗
PubMed1988

Dietary sodium change in primary aldosteronism. Atrial natriuretic factor, hormonal, and vascular responses.

Atrial natriuretic factor (ANF) may be physiopathologically involved in several clinical conditions including human hypertension. However, few data are available regarding this putative hormone and its relationship to aldosterone, blood pressure, and vascular responsiveness to alpha-adrenergic receptor stimulation in primary aldosteronism, a volume-expanded, low-renin model of human hypertension. For this reason, the behavior of supine and upright plasma ANF as related to aldosterone, blood pressure, and forearm alpha-adrenergic sensitivity (plethysmographic technique) to intra-arterial norepinephrine infusion was studied in eight patients with primary aldosteronism (five with adenomas, three with hyperplasia) before and at the end of two sequential 1-week low (20 mmol/day) and high sodium (200 mmol/day) diet periods. Basal, predict ANF concentrations decreased and increased after low and high sodium intakes, respectively. Furthermore, highly significant postural ANF decrements after 1 hour of standing occurred with each diet, although they were lower after the low than after the high sodium diet. Plasma aldosterone, either supine or upright, was insensitive to dietary sodium manipulations, suggesting the absence of ANF-mediated control of aldosterone secretion in our patients. In spite of about twofold higher ANF concentrations during the high than during the low sodium diet, forearm vascular sensitivity to intra-arterial norepinephrine infusion did not change during the study. Furthermore, systemic arterial blood pressure rose to a highly significant extent after dietary sodium content was increased, thus casting doubt on a role for ANF as an endogenous long-term modulator of systemic blood pressure and peripheral alpha-adrenergic sensitivity in patients with primary aldosteronism.

Adult↗
PubMed1988

Dipyridamole echocardiography in essential hypertensive patients with chest pain.

The exercise-electrocardiography test shows limited feasibility and diagnostic accuracy for the noninvasive detection of coronary artery disease in hypertensive patients. Recently, the dipyridamole-echocardiography test (two-dimensional echocardiographic monitoring with dipyridamole infusion, up to 0.84 mg/kg over 10 minutes) has been proposed as an exercise-independent method for the diagnosis of coronary artery disease. The diagnostic usefulness of the exercise-electrocardiography test and the dipyridamole-echocardiography test was evaluated in 63 consecutive inpatients with history of chest pain, essential hypertension, and no previous myocardial infarction. The criterion of positivity for the exercise-electrocardiography test was a horizontal or downsloping ST segment shift exceeding 0.1 mV and for the dipyridamole-echocardiography test, a transient dyssynergy of contraction. Fifteen patients could not perform a diagnostic exercise-electrocardiography test because of an inability to exercise adequately (two patients), severe hypertension in spite of full antihypertensive therapy (six patients), or excessive blood pressure rise at the first step of the exercise-electrocardiography test (seven patients). Five patients could not perform the dipyridamole-echocardiography test because of a poor acoustic window. The overall feasibility was 76% for the exercise-electrocardiography test and 92% for the dipyridamole-echocardiography test (p less than 0.05). All 43 patients who performed both tests underwent coronary angiography; 30 had significant coronary artery disease (greater than 70% lumen reduction of at least 1 major coronary vessel). Sensitivity was 67% for both the exercise-electrocardiography test and the dipyridamole-echocardiography test (p = NS); specificity was 46% for the exercise-electrocardiography test and 92% for the dipyridamole-echocardiography test (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Angiography↗
PubMed1987

Plasma renin activity does not predict the antihypertensive efficacy of chlorthalidone.

It has been established that angiotensin II stimulation may limit the antihypertensive potential of diuretic therapy in some patients. It is less clear, however, whether renin-angiotensin II stimulation is the cause of the flat blood pressure dose-response relationship to diuretics. To investigate this, 75 out-patients with essential hypertension were treated with chlorthalidone 12.5, 25 or 50 mg o.d. for 3 weeks, in a double-blind, placebo controlled cross-over study. Chlorthalidone significantly reduced blood pressure in all the groups, a plateau being reached at 25 mg o.d. Similarly, plasma renin activity was increased by each dose level of chlorthalidone, but it showed a different trend, being increased to a comparable extent at 12.5 mg and 25 mg o.d., and still higher at 50 mg o.d. Thus, greater stimulation of renin was coincident with the levelling of the blood pressure response to chlorthalidone. However no significant correlation was found between interindividual plasma renin activity and change in blood pressure, either in the entire series, or in each treatment subset. The data suggest overall that renin stimulation may influence the characteristic dose-hypotensive response relationship to diuretic agents in antihypertensive therapy, but it is unlikely that measurement of individual plasma renin activity will provide an useful guide to the optimal dose of a diuretic agents.

Adult↗
PubMed1987

Captopril and nifedipine interactions in the treatment of essential hypertensives: a crossover study.

In order to evaluate the antihypertensive effect and the tolerability of combination therapy with an angiotensin converting enzyme inhibitor (captopril) and a dihydropyridine calcium antagonist (nifedipine) compared with monotherapy and placebo, we studied 32 uncomplicated essential hypertensives. At the end of a 1-month placebo washout period, their diastolic blood pressure was greater than 105 and less than 120 mmHg. The subjects then received, according to a double-blind randomized crossover design, captopril (50 mg twice daily), nifedipine (20 mg twice daily), captopril plus nifedipine at the same doses and the corresponding placebo, each treatment being given for 1 month. Both captopril and nifedipine significantly reduced mean blood pressure, which was further and significantly reduced by the combination of the two drugs. The decreases in mean blood pressure induced by nifedipine were significantly greater than those induced by captopril, and those induced by the combined therapy were significantly greater than those induced by either drug on monotherapy. The heart rate was significantly increased only by nifedipine, and to a similar, but not significant, extent by the combination therapy. Plasma renin activity was similarly and significantly increased and urinary aldosterone tended to decrease to a similar extent under the three active treatments. Adverse effects were mild to moderate in intensity; their incidence under captopril was lower than that under placebo, while the incidence under nifedipine and combined therapy was greater than under placebo. Ankle oedema disappeared under the combined therapy in three out of four patients who developed this side effect under nifedipine, although one additional patient developed ankle oedema under combination therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

A renin-secreting tumor.

A 23-year-old white male was referred for hypertension resistant to triple antihypertensive treatment, with hypokalemia, hyperaldosteronism and elevated levels of circulating plasma renin activity (PRA). Renal angiography and echoscans put in evidence an avascular solid mass at the midlower level of the right kidney. Renal vein catheterization with sampling of blood from the lower branches of the right renal vein showed lateralization of renin secretion from that side. After surgical exeresis, the mass (1.0 cm) was diagnosed as a renal hemangiopericytoma on the basis of light and electron microscopy. Tumor exeresis was followed by a prompt normalization of blood pressure and plasma potassium, with a decrease in PRA and aldosterone. Two months after surgery the patient was still normotensive. Circulating levels of inactive (trypsin-activable) renin were around 60% of the total pool of plasma renin, i.e. much lower than those reported in other cases of renin-secreting tumors. After surgery, inactive and active renin fell in parallel, implying that both were secreted by the tumor. Tumoral PRA responded to postural stimulation, but was unresponsive to acute converting enzyme inhibition, suggesting that sympathetic stimuli were still operative, but the negative feedback inhibition by angiotensin II on renin secretion was lost. Acute converting enzyme inhibition by captopril dropped blood pressure; however, during long-term treatment, the drug (3 X 50 mg/day) was ineffective in terms of either blood pressure normalization or relief of secondary hyperaldosteronism. Acute calcium entry blockade by nifedipine (10 mg p.o.) caused an evident blood pressure drop.

Adult↗
PubMed1987

Indomethacin reduces the antihypertensive action of enalapril.

We evaluated the influence of indomethacin on the pharmacological actions of Enalapril in 9 uncomplicated essential hypertensives. While on chronic treatment with Enalapril, these patients randomly received indomethacin (50 mg bid) or a corresponding placebo for 1 week and the opposite treatment after a 2 week interval. Indomethacin, which decreased serum thromboxane B2 and urinary 6-keto prostaglandin-F1 alpha, reduced the plasma renin activity (PRA) increased by Enalapril. Indomethacin did not modify serum ACE, whose activity had been reduced by the ACE inhibitor. Mean blood pressure (MBP) values, which were significantly and to a similar extent reduced by Enalapril at the beginning of the cross-over, after placebo addition and at the end of the two week interval, were significantly increased by indomethacin, despite being still significantly lower than baseline values. These data show that systemic and renal prostaglandin (PG) synthesis inhibition induced by indomethacin can blunt the antihypertensive effect of chronic Enalapril treatment in patients with essential hypertension.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Acute hemodynamic effect of nifedipine in hypertensives with chronic renal failure: the influence of volume status.

To study the influence of sodium on the antihypertensive effect of a calcium entry blocker (CEB), 11 hypertensives with chronic renal failure (CRF), whose blood pressure was uncontrolled by hemodialysis, randomly received nifedipine (10 mg p.o.) or the corresponding placebo before and after dialysis, reversing the sequence the next week. Dialysis induced a similar sodium loss during the two experimental periods (-339.0 +/- 26.7 vs. -348.8 +/- 26.4 mEq) and did not significantly change blood pressure. When compared with placebo, nifedipine significantly (p less than 0.05 or less) reduced mean blood pressure and increased heart rate both before and after dialysis, with a peak effect at the first hour. However, both absolute and percentage decrements of mean blood pressure induced by nifedipine before dialysis were significantly (p less than 0.05 or less) greater than those after dialysis. These data indicate that the acute hypotensive effect of nifedipine is greater during sodium repletion than during sodium depletion, a finding that suggests a positive interaction between sodium and the antihypertensive action of CEBs.

