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At least 1,351 records · Page 75Linked to original sources
PubMed1979

Antianginal efficiency of nifedipine with and without a beta-blocker, studied with exercise test. A double-blind, randomized subacute study.

Twenty-one patients, mean age 60.3 years, with stable angina pectoris earlier treated with beta-blockers, were investigated with standardized exercise tests to evaluate the action of nifedipine alone and in combination with a beta-blocker. The first exercise test was performed 3 weeks after treatment with the patient's usual beta-blocker. Following this, the patients were tested twice after a double-blind cross-over 3-week trial with nifedipine and placebo. The patients were subsequently treated for 3 weeks with nifedipine 10 mg 3 times daily or placebo and then performed an exercise test. During the 4th period of 3 weeks the patients took a combination of nifedipine, 10 mg 3 times daily, and their usual beta-blocker and then performed the final exercise test. Nifedipine alone raised the heart rate by 5 beats/min at rest and diminished the systolic blood pressure at rest by 17 mm Hg. During exercise at comparable load the heart rate did not change significantly, but the systolic blood pressure decreased with 22 mm Hg. The exercise tolerance expressed as total work increased on a average by 20%, range-14 - + 194%. Nifedipine in combination with a beta-blocker gave a further decrease in the systolic blood pressure, totally 37 mm Hg at comparable load. The exercise tolerance increased more, totally by an average of 41%. There was a significant correlation between basal values for systolic blood pressure registered during the placebo period at rest and the percentage change in total work. The atrioventricular conduction time did not change significantly compared to placebo during treatment with nifedipine or the combination nifedipine + beta-blocker. No serious side-effects were observed during the study.

Aged↗
PubMedDate not supplied

Hemodynamic assessment of prenalterol: a cardioselective beta agonist in patients with imparied left ventricular function.

The hemodynamic effects of a new cardioselective beta agonist, prenalterol, were evaluated in 12 patients with moderate or severe impairment of left ventricular function due to coronary heart disease or primary cardiomyopathy. In doses up to 7 mg the drug led to a substantial increase of left ventricular pressure rise (+55%) and mean circumferential fiber shortening (+59%) and a decrease of left ventricular end-diastolic pressure (-52%), mean pulmonary artery pressure (-24%) and pulmonary vascular resistance (-37%) indicating augmented myocardial contractility and reduced left ventricular preload. Cardiac output was increased only in 4 of 12 patients, heart rate, left ventricular systolic and mean right atrial pressures and the pressure-rate product as an index for myocardial oxygen demand remained essentially unchanged. The same is true for stroke index, stroke work index, total peripheral resistance, left ventricular end-diastolic and end-systolic volume and ejection fraction. The positive inotropic effect was achieved with good tolerance and without arrhythmogenic or other side effects. Prenalterol may be especially useful in patients with low sympathetic activity and hypotension. In patients with diffuse congestive cardiomyopathy, high sympathetic activity, pronounced peripheral vasoconstriction and normal blood pressure, vasodilator therapy alone or in combination with prenalterol should be considered.

Adrenergic beta-Agonists↗
PubMed1984

A dose response study with oral prenalterol in patients with chronic congestive cardiac failure.

Prenalterol is an orally active cardioselective beta agonist, with a long half-life. Previous studies have confirmed its inotropic activity following intravenous infusion in patients with heart failure. It has little chronotropic activity and no significant arrhythmogenicity. We have studied the response to sustained-release oral prenalterol given over four weeks at doses of 20, 40, 100, and 200 mg daily in 10 patients with New York Heart Association class II and III heart failure due to ischemic heart disease. All were in sinus rhythm and already receiving diuretics and digoxin. The drug was well tolerated and without side effects. Nine patients showed a dose-related improvement in their exercise tolerance as measured on the treadmill, up to a dose of 100 mg daily, with a significant increase in estimated oxygen uptake. There was a dose-related reduction in maximum heart rate, systolic blood pressure, and rate-pressure product during exercise, which is suggestive of a reduction in myocardial oxygen consumption. We conclude that prenalterol improves exercise tolerance without any significant cardiovascular or other side effects, and produces a clinically relevant and sustained improvement in patients with chronic heart failure. M-mode echocardiographic measurements of left ventricular dimension and function at rest did not show any change during the study.

Administration, Oral↗
PubMed1983

Cardiovascular malformations associated with administration of prenalterol to young chick embryos.

