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 RESEARCH PAPER
Year : 1996  |  Volume : 28  |  Issue : 2  |  Page : 77-83

Interaction of alpha-adrenoceptor antagonists with various agonists in isolated aorta and ventricle from normal and diseased rats



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Bhugra Praveen


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The present study attempts to investigate the interactions of alpha-adrenoceptors with various agonists. In isolated ventricle preparations obtained from rats chronically treated with prazosin there was a decrease in the pD2 value of nor-adrenaline (NA) and no change in maximal response suggesting that calcium fluxes do not play a role. However, with yohimbine there appeared to be a down regulation of the alpha, receptor. In hypertensive rats there was an increase in the pD2 value of NA and terbutaline (TA) with no change (NA) or increase (TA) in maxima suggesting increase in beta, receptor and increased calcium influx. The pD2 value of NA was reduced with chronic prazosin treatment which is in line with that observed in normotensive preparation. The increase in the pD2 value in hyperthyroid rat preparations may be due to thyroid hormone induced changes in various receptor effector coupling factors. Simultaneous treatment with alpha- adrenoceptor blockers suggest increase in alpha, receptor density and increase in calcium influx with NA. In aortic strip preparations chronic prazosin treatment abolished responses to NA and phenylephrine (PE) which could simply be due to alpha, blocking action of prazosin. However, the increase in pD2 value of NA and PE suggest that this could be due to block of presynaptic alpha, receptors. In DOCA-saline hypertensive rats chronic treatment with prazosin reduced the pD2 value and maxima of NA and abolished that of PE which is in line with the known mechanism of prazosin. With chronic yohimbine treatment the increase in pD2 value of PE may be due to the inhibitory action of alpha, receptors. The changes seen in the hyperthyroid rats or in those simultaneously treated with alpha adrenoceptor blocker may be secondary to the primary effect on the heart and due to generalised reduced sensitivity of the rat aorta.






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