Adult↗
PubMed1987

Verapamil and alpha-mediated vasoconstriction in human forearm: a comparison between norepinephrine and selective alpha 1- and alpha 2-adrenergic agonists.

To evaluate the hypothesis of alpha-antagonism as a contributing factor to the vascular action of calcium entry blockade (CEB) in man, we have compared the action of verapamil, a CEB, on nonselective (norepinephrine, NE) and selective alpha 1-(methoxamine, MET) and alpha 2-(B-HT 933, BHT) adrenergic agonists in human forearm vasculature. All drugs were infused into the brachial artery at systemically ineffective rates. Blood pressure and heart rate were continuously monitored; forearm blood flow was measured through strain gauge plethysmography. Sixteen mild, untreated hypertensive patients were studied. Cumulative forearm blood flow dose-response curves to three cumulative infusion rates (3 min each) of NE (0.015, 0.05, 0.15 micrograms/100 ml tissue/min), MET (0.06, 0.6, 6 micrograms/100 ml tissue), and BHT (3, 10, 30 micrograms/100 ml tissue/min) were obtained during saline and after verapamil (0.9 micrograms/100 ml tissue/min X 15 min) infusion. Verapamil did not modify to any significant extent NE-mediated vasoconstriction, but clearly blunted the vascular action of either MET or BHT. Because NE is the physiological neurotransmitter, the data cast doubts about the relevance of alpha-antagonism as a mechanism of action of calcium entry blockade through verapamil. Besides, the data caution against generalizing by using data obtained through several compounds, including CEBs, of alpha-adrenergic stimuli.

Adrenergic alpha-Agonists↗
PubMed1987

Haemodynamic (systemic and renal) and humoral interactions between nicardipine and domperidone in hypertensives.

We studied the haemodynamic (systemic and renal) and humoral effects of nicardipine, a dihydropyridine calcium entry blocker in essential hypertensives and whether DA2 dopaminergic receptor blockade, induced by domperidone, might modify these effects. Eight uncomplicated mild to moderate hypertensives received placebo (saline) for 30 min followed by i.v. nicardipine (0.06 mg/min) for 30 min and repeated the same sequence introducing domperidone (10 mg i.v.) between saline and nicardipine; the effects of each treatment were followed for 30 min. The sequence was randomized with a 72-h interval between each study. Compared with placebo, nicardipine significantly reduced mean blood pressure (-14%) and renovascular resistance (-28%), increased heart rate (+15%), renal plasma flow (RPF; +21%), glomerular filtration rate (GFR; +43%) and urinary sodium excretion (+181%). The acute natriuretic effect of nicardipine was associated with an increase in the amount of filtered sodium (+43%) and with fractional sodium excretion (+110%), and a direct correlation was found between changes in RPF and in urinary sodium excretion (r = 0.68) and fractional sodium excretion (r = 0.57). Plasma renin activity (PRA) did not change, plasma aldosterone was significantly reduced (-10%) and plasma noradrenaline significantly increased (+63%). Domperidone pretreatment prevented the GFR increase induced by nicardipine and increased the noradrenaline response (+107%), but did not change the other actions of nicardipine. These data show that nicardipine, when acutely infused in essential hypertensives, while reducing blood pressure and reflexly activating the sympathetic nervous system, significantly increases urinary sodium excretion, RPF and GFR.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

The interference of indomethacin and of imidazole salicylate on blood pressure control of essential hypertensive patients treated with atenolol. Preliminary report.

To evaluate whether imidazole salicylate, a recently developed NSAID, can interfere with the antihypertensive effect of atenolol and to compare its action with that of indomethacin, 9 essential hypertensives, while on prolonged (more than 1 month) treatment with atenolol (100 mg qd) received, according to a double-blind cross-over study, imidazole salicylate (750 mg t.i.d.) or indomethacin (50 mg b.i.d. plus a placebo tablet) for 1 week, reverting the treatment after a 2-week wash-out period. While indomethacin addition significantly increased blood pressure, when compared to atenolol alone, imidazole salicylate did not change it. These data show that imidazole salicylate, unlike indomethacin, does not reduce the antihypertensive effect of atenolol.

Adult↗
PubMed1986

Antihypertensive and renal effects of tertatolol, a new beta-blocking agent, in hypertensive patients.

Tertatolol, a new nonselective beta-adrenoceptor blocker, was administered to 11 hypertensive patients in a short-term study. Systolic and diastolic blood pressure and heart rate were significantly decreased when compared to the placebo period: in spite of that glomerular filtration rate and renal plasma flow were unchanged. The administration of metoclopramide (a dopaminergic receptor antagonist) caused a significant reduction of renal plasma flow and a significant rise of renal vascular resistances during placebo, but no change during tertatolol therapy. A possible interference of tertatolol on dopaminergic receptors is discussed as the mechanism responsible for the unmodified renal plasma flow despite the significant blood pressure lowering with tertatolol.

Adrenergic beta-Antagonists↗