Drugs online research references
Teratology. 1983 Aug;28(1):9-14.
Reduction of catecholamine-induced cardiovascular malformations in the chick embryo with metoprolol.
Kuhlmann RS, Kolesari GL, Kalbfleisch JH.
It has been documented that activation of the beta 1-adrenergic receptor mechanism is directly related to cardiovascular malformations associated with the heart and great vessels of the embryonic chick. These adrenergic receptors are believed to be present and functional in the innervated and noninnervated embryonic heart at early stages of development. The present study examined the effects of four sympathomimetic cardioactive amines on chick cardiovascular morphogenesis at Hamburger and Hamilton stage 24. Special attention was directed toward understanding dopamine teratogenicity. In order of decreasing potency at the maximum teratogenic dose (dopamine greater than isoproterenol greater than epinephrine greater than norepinephrine) each drug was found capable of producing aortic arch anomalies of the third, fourth, and sixth aortic arches and ventricular septal defects (VSD). A new specific beta 1-adrenergic antagonist, metoprolol tartrate, was employed in an attempt to lower the incidence of these cardiovascular malformations. Pretreatment with this selective beta 1-blocker profoundly reduced the incidence of malformations within any amine-treated group. These experiments demonstrate that dopamine, as well as the other sympathomimetic amines, is a potent teratogen and most likely produces these cardiovascular malformations by primarily stimulating the beta 1-adrenoreceptor in the embryonic chick.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6636001&dopt=Abstract
Cardiovasc Res. 1993 Dec;27(12):2146-51.
Acute effects of catecholamines on function of the rat right heart.
Irlbeck M, Zimmer HG.
Department of Physiology, University of Munich, Munchen, Germany.
OBJECTIVE: Although the haemodynamic effects of catecholamines on the rat left ventricle have been investigated extensively, only few systematic in vivo studies have been performed on the right ventricle. The aim was to examine the acute effects of noradrenaline and isoproterenol on rat right ventricular function. METHODS: Haemodynamic variables were measured during acute, 20 minute infusion of noradrenaline (0.1 mg.kg-1 x h-1) or isoproterenol (12 micrograms.kg-1 x h-1) in female Sprague Dawley rats. To estimate the contribution of alpha and beta receptor stimulation to these effects, eight rats each were infused with prazosin (0.1 mg.kg-1 x h-1), metoprolol (1.0 mg.kg-1 x h-1), or the alpha and beta antagonist carvedilol (0.5 and 1.0 mg.kg-1 x h-1) alone and in combination with noradrenaline or isoproterenol. RESULTS: Noradrenaline and isoproterenol increased right ventricular systolic pressure (RVSP) from 30.3 (SEM 0.5) (n = 32) to 72.7(2.7) (n = 24) and 72.3(4.4) (n = 8) mm Hg, right ventricular (RV) dP/dtmax from 1848(70.3) to 4058(301) and 3612(366) mm Hg.s-1, and heart rate from 329(6) to 371(6) and 420(8) beats.min-1, respectively. Metoprolol completely prevented the isoproterenol induced haemodynamic changes, but neither metoprolol nor prazosin was able to significantly affect the pressure effect of noradrenaline (noradrenaline + metoprolol: 67.3(6.9) mm Hg, noradrenaline + prazosin: 67.0(3.8) mm Hg). The combination of both blockers, however, prevented the noradrenaline induced rise in RVSP (noradrenaline + metoprolol + prazosin: 36.5(5.1), and noradrenaline + prazosin + metoprolol: 30.0(1.2) mm Hg). Carvedilol (1.0 mg.kg-1 x h-1) significantly attenuated the noradrenaline induced RVSP increase (39.1(3.0) mm Hg), but not to the control range. Metoprolol or carvedilol completely prevented the noradrenaline elicited increases in heart rate (254(7) and 287(20) min-1) and RVdP/dtmax, but prazosin alone had no effect on the heart rate and RVdP/dtmax increase. Thus beta receptor blockade alone failed to significantly influence the noradrenaline induced increase of RVSP despite prevention of the increase in heart rate and RVdP/dtmax. Prazosin had a significant effect on RVSP only in combination with metoprolol. CONCLUSIONS: The combined effect of both alpha and beta blockade exceeds the pure addition of the single effects in the rat right ventricle. Moreover, we speculate that the failure to reduce the noradrenaline induced increase in RVSP by either alpha or beta blockade alone is due to the stimulation of the receptor that is not affected by the respective blocker.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7906201&dopt=Abstract
Proc Soc Exp Biol Med. 1985 Oct;180(1):144-8.
Effect of various catecholamine antagonists on prolactin secretion in conscious male rabbits.
Kaji H, Chihara K, Minamitani N, Kodama H, Kita T, Fujita T.
To clarify physiological roles of catecholaminergic systems in the control of rabbit prolactin (PRL) release, the effect of various catecholamine receptor antagonists on plasma PRL levels was examined in conscious, freely moving male rabbits. An intravenous (iv) injection of yohimbin (2.5 mg/kg body wt), an alpha 2-adrenoreceptor antagonist, but not prazosin (2 mg/kg body wt), an alpha 1-adrenergic receptor antagonist, resulted in a significant elevation of plasma PRL. Conversely, propranolol (2.5 mg/kg body wt, iv), a nonselective beta-adrenoreceptor antagonist, and metoprolol (2.6 mg/kg body wt, iv), a beta 1-adrenergic antagonist, slightly but significantly suppressed basal levels of plasma PRL. On the other hand, haloperidol (0.5 mg/kg body wt, iv), pimozide (0.3 mg/kg body wt, iv), sulpiride (5 mg/kg body wt, iv), chlorpromazine (3 mg/kg body wt, iv), and YM-09151-2 (0.2 mg/kg body wt, iv), all dopamine receptor antagonists caused a significant increase in plasma PRL. These results suggest that dopaminergic and alpha 2-adrenergic mechanisms exert a tonic inhibitory role and beta-adrenergic mechanisms, probably beta 1, a tonic stimulatory role in the regulation of PRL release in the rabbit.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2863827&dopt=Abstract
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