Drugs online research references
Sheng Li Xue Bao. 1994 Feb;46(1):1-7.
[Effect and its mechanism of substance P on contractile activity of isolated antral muscle strips of rat]
[Article in Chinese]
Liu X, Lin KW.
Department of Physiology, Dalian Medical College.
The present study was aimed at investigating the effect of substance P (SP) on the contractile activity of isolated antral muscle strips of rat and its underlying mechanism. Isolated strips were incubated in an organ bath into which SP was added with or without pretreatment of some antagonists or inhibitors. The results were as follows: (1) SP increased the contractile amplitude of the strips in a dose-dependent manner from 8 x 10(-11) to 8 x 10(-7) mol. At 4 x 10(-8) mol the amplitude was increased by 160.9 +/- 23.0%, while the automaticity of the strips was not affected. (2) This effect of SP could be partially inhibited by hexamethonium (ganglionic blocker), cyproheptadine (blocker of 5-HT2 receptor), diphenhydramine (blocker of H1 receptor), or aminophylline (inhibitor of phosphodiesterase), but not by atropine, propranolol, phentolamine, haloperidol, or naloxone. These results suggested that SP might be a non-cholinergic excitatory transmitter. Its spasmogenic action might be mediated by activating 5-HT neurons, which elicited release of histamine or directly acted on muscle cells.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7521970&dopt=Abstract
Am J Respir Crit Care Med. 1994 Nov;150(5 Pt 1):1379-83.
Potassium channel opener, YM 934, inhibits neurogenic plasma leakage in guinea pig airways.
Ishikawa J, Ichinose M, Nakajima N, Takahashi T, Yamauchi H, Miura M, Shirato K.
First Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.
The effect of a potassium channel opener, YM 934, on neurogenic airway plasma leakage was examined in anesthetized guinea pigs. Airway plasma leakage was evoked by stimulation of both vagal nerves in the presence of atropine (1 mg/kg, intravenous) and propranolol (1 mg/kg, intravenous), and was measured by extravasation of Evans blue dye (30 mg/kg, intravenous) in trachea (Tr), main bronchi (MB), and central (cIPA) and peripheral intrapulmonary airways (pIPA). Vagal stimulation significantly increased the dye leakage in all portions of the airway. YM 934 (10, 30, and 100 micrograms/kg, intravenous) inhibited vagally-induced plasma leakage in Tr, MB, cIPA, and pIPA, and this inhibitory effect of YM 934 was reduced by the ATP-sensitive potassium channel blocker, glibenclamide (25 mg/kg, intravenous). By contrast, YM 934 (100 micrograms/kg, intravenous) had no inhibitory effect on exogenous substance P (0.5 and 1 micrograms/kg, intravenous)-induced plasma leakage in any parts of the airway. These results indicate that YM 934 inhibits airway neurogenic inflammation by modulating the release of neuropeptides from the sensory nerve endings, and that the inhibitory effect can be attributed to the potassium channel opening activity of this compound.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7524979&dopt=Abstract
J Cardiovasc Pharmacol. 1994 Aug;24(2):336-43.
Beta-adrenoceptor antagonism and the hyperthyroid rat heart.
Amos G, Kerr D, Sernia C, Brown L.
Department of Physiology and Pharmacology, University of Queensland, Australia.
beta-Adrenoceptor antagonists such as propranolol and atenolol ameliorate the symptoms of human hyperthyroidism. We wished to define whether the cardiac changes of hyperthyroidism are attenuated by treatment with the beta-adrenoceptor antagonist atenolol. Rats were treated with triiodothyronine (T3) [1 mg/kg/day subcutaneously (s.c.) for 14 days] together with oral atenolol (100 mg/day on days 8-14); physiological parameters, inotropic and chronotropic responses in isolated cardiac tissues to compounds that increase intracellular cyclic AMP, and ventricular beta 1- and beta 2-adrenoceptors were measured. Administration of T3 produced marked hyperthyroidism, leading to increased metabolism, cardiac hypertrophy, tachycardia, hypertension, marked decrease in or loss of positive inotropic responses to calcium chloride, norepinephrine (NE), forskolin, and theophylline and increased ventricular beta 1- and beta 2-adrenoceptor density. Atenolol treatment of hyperthyroid rats attenuated the increases in heart rate (HR), rectal temperature, and O2 consumption but did not alter cardiac hypertrophy, hypertension, decreased positive inotropic responses or increased beta-adrenoceptor density. We conclude that beta-adrenoceptor antagonists produce only limited changes in hyperthyroidism-induced cardiovascular responses; furthermore, beta-adrenoceptor antagonists are unlikely to attenuate the cardiovascular risk factors of hyperthyroidism.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7526070&dopt=Abstract
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