INCREASED SENSITIVITY TO INHIBITION BY NIFEDIPINE OF RESPONSES OF THE MESENTERIC-ARTERY BED OF THE SHRSP TO NORADRENALINE IS NOT DEPENDENT ON ALPHA(1)-ADRENOCEPTOR SUBTYPES

The effects of noradrenaline (NA) on the perfusion pressure of mesenteric vascular bed preparