Histamine and 2-(2-pyridyl) ethylamine (PEA), a specific H1 receptor agonist, produced dose dependent contraction of guinea-pig gall bladder strip.Mepyramine maleate, the specific H1 receptor antagonist inhibited the responses to histamine and PEA, while metiamide the specific H2 receptor antagonist, had no significant effect. Dimaprit, a specific H2 receptor agonist, produced dose related relaxation of the depolarised gall bladder strip. Metiamide inhibited the responses to dimaprit while mepyramine did not produce any significant effect on the responses to dimaprit. Reserpine pretreatment (5 mg/kg. ip 24 h) did not significantly affect the responses to histamine. Neither atropine sulphate nor propranolol significantly altered the responses to histamine. Our findings suggest that the gall bladder contains excitatory Hl histaminergic receptors and inhibitory H2 histaminergic receptors. Further more, responses are due to its direct effects on the smooth muscle.

5-Hydroxytryptamine (5 HT), produced dose-dependent cotraction in the rat anococcygeus muscle. Cyproheptadine (1 x 10-6M), a specific 5HT receptor blocker failed to inhibit the responses to 5HT. However phentolamine (1 x l0-6M), a specific ( receptor blocker produced competitive antagonism (PA2 = 8.3) with 5HT. Responses to SHT were also inhibited in the reserpinised (5 mg/kg ip, 24 h before) and 6-hydroxy dopamine (60HDA) pretreated preparations. Repeated doses of 5HT produced tachyphylaxis.Imipramine, a 5HT uptake blocker, produced non-competitive inhibition of the responses to 5HT (pD'2 = 7.73(0.1). Nialamide, a MAO inhibitor and pyrogallol, a COMT inhibitor, significantly potentiated the responses to 5HT. However the combined effect of tyramine and 5HT responses were not additive. Our data suggest an indirect effect of 5HT in rat anococcygeus muscles. Further more the mechanism of release appears to be tyramine-like.

BDPU [ (1-butyl-3(1,(6-7-dimethoxyquinoline-4-yl) piperidine 4-yl urea)] produced dose dependent (20 'g to 160 'g) positive inotropic effect on the isolated heart of guinea-pig. Reserpine pre-treatment (5 mg/kg., ip, 24 h) shifted the BDPU dose response curve to the 1eft. This may, be a supersensitive phenomena. In the anesthetized dog BDPU did not produce significant changes in blood pressure at doses 50, 100 and 200 'g/kg. At higher dose 400 'g/kg a fall in the mean arterial pressure was observed.Neither propranolol (l0-7M) nor phentolamine(10-7 M) produced any shift of the dose response curve of BDPU. Theophylline (l0-3M) and imidazole (20mM) perfusion did not alter BDPU responses. The positive inotropic responses of BDPU seem to be due to direct changes in calcium availability in the myocardium.

Sodium potassium activated-adenosine-triphosphatase is intimately involved in the active transport of electrolytes across the biologic membranes.This presentation aims to review the evidence for a role of Na+K+ ATpase in tissue injury with different drugs, with particular reference to the liver. Rat liver has been used as an experimental model.Chronic liver injury has been produced by (i) carbon tetrachloride (ii) paracetamol and (iii) aflatoxin. The altered activity of Na+K+ATpase with toxic hepatic injury indicates the role of Na+K+ATpase at the cellular level, which is also correlated with the altered function of enzymes such as hepatic glutamic oxaloacetic and pyruvic transaminases. The effect of Picrorhiza kurroa and Eclipta alba have been studied to know their protective effect against the toxic hepatic injury. Restoration of Na+K+ATpase activity to normal by these two indigenous drugs indicates their hepatoprotective role against toxic hepatic injuries by various hepatotoxic agents used in the experimental study.

Adrenaline, noradrenaline and phenylephrine produed dose dependent relaxation of estrogen primed rat uterus. The responses to all three agonists were blocked competitively by propranolol (1.0x 10-6M to 1.0 x l0-7M), a specific ( receptor antagonist. Phentolamine (1.0x l0-6 M), a specific a receptor antagonist failed to inhibit these responses. The response to phenylephrine and noradrenaline were potentiated by caffeine perfusion (5.1 x l0-5M), a phosphodiesterase inhibitor, whereas imidazole perfusion (1.4x 10-4 M) inhibited the responses to phenylephrine and noradrenaline. Our data suggest specific ( receptor action of phenylephrine and noradrenaline in estrogen primed rat uterus. It is also suggestive that ( receptor action may be associated with adenylate cyclase cyclic 3'-5' adenosine monophosphate, (CAMP) system in this tissue.

Sodium stearate (5 x10-5M to 8x I0-4M) and sodium oleate (1 x 10-4M to 1.6 x I0-3M) exhibited positive inotropic effect on isolated frog's heart. The inotropic action to these fatty acids were blocked competitively by propronolol (1 x 10-6M), while phentolamine (1 x 10-6M) did not alter the responses to these fatty acids significantly. Imidazole (I x I0-4M) perfusion inhibited the fatty acids induced positive inotropic action, whereas caffeine (1 x l0-4M) potentiated the responses to these fatty acids. Moreover, there was decrease in responses upon repeated administration of submaximal dose of fatty acids. Our data suggests that sodium stearate and sodium oleate produced cardiotonic effect which could be through the release of catecholamince