Drugs online research references
J Pharmacol Exp Ther. 1995 Jan;272(1):379-84.
Isoproterenol causes hyperpolarization through opening of ATP-sensitive potassium channels in vascular smooth muscle of the canine saphenous vein.
Nakashima M, Vanhoutte PM.
Center for Experimental Therapeutics, Baylor College of Medicine, Houston, Texas.
Experiments were designed to determine how isoproterenol affects the cell membrane potential of smooth muscle cells of the canine saphenous vein. Measurements of membrane potential were performed using glass microelectrodes. Isoproterenol (10(-9) to 10(-6) M) caused sustained, concentration-dependent membrane hyperpolarizations in tissues with and without endothelium. ICI 118,551 (a selective beta 2-adrenoceptor antagonist), but not atenolol (a selective beta 1-adrenoceptor antagonist), abolished the hyperpolarization to isoproterenol. Forskolin, an activator of adenylate cyclase, produced sustained hyperpolarizations, which were not mimicked by 1,9-dideoxyforskolin. Incubation with either ouabain or extracellular K(+)-free solution did not inhibit the electrical response to isoproterenol. Glibenclamide (a selective ATP-sensitive K+ channel antagonist) attenuated the hyperpolarizations induced by either isoproterenol or forskolin, whereas charybdotoxin (an inhibitor of large conductance Ca(++)-activated K+ channels) did not. These findings suggest that isoproterenol opens ATP-sensitive K+ channels indirectly through activation of adenylate cyclase in the smooth muscle of the canine saphenous vein. The adrenergic receptor involved belongs to the beta 2-adrenoceptor subtype.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7529310&dopt=Abstract
Integr Physiol Behav Sci. 1991 Apr-Jun;26(2):98-107.
Blood pressure hyperreactivity in non-human primates during dietary sodium combined with behavioral stress.
Turkkan JS, Story MK.
Division of Behavioral Biology, Johns Hopkins University School of Medicine, Baltimore, MD 21205.
The potential for behavioral stress alone or combined with dietary salt to augment pressor reactivity to the onset of daily experimental sessions was examined in normotensive, intact baboons over the course of four months. During twice daily experimental sessions, adult male baboons experienced food/shock conflict such that lever pulling not only served to earn food, but was also occasionally punished with cued mild electric shock. Blood pressure and heart rate were measured during a baseline period of fixed-ratio food reinforcement (3 weeks), during conflict stress (2 weeks), and after dietary salt was added to the daily conflict protocol (CONFLICT + SODIUM, 3 weeks). Reactivity, i.e., acute changes in blood pressure and heart rate to the daily experimental sessions, was not evident during food reinforcement sessions nor during the CONFLICT stress alone condition. The addition of a high salt diet virtually doubled blood pressure increases and heart rate decreases to the onset of experimental sessions. Average reactivities during CONFLICT + SODIUM periods were 11.2/7.9% delta for SBP/DBP (systolic/diastolic blood pressure, mmHg), and -5.65% delta for HR (heart rate, BPM). Neither atenolol nor hydrochlorothiazide diuretic significantly altered cardiovascular reactivity during CONFLICT + SODIUM in comparison to a preceding non-drug CONFLICT + SODIUM period. When atenolol and diuretic effects were directly compared, atenolol mildly augmented, while diuretic mildly decreased DBP but not SBP reactivity during CONFLICT + SODIUM. Reactivity was eliminated after salt loading and behavioral sessions were terminated. These findings provide evidence that enhanced salt ingestion may synergistically act with behavioral stress to produce pressor hyperresponsiveness to otherwise benign environmental events.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1878323&dopt=Abstract
Jpn J Pharmacol. 1990 Feb;52(2):195-200.
Characteristics of 125I-iodocyanopindolol binding to beta-adrenergic and serotonin-1B receptors of rat brain: selectivity of beta-adrenergic agents.
Tsuchihashi H, Nakashima Y, Kinami J, Nagatomo T.
Department of Pharmacology, Niigata College of Pharmacy, Japan.
The present study was designed to examine the specificity of beta-adrenergic antagonists for beta 1-, beta 2-adrenergic and 5HT1B-serotonergic receptors by the competitive interaction with 125I-iodocyanopindolol (125I-ICYP) as a radioligand. The beta 1-adrenoceptors were preferred by acebutolol, atenolol, betaxolol, practolol, and l-, dl- and d-metoprolol, while butoxamine and lCl-118,551 preferred beta 2-adrenoceptors. The selectivities of these beta 1- and beta 2-antagonists are well-known, but alprenolol which is known as a non-selective antagonist was 7.2-fold more selective for the beta 2-adrenoceptors in the present study. All beta-antagonists used were more selective towards beta-adrenoceptors as compared with 5HT1B-receptors. Good correlations were observed between the potencies of beta-adrenoceptor antagonists for inhibition of 125I-ICYP binding to beta 1- and beta 2-adrenoceptor sites and their potencies for inhibiting the binding of the same radioligand to 5HT1B-serotonergic receptor sites. These results suggest that beta-adrenoceptor antagonists can bind to beta-adrenoceptors and 5HT1B-receptors.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1968985&dopt=Abstract
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