Drugs online research references
Biochim Biophys Acta. 1987 Apr 3;918(2):168-74.
Inhibition of purified bovine milk lipoprotein lipase by propranolol and other beta-adrenergic blockers in vitro.
Kubo M, Hostetler KY.
Numerous clinical studies have shown that propranolol administration causes hypertriglyceridemia and a decrease in high-density lipoprotein in man. Although these findings have been attributed to diminution of triacylglycerol-rich lipoprotein catabolism by lipoprotein lipase, biochemical studies of the effects of propranolol on lipoprotein lipase activity in vitro have not been previously reported. We purified lipoprotein lipase from raw bovine skimmed milk and examined the effect of propranolol using as substrate phospholipid-stabilized, triolein emulsions containing purified human apolipoprotein C-II. These studies demonstrate that propranolol inhibits lipoprotein lipase activity. The inhibition was found to be noncompetitive with a Ki for propranolol of 0.55 mM. In addition, propranolol was shown to bind to phospholipid-stabilized triolein emulsions reaching local concentrations at the particle surface many times higher than its bulk concentration. Metoprolol, timolol and practolol, which are less hydrophobic than propranolol, were less inhibitory. Atenolol was the weakest inhibitor of purified bovine lipoprotein lipase in vitro.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2881580&dopt=Abstract
Res Commun Mol Pathol Pharmacol. 1996 Sep;93(3):301-18.
Beta 2- but not beta 1-adrenoceptors mediate the adrenergic component of reflex tracheal dilatation during bronchoconstriction in guinea pigs in vivo.
Takahashi Y, Ohno H, Misawa M.
Department of Pharmacology, SS Pharmaceutical Co., Ltd., Chiba, Japan.
Involvement of beta 1- and/or beta 2-adrenoceptors in vagal reflex-mediated tracheal dilatation during bronchoconstriction was investigated using the in vivo guinea pig tracheo-bronchi separated preparation. Inhalation of 0.01% (w/v) histamine to the bronchial site produced vagal reflex-mediated tracheal constriction followed by dilatation slightly after bronchial constriction. The latter reflex dilatation was significantly inhibited not only by 1% propranolol, a nonselective beta-adrenoceptor antagonist, but also by 0.1% butoxamine and 0.01% ICI-118,551, selective beta 2-adrenoceptor antagonists. However, 0.1% atenolol, a selective beta 1-adrenoceptor antagonist failed to inhibit the dilatation. Furthermore, the dilatation was also inhibited by 0.1% guanethidine treatment or adrenalectomy. All of noradrenaline, adrenaline and cyclic AMP contents in the tissue of the tracheal site significantly increased during the reflex tracheal dilatation after bronchoconstriction. The increase in cyclic AMP was reduced by 1% propranolol. Furthermore, local treatment of the tracheal site with 0.01% noradrenaline or 0.01% adrenaline induced tracheal dilatation, which was significantly inhibited by 0.1% butoxamine or 0.001% ICI-118,551 but not by 0.1% atenolol. These results suggest that the reflex tracheal dilatation during bronchoconstriction may be mediated by mainly beta 2-adrenoceptors activated by adrenaline released from the adrenal medulla and by noradrenaline released from the adrenergic nerve terminals.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8896042&dopt=Abstract
Brain Res Bull. 1997;44(1):97-103.
Intracerebroventricular administration of NPY increases sympathetic tone selectively in vascular beds.
Hu Y, Dunbar JC.
Department of Physiology, Wayne State University School of Medicine, Detroit, MI 48201, USA.
NPY is widely distributed and has broad regulatory actions in the peripheral and central nervous system (CNS) and is especially important in the regulation of cardiovascular responses. CNS administered NPY has been demonstrated to produce both increases and decreases in cardiovascular tone. In this study we evaluated the effect of intracerebroventricular (ICV) administered NPY on cardiovascular tone, regional blood flow dynamics, as well as the mechanism of this action in normal animals. Male rats were instrumented with ICV cannulas and allowed to recover. At the time of the experiment the rats were anesthetized with urethane/chloralose and the femoral artery cannulated for blood pressure determinations. The abdomen was opened and Doppler flow probes were placed around the iliac, renal, and superior mesenteric artery. Mean arterial pressure (MAP), heart rate (HR), iliac, renal, and superior mesenteric flow, as well as the calculated iliac, renal, and superior mesenteric conductance were determined. ICV administered NPY resulted in an increase in MAP and HR, which was associated with decreased flows in the iliac and superior mesenteric vessels while increasing renal flow. Conductance was decreased in the iliac and superior mesenteric vascular beds but not the renal artery. ICV administration of NPY in the presence of a systemically administered alpha1-adrenergic inhibitor, prazosin, attenuated the NPY-mediated effects on MAP as well as vascular conductance in the iliac and superior mesenteric vessels. Additionally, ICV administration of NPY in the presence of a systemically administered beta1-adrenergic inhibition, atenolol, also attenuated the NPY-mediated increase in HR and MAP. Blood flow responses and iliac and superior mesenteric vascular conductance were also attenuated by atenolol pretreatment. In these studies we conclude that lateral ventricular administration of NPY acts to increase systemic MAP and HR and the response is mediated by an increase in sympathetic tone to the heart and especially the splanchnic and skeletal muscle vasculature.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9288836&dopt=Abstract
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