Drugs online research references
Life Sci. 1996;59(14):PL221-6.
Alpha 1- and beta-adrenergic and muscarinic-cholinergic regulation in the spontaneous beating and Ca2+ oscillations in cultured neonatal rat cardiac myocytes.
Takemura H, Kimura H, Hatta S, Amemiya N, Kawana S, Imoto K, Ohshika H.
Department of Pharmacology, Sapporo Medical University, Japan.
alpha 1- and beta-adrenergic and muscarinic-cholinergic regulation in spontaneous beating and Ca2+ oscillations in neonatal rat cardiac myocytes at day 6 of culture was investigated. The spontaneous beating in myocytes decreased in the presence of 10 microM norepinephrine (NE). This negative chronotropic action was antagonized by prazosin. Carbachol (CCh) also showed negative chronotropic action which was inhibited by atropine. On the other hand, isoproterenol (ISP) increased the beating rate which was antagonized by propranolol. NE increased inositol phosphate formation whereas CCh and ISP did not. NE and CCh suppressed the frequency of the spontaneous Ca2+ oscillations but ISP increased. The present results suggest that alpha 1-adrenergic and muscarinic receptors regulate chronotropism to be negative whereas beta-adrenoceptor regulates chronotropism to be positive in cultured neonatal rat cardiac myocytes.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8831806&dopt=Abstract
Eur J Pharmacol. 1996 Jul 11;308(1):81-6.
Stimulation of phospholipase C activity by norepinephrine, t-ACPD and bombesin in LA-N-2 cells.
Sorrentino G, Singh IN, Massarelli R, Kanfer JN.
Istituto di Scienze Neurologiche, II Universita degli Studi di Napoli, Italy.
The release of [3H]inositol phosphates from myo-[3H]inositol-prelabeled LA-N-2 cells was measured in the presence of beta-adrenoceptor, metabotropic glutamate and bombesin agonists. Norepinephrine and isoproterenol increased the formation of [3H]inositol phosphates in a dose-dependent manner, with an EC50 of 100 microM for norepinephrine and an EC50 of 5 microM for isoproterenol. These stimulations were abolished by propranolol, a beta-adrenoceptor antagonist, with an IC50 in the range of 50-55 microM for both norepinephrine and isoproterenol. The stimulation of [3H]inositol phosphate appearance occurred with varying concentrations of trans-1-amino-1,3-cyclopentanedicarboxylic acid (t-ACPD), a metabotropic glutamate receptor agonist. This release of [3H] inositol phosphates was blunted by its antagonist, 2-amino-3-phosphonopropionic acid (AP-3). Bombesin and neuromedin-B, a bombesin-like peptide, also increased the appearance of [3H]inositol phosphates. This was blunted by the antagonist [Tyr4, D-Phe12] bombesin. The appearance of [3H]inositol phosphates stimulated by t-ACPD was coupled through a cholera toxin-sensitive G-protein and the bombesin-stimulated appearance of [3H]inositol phosphates was coupled through a pertussis toxin-sensitive G-protein. The norepinephrine-stimulated appearance of [3H]inositol phosphates was toxin insensitive. The stimulation of the [3H]inositol phosphate appearance by these three agonists was protein kinase and Ca2+ independent.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8836635&dopt=Abstract
Eur J Pharmacol. 1996 Jan 25;296(2):173-80.
Local exposure to salbutamol or Bt2 cyclic AMP inhibits pleural exudation and leukocyte influx caused by antigen in rats.
Diaz BL, Serra MF, Alves AC, Cordeiro SB, Martins MA, e Silva PM.
Departamento de Fisiologia e Farmacodinamica, Instituto Oswaldo Cruz/FIOCRUZ, Rio de Janeiro, Brazil.
The local effect of salbutamol and N6,2'-O-dibutyryl adenosine 3':5'-cyclic monophosphate (Bt2 cyclic AMP) on the rat pleural inflammation caused by allergen was investigated. Antigen (ovalbumin, 12 micrograms/cavity) intrathoracically administered to immunized rats led to a marked pleural protein extravasation and leukocyte infiltration, as attested by the quantification of protein and enumeration of leukocytes recovered from the pleural cavity. Salbutamol (10-40 micrograms/cavity) and the cell-permeable cyclic AMP analogue, Bt2 cyclic AMP (20-160 micrograms/cavity), injected 1 h and 5 min before the antigen, respectively, inhibited the exudation occurring within 30 min, and neutrophil and eosinophil accumulation occurring 4 and 24 h, respectively. The late eosinophilia was also markedly attenuated by salbutamol administered 10 min post-challenge, when mast cells had already been degranulated. Pretreatment with the beta-adrenoceptor antagonist propranolol (1 mg/kg, i.v.) failed to modify the inhibitory effect of Bt2 cyclic AMP, but abolished the blockade caused by salbutamol of leukocyte infiltration under conditions where the salbutamol anti-exudatory activity was impaired to about 80%. In another set of experiments, salbutamol (20 and 40 micrograms/cavity) markedly inhibited the exudation caused by histamine and 5-hydroxytryptamine (5-HT) which, though to a lesser extent, was also sensitive to Bt2 cyclic AMP (80 micrograms/cavity). As observed with allergic pleurisy, propranolol impaired the inhibition by salbutamol of histamine- and 5-HT-induced exudation, whereas the Bt2 cyclic AMP inhibition was not affected. We conclude that salbutamol and Bt2 cyclic AMP share the ability to inhibit pleural exudation and leukocyte recruitment caused by allergen in immunized rats, suggesting that the anti-inflammatory effect of salbutamol may be mediated by a cyclic AMP signaling pathway, probably via beta 2-adrenoceptor activation.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8838454&dopt=Abstract
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