Search PubMed⌕ Search

Biomedical subjects

L Terzoli

Publications and source records attributed to L Terzoli.

At least 37 records · Page 2Linked to original sources
PubMed1980

Time-course of the anti-hypertensive action of atenolol: comparison of response to first dose and to maintained oral administration.

To show whether repeated administration of atenolol for several days would influence its pharmacokinetic parameters and the extent and duration of the pharmacologic responses, the plasma level of atenolol and changes in heart rate, blood pressure and plasma renin activity were measured in 12 hypertensive patients at various times of day (9 a. m., 12 noon, 3 p. m. and 7 p. m.) after oral administration of the first dose of atenolol 100 mg, again during the 7th and 14th days of continued once-daily administration of the same dose, and finally during the three days following withdrawal of the drug. The peak plasma concentration of atenolol (about 600 ng/ml) was found 3 h after administration of the first dose, and measurable amounts (50-70 ng/ml) were found after 24 h. None of the pharmacokinetic characteristics were changed by administration of a single daily dose for two weeks. After withdrawal of the drug, detectable amounts of atenolol were found in plasma for at least 48 h. The first dose of atenolol caused prompt (3 h) and prolonged (up to 24 h) lowering of supine and standing systolic and diastolic blood pressures, slowing of supine and standing heart rate, reduction of the blood pressure and heart rate responses to dynamic exercise, and a decrease in plasma renin activity. The extent and time-course of all these responses were not influenced by repeated once-daily administration of the 100 mg dose for two weeks. Most of the effects continued during the withdrawal days, the lowering of blood pressure being somewhat more prolonged than the slowing of heart rate. It is concluded that a once-daily dose of atenolol 100 mg decreases blood pressure and heart rate throughout the following 24 h, without excessive daily fluctuation in its effects, and without signs of tolerance or accumulation.

Administration, Oral↗
PubMed1980

Antihypertensive and renal effects of orally administered verapamil.

In 12 in-patients with moderate uncomplicated hypertension, maintained on constant sodium intake for 15 days, single-blind oral administration of verapamil 80-160 mg t.i.d. for 10 days had a significant antihypertensive effect: in the supine position systolic blood pressure decreased from 177 +/- 5 to 150 +/- 3 mmHg, and diastolic pressure from 111 +/- 3 to 96 +/- 2 mmHg; standing values were similarly lowered from 171 +/- 7 to 143 +/- 4 mmHg, systolic, and from 118 +/- 4 to 97 +/- 2 mmHg, diastolic. The heart rate did not show any significant change (from 79 +/- 3 to 77 +/- 2 beats/min, supine, and from 92 +/- 3 to 87 +/- 3 beats/min, upright). The antihypertensive effect was uniform throughout the day, being similar 2, 3, 6 and 8 h after administration of a dose. Dynamic exercise (75-100 watts on a cycle-ergometer) caused identical increases in arterial pressure and heart rate on the last day of placebo and again on the last day with verapamil, but the peak levels of systolic pressure reached during exercise were lower after verapamil than with placebo, because of the lower blood pressure before exercise. Reduction of arterial pressure by verapamil was not accompanied by increased plasma renin activity, or by renal retention of sodium and water: there was a small increase in sodium excretion, at least during the first days of verapamil administration (from 107 +/- 15 to 113 +/- 15 mEq Na+/day), and a slight significant reduction in body weight (from 74.2 +/- 3.7 to 73.5 +/- 3.7 kg). It is concluded that oral administration of verapamil significantly lowers blood pressure without simultaneously inducing cardiac stimulation, renin secretion or salt and water retention.

Adult↗
PubMed1980

Dose-response curve and time course of the antihypertensive effect of SKF 92 657, a beta-receptor-blocking and vasodilating compound.

1. The antihypertensive effect of the new drug, SKF 92 657, a hydrazinopyridazine derivative, possessing both beta-adrenoreceptor-blocking and vasodilating properties, was investigated in essential hypertension. 2. Single oral doses of 1.0 or 2.0 mg/kg did not produce any consistent decrease in blood pressure; 4.0 mg/kg was the threshold dose for a mild but not significant blood pressure reduction, whereas 8.0 mg/kg caused a significant and marked blood pressure decrease without clinically relevant changes in heart rate. 3. Continued administration of the drug for 7 days induced a significant and uniform reduction in blood pressure without tachycardia. The increase in systolic blood pressure and in heart rate caused by dynamic exercise was left unaffected by the drug.

Adrenergic beta-Antagonists↗
PubMed1978

Relationship between the hypotensive and renin-stimulating actions of diuretic therapy in hypertensive patients.

1. The pressor role of renin stimulated by chronic diuretic therapy has been assessed in 31 patients with essential hypertension by infusing the angiotensin II antagonist, saralasin, immediately before and at the end of 2 weeks' treatment with the diuretic, chlorthalidone. 2. Under diuretic therapy the change in blood pressure caused by saralasin was found to be correlated to plasma renin activity values, in such a way that small pressor responses were again observed in patients whose renin was mildly stimulated by the diuretic, whereas a marked depressor response occurred in patients whose renin was markedly increased. 3. On the other hand, the hypotensive effect of chlorthalidone was correlated to values of plasma renin activity under diuretic therapy in an opposite direction: indeed little or no decrease and sometimes an increase in blood pressure were observed in patients with marked renin activation by diuretic therapy. 4. It is concluded that stimulation of renin release by chronic diuretic therapy can be considered a factor limiting the hypotensive activity of diuretic drugs.

Adult↗
PubMed1978

Considerations on physiopathological approaches to the treatment of hypertension.

1. Two main physiopathological approaches to the treatment of hypertension are discussed, the first based on renin profiling and the second on haemodynamic measurements. 2. Reduction in plasma renin activity does not appear to be a clinically important mechanism in the hypotensive effect of beta-adrenergic blockers and of alpha-methyldopa. In particular, alpha-methyldopa has been found equally effective as a hypotensive agent both in normal renin and in low renin hypertensive patients. 3. Diuretics are certainly possessed of a renin-stimulating action, but in most patients this action does not obscure the hypotensive effect of these drugs. 4. Responders and non-responders to the hypotensive activity of beta-adrenergic blockers do not differ among them in their control haemodynamics.

Adrenergic beta-Antagonists↗
PubMed1976

Control of renin release: a review of experimental evidence and clinical implications.

Present knowledge of the mechanisms regulating release of renin is reviewed with particular emphasis on neural factors. Evidence is given for a direct effect of renal innervation on beta adrenergic receptors in juxtaglomerular cells, and for the involvement of reflex release of renin in conditions such as tilting and acute salt depletion. Participation of neural and nonneural mechanisms of control is also shown to occur in other conditions, such as aortic constriction and hemorrhage. The view is held that neural sympathetic factors might explain some of the renin disturbances found in essential hypertension. First, in patients with high renin hypertension part of the hypertension is renin-dependent, and these pressor levels of renin seem to be neurally induced since they can commonly be suppressed by beta adrenoreceptor blocking agents. Second, the hypothesis is presented that patients with low renin hypertension, at least those who have no volume disturbance, have a blunted sympathetic control of renin release. Therefore a sufficiently precise test of sympathetic activity, and possibly of body fluid volumes, should be associated with renin profiles for a better understanding of the pathophysiology of arterial hypertension and as a better guide to therapeutic management. Indeed, most of the available antihypertensive drugs act on sympathetic activity, body fluid volume or renin, and this multifaceted profile would provide more rational guidelines for treatment.

Adrenergic beta-Antagonists↗