Drugs online research references
Basic Res Cardiol. 1989 Jul-Aug;84(4):359-70.
Triiodothyronine-induced changes in function, metabolism and weight of the rat heart: effects of alpha- and beta-adrenergic blockade.
Zierhut W, Zimmer HG.
Department of Physiology, University of Munchen, FRG.
The involvement of alpha- and beta-adrenergic receptors in the triiodothyronine (T3)-induced hemodynamic and metabolic alterations and in the development of cardiac hypertrophy was analyzed in time-course studies. Female Sprague-Dawley rats received daily injections of T3 (200 micrograms/kg s.c.) and a continuous i.v. infusion of 0.9% NaCl or alpha- or beta-receptor blocking agents. NaCl-injected animals served as controls. Eighteen hours after T3 administration, heart rate and LV dP/dtmax were considerably elevated. Cardiac output (CO) was not significantly changed. These alterations were abolished by simultaneous infusion of the beta-adrenergic blocker metoprolol. After 48 hours, CO as well as the cardiac RNA concentration were markedly elevated. The rise in LV dP/dtmax and heart rate was similar to the 18-h-value and was prevented by metoprolol. However, metoprolol did not influence the increase in CO and RNA concentration. Likewise, after 72 hours, metoprolol antagonized the T3-induced increase in heart rate and LV dP/dtmax, but had no effect on the elevation of CO and RNA concentration, the enhancement of adenine nucleotide synthesis and cardiac hypertrophy. Like metoprolol, the alpha-adrenergic blocker prazosin did not influence the T3-evoked cardiac hypertrophy. Thus, the development of cardiac hypertrophy in this model can occur independently of alpha- and beta-adrenergic stimulation.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2479371&dopt=Abstract
Klin Wochenschr. 1979 Apr 1;57(7):331-9.
[Hemodynamic and humoral changes during administration of a sympathomimetic and a sympatholytic drug with special notes on the regulation of renin release (author's transl)]
[Article in German]
Meurer KA, Geuchen H, Lang R, Kaufmann W.
Studies in normal volunteers documented the positive inotropic effects of Etilefrin-HCL, a direct sympathomimetic drug, with increases of systolic blood pressure, renal blood flow and glomerular filtration rate. Sodium and potassium excretion as well as serum potassium decreased. After an additional injection of Metoprolol, a beta 1-sympatholytic drug, blood pressure, renal blood flow and glomerular filtration rate normalized, whereas electrolyte excretion decreased further. Renin release was decreased during administration of Etilefrin as well as during combined Etilefrin and Metoprolol application. Reziprocal to changes of blood pressure, plasma norepinephrine concentration decreased during Etilefrin and increased during combined administration of Etilefrin and Metoprolol. The results lead to the following interpretation: Changes of blood pressure and renal hemodynamics are mediated by beta 1-adrenergic effects of Etilefrin, whereas the electrolyte excretion is influenced by beta 2-adrenergic effects. Renin release seems to be influenced by beta 1 as well as beta 2-adrenergic receptors.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=35650&dopt=Abstract
J Androl. 1990 May-Jun;11(3):293-300.
Identification and characterization of a beta-adrenergic receptor in hamster Sertoli cells.
Skinner TJ, Heindel JJ.
Department of Biology, University of Mississippi.
Sertoli cells cultured from immature hamsters contain a beta-adrenergic receptor which is coupled to the cAMP second messenger system. Thus, isoproterenol, epinephrine, and norepinephrine, which act via beta-adrenergic receptors, all stimulate cAMP accumulation in Sertoli cells cultured for 4-5 days. This cAMP response to isoproterenol is inhibited stereospecifically by the beta-receptor blocker, propranolol. It is also sensitive to inhibition by beta-adrenergic antagonists in this order of potency: nonspecific beta receptor antagonists, propranolol, timolol, hydroxypindolol greater than beta 1 selective antagonists, oxyprenolol, metoprolol much much greater than beta 2 selective antagonist, butoxamine. Butoxamine was at least 1000-fold less sensitive than either the nonspecific or the beta 1 selective antagonists at inhibiting the response of either isoproterenol (nonspecific), dobutamine (beta 1 selective) or zinterol (beta 2 selective). The hamster Sertoli cell beta receptor is, therefore, predominantly of the B1 subtype. This beta receptor mediated increase in cAMP is sensitive to homologous desensitization and is stimulated synergistically by forskolin. In addition, Seroli cells freshly isolated from immature hamsters contain an active beta receptor. However, this beta receptor mediated increase in cAMP is dependent on the type of trypsin used in the cell preparation. In agreement with Kierszenbaum et al (1985), freshly isolated Sertoli cells from immature rats never responded to the catecholamines regardless of the type of trypsin used; indicating an important physiologic difference between rat and hamster Sertoli cells.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1974547&dopt=Abstract
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