Calcium entry blockers inhibit vasoconstrictor responses to sympathetic nerve stimulation mediated by alpha 1-adrenoceptors.

Stimulation of the sympathetic outflow (spinal cord segments T 7-9) in pithed rats resulted in an increase in mean arterial pressure, heart rate, total peripheral vascular resistance and cardiac output. The increase in blood pressure and peripheral resistance was markedly depressed by prazosin and to a lesser extent by yohimbine, suggesting that these responses were mediated primarily by postjunctional alpha 1-adrenoceptors. The calcium entry blockers nifedipine, tiapamil and verapamil also depressed pressor responses and the increase in total peripheral resistance to electrical stimulation of the sympathetic outflow in these rats. This depression resulted primarily from an effect on peripheral vascular resistance components, as cardiac output remained unaffected by the calcium entry blockers. This conclusion was supported by studies on isolated, perfused rat renal arteries. Vasoconstrictor responses of this in vitro preparation to perivascular nerve stimulation were depressed by 1,000-fold lower concentrations of prazosin than rauwolscine, demonstrating the predominantly alpha 1-adrenoceptor nature of these effects. Likewise, these vasoconstrictor responses were depressed by nifedipine, tiapamil and verapamil in a concentration-dependent manner. The results of this study suggest that vasoconstrictor responses of rat resistance vessels to sympathetic nerve stimulation are mediated primarily by postjunctional alpha 1-adrenoceptors and can be inhibited by calcium entry blockers. This implies that contractile responses of these resistance vessels to alpha 1-adrenoceptor stimulation are not independent of the availability of extracellular calcium.