Tissue specific susceptibility of alpha-adrenoceptor mediated vasoconstriction to nifedipine

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Abstract
The influence of the calcium antagonist nifedipine on α1- and α1-adrenoceptor vasoconstrictor effects was investigated in vitro. Changes in tension were monitored isometrically on helical strips of canine circumflex coronary and saphenous arteries suspended in 10 ml organ baths and of saphenous veins superfused with Krebs-Henseleit solution. Distinction between α1- and α2-adrenoceptor was made by using selective α-adrenoceptor blocking drugs such as rauwolscine, yohimbine, corynanthine and prazosin, and the agonists noradrenaline, phenylephrine and guanfacine. In venous and both arterial vascular smooth muscles, the contractile process could be triggered by stimulation of both α1- and α2-like adrenoceptors. Nifedipine inhibited the venoconstrictor response to the α2-agonist guanfacine, leaving that to the α1-agonist phenylephrine unchanged. In saphenous arteries, nifedipine in addition to guanfacine also antagonized constrictor responses to phenylephrine, though to a significantly weaker extent. In circumflex coronary arteries, nifedipine was equally potent in antagonizing responses to both α1- and α2-adrenoceptor stimulation. It is suggested that the susceptibility of α-adrenoceptormediated vasoconstrictor effects to blockade by calcium antagonists depends not only on the subtype of α-adrenoceptor but, in addition, on the type and origin of vascular smooth muscle and may be a reflection of tissue variations in intracellular calcium stores.