Evidence against the role of α1-adrenoceptor reserve in buffering the inhibitory effect of nifedipine on the contractility of canine vascular smooth muscle
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abstract
The relationship between the postsynaptic α1-adrenoceptor reserve and the sensitivity of vasoconstriction induced by α-adrenoceptor agonists to the dihydropyridine Ca2+ entry blocker nifedipine was investigated in isolated muscle strips of dog mesenteric artery (DMA) and saphenous vein (DSV). The amplitudes of the contractile responses of DMA induced by phenylephrine were the same as those in DSV in the presence and in the absence of extracellular Ca2+. The use of 3 × 10−9 M phenoxybenzamine to irreversibly block the α1-adrenoceptors revealed a marked difference in the size of the α1-adrenoceptor reserve between DMA (40%) and DSV (7%). In spite of a larger receptor reserve, the contractile responses induced by phenylephrine in DMA were more sensitive to nifedipine compared with those in DSV. These results suggest that the postsynaptic α1-adrenoceptor reserve in vascular smooth muscle, at least in DMA and DSV, does not play an important role in buffering the inhibitory effect of nifedipine on the contractile response to a full agonist of α1-adrenoceptors. Other factors, such as the difference in the membrane depolarizing effect, the ability to utilize intracellular Ca2+ for contraction, and the possible existence of α1-adrenoceptor subtypes, may contribute to the different inhibitory effects of nifedipine on these blood vessels.Key words: adrenoceptors, nifedipine, smooth muscle, calcium, saphenous vein, mesenteric artery.
