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S C Verma

Publications and source records attributed to S C Verma.

58 records · Page 4Linked to original sources

Evidence for histamine and 5-hydroxytryptamine like effects of MK-212 on guinea pig ileum, taenia coli and rat fundus strip.

MK-212 (1 x 10(-7)M -- 1 x 10(-5)M) produced dose-dependent contractions of guinea pig ileum, taenia coil and rat fundus strip. The responses to MK-212 in all three preparations were blocked competitively by cyproheptadine (1 x 10(-8)M) a 5-HT receptor antagonist. Mepyramine (1 x 10(-8)M)-H1 receptor antagonist also inhibited competitively the responses of guinea pig ileum and taenia coli to MK-212. However, it failed to block significantly the responses of rat fundus strip to MK-212. Metiamide (1 x 10(-6)M), propranolol (1 x 10(-6)M) or atropine (1 x 10(-6)M) did not produce any significant effects on MK-212 induced contractile responses of guinea pig ileum, taenia coli and rat fundus strip. Our findings suggest that MK-212 produces both 5-HT as well as histamine like effects on the guinea-pig ileum, taenia coli and rat fundus strip.

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Blockade by burimamide of the effects of clonidine on cardiac contractility phosphorylase activation and cyclic adenosine monophosphate in isolated guinea pig heart.

Clonidine in a dose-range of 2.5 microgram to 80 microgram caused positive inotropic effect, which was accompanied by increase in the cyclic AMP levels and phosphorylase-activation of the isolated perfused guinea pig heart. Clonidine-induced biochemical and mechanical effects were blocked by burimamide, an H2-receptor antagonist Propranolol (1 x 10(-6)M), phentolamine (1 x 10(-6)M) or reserpine pretreatment, did not affect the clonidine responses on the perfused guinea pig heart. Clonidine reduced the 4-methyl-histamine (H2-agonist) responses of guinea pig heart. Our data suggest that the cardiac effects of clonidine may be due to stimulation of H2-type of receptors.

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The cardiac inotropic responses to insulin in the rat heart.

Insulin (5 to 40 I.U.) produced dose-dependent positive inotropic effect in the isolated rat heart. The responses to insulin were markedly inhibited in the presence of propranolol (1 . 1X10(-6) M). Insulin responses were markedly reduced in reserpine pretreated (5 mg/kg, i.p.) rats. Theophylline (4.4 mM), the phosphodiesterase inhibitor, potentiated the responses to insulin, whereas imidazole (20 mM), the phosphodiesterase stimulator inhibited the responses to insulin. The data suggest that the positive inotropic effects of insulin in rat heart is mediated through the release of cardiac catecholamines which stimulates beta-adrenoceptors. The final mediator of cardiac action seems to be cyclic-AMP.

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