Prenalterol (levo-1-[4-hydroxyphenoxy]-3-isopropyl-amino-2-propanol), a new stimulant of cardiac beta-adrenergic receptors in man, induces cardiovascular malformations when topically administered to 2 1/2- through 5 1/2-day chick embryos (Hamburger-Hamilton stages 17-27). Ventricular septal defects (VSD) located in the middle portion of the conal septum and classified as the simple, punched-out type VSD without septal malalignment were the predominant malformations observed throughout the developmental period tested. Arch malformations of the aortic circulation were also observed throughout the test interval, while anomalies of the pulmonary system were observed only at Hamburger-Hamilton stages 17 and 26-27. At stage 25 prenalterol demonstrated an acute toxicity significantly less than (1/50-1/20) epinephrine (P = .035 at concentrations of 8-10 mM) but was relatively equipotent with epinephrine in producing cardiovascular malformations. The effective median concentrations of the two agents were comparable (0.5-1.0 mM). The spectra of malformations induced by prenalterol and epinephrine were qualitatively similar. Malformations included absence of the right and/or left third aortic arch (innominate arteries), persistent remnant of the left fourth aortic arch, and VSD. These results support a previously proposed theory by these investigators that hyperstimulation of cardiac beta-adrenergic receptors in the chick embryo produces cardiovascular malformations.

Abnormalities, Drug-Induced↗
PubMed1984

Inotropic effect of prenalterol in amitriptyline poisoning.

A case of severe amitriptyline poisoning with grade IV coma, seizures, bradycardia and hypotension who did not respond to dopamine was successfully treated with prenalterol, a new cardioselective beta-agonist. The case is discussed with respect to plasma concentrations of dopamine, prenalterol and amitriptyline. Prenalterol, hydrocortisone and insulin may be useful as inotropic agents in tricyclic poisoning where dopamine fails to provide an adequate response.

Adrenergic beta-Agonists↗
PubMed1982

Effect of norepinephrine, prenalterol and metoprolol on the histochemical localization of adenylate cyclase activity in the brown adipose tissue of newborn rat.

Norepinephrine-stimulated adenylate cyclase enzyme (EC 4.6.1.1.) was histochemically demonstrated by electron microscope in the plasmalemmas of the newborn rat adipocytes. The precipitating agent in the histochemical reaction was cobalt salt. Metoprolol, a selective beta 1-blocker given in vivo abolished almost totally the reaction products from the outer surfaces of the plasmalemmas. In vitro treatment did not yield constantly reproducible results. Prenalterol (H 133/22-CGP 7760/B Hässle) a selective beta-agonist given in vivo stimulated enzyme activity in the plasmalemmas. The reaction, however, showed different localization patterns and enhanced amounts of reaction products in the membranes. It is proposed that the histochemical demonstration of amine-stimulated adenylate cyclase activity in the adipocyte plasmalemmas corresponds to the hormonal receptor sites. The question of the sensitivity of the receptors is discussed.

Adenylyl Cyclases↗
PubMed1985

Cytochemical demonstration of adenylate cyclase activity with cerium.

Cerium was applied for the ultrastructural, cytochemical localization of adenylate cyclase (EC 4.6.1.1.). The enzyme activity was stimulated with norepinephrine, prenalterol and cholera toxin in the brown fat cells of newborn rats. The final reaction product was observed in the plasmalemmas of the stimulated adipocytes. The precipitate was finely crystalline, easily visible in the electron microscope and in the X-ray microprobe analysis it yielded cerium and phosphate peaks, respectively. The use of cerium offers a new tool valid for the cytochemical localization of adenylate cyclase enzyme related to the membrane receptors.

Adenylyl Cyclases↗
PubMed1984

Effects of in vivo treatment with isoprenaline or prenalterol on beta-adrenoceptor mechanisms in the heart and soleus muscle of the cat.

The full agonist isoprenaline (5.3-6.6 nmol/kg . min) and the partial beta-adrenoceptor agonist prenalterol (10.6-13.3 nmol/kg . min) were administered to cats continuously via osmotic minipumps (i.p.). After seven days the functional and adenylate cyclase responsiveness to the agonists, as well as the beta-adrenoceptor-binding characteristics, were studied in cardiac and soleus muscle preparations in vitro. After isoprenaline pretreatment, the papillary muscles and soleus muscle strips wer 15-18 times less sensitive to isoprenaline compared with muscles from control cats. The stimulatory potency (pD2) of prenalterol in the papillary muscle was not changed significantly. The affinity of the agonists to the beta-adrenoceptors was unaffected in both tissues by the pretreatment, but the densities of beta-adrenoceptors were significantly reduced, by 36% (myocardium) and 47% (soleus) respectively. In the cat papillary muscle the intrinsic sympathomimetic activity (ISA) of prenalterol on contractile parameters was reduced from 84 (Tmax), 69 (dT/dtmax) and 71% (dT/ dtmin ) in control animals, to 33, 22 and 28%, respectively in the animals pretreated with isoprenaline. Prenalterol pretreatment did not induce any marked changes, either in the stimulatory potency or affinity of the agonists in the two tissues or in the maximal response (ISA) of prenalterol in the papillary muscle. The marked reduction in the stimulatory potency of isoprenaline and the reduced ISA of prenalterol in the myocardium after isoprenaline pretreatment can not be explained by the reduction in beta- adrenoceptor density alone. Since the affinity to the beta- adrenoceptors is unaffected, a reduced efficiency in the signal transmission must be the main cause.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenylyl Cyclases↗
PubMed1982

beta 1-and beta 2-adrenoceptor stimulatory effects of prenalterol.

Prenalterol, previously characterized as a functionally cardioselective partial beta-adrenoceptor agonist, was shown to relax K+ -elicited contractures in the uterine muscle from progesterone pretreated rats (pD2 7.7) and to increase beating rate in the rat right atrium (pD2 8.0) at about the same concentrations with maximal effects corresponding to 94 and 82% respectively of those of isoproterenol. Terbutaline, with equal maximal effects as isoproterenol, was 50 times more potent in the uterus (pD2 7.8) than in the right atrium (pD2 6.1). Both tissues displayed a high sensitivity to isoproterenol (pD2 9.1 in both tissues) indicating large receptor reserves for the full agonist. The maximal relaxing effect of prenalterol in the uterus was obtained at about a three-fold increase of the cyclic AMP content, which is similar to that obtained with isoproterenol at a corresponding relaxation. The effects in the uterine muscle of all three agonists were mediated through beta 2-adrenoceptors since beta 2-adrenoceptor blockers (ICI 118, 551 and IPS 339) antagonized the effects in concentrations which had only marginal effects on the atrial responses of the agonists. The beta 1-antagonists pafenolol and pamatolol in concentrations higher than those, which blocked the effects of the agonists on beating rate, were devoid of inhibitory effects in the uterus. These results indicate that prenalterol possesses the ability to elicit a functional response by stimulation of either beta 1-or beta 2-adrenoceptors provided that the tissue has a large spare receptor reserve for full agonists.

Adrenergic beta-Agonists↗
PubMed1982

Cardiostimulatory effects of prenalterol, a beta-1 adrenoceptor partial agonist, in vivo and in vitro. Correlation between physiological effects and adenylate cyclase activity.

The cardiostimulatory effects of prenalterol, a beta-1-adrenoceptor partial agonist, were studied in vivo and in vitro and compared to those evoked by isoprenaline, a full agonist, and to those of other partial agonists. In the anaesthetized rat, prenalterol and terbutaline were found not to elevate the myocardial cyclic AMP content; this was in sharp contrast to isoprenaline. Both partial agonists did, however, produce significant effects on heart rate. In the anaesthetized cat, prenalterol exhibited chronotropic and inotropic intrinsic activities of 88 and 76% respectively in relation to isoprenaline. No statistically significant increase in myocardial cyclic AMP content could however be detected. Prenalterol did not stimulate adenylate cyclase significantly in the cat myocardial homogenate. This was also true of the beta-2-adrenoceptor selective partial agonist procaterol. In this preparation, isoprenaline, noradrenaline and adrenaline acted as full agonists. Furthermore, prenalterol produced a concentration-dependent inhibition of isoprenaline-activated adenylate cyclase. Our data indicate that maximal cardiac stimulation occurs at a low level of adenylate cyclase activation and low myocardial cyclic AMP concentration when provoked by a full beta-adrenoceptor agonist. The maximal physiological effects of a partial agonist such as prenalterol may consequently be achieved at a marginal activation of the adenylate cyclase. The present data may thus support the hypothesis of a large beta-adrenoceptor reserve for full agonists in the heart.

Adenylyl Cyclases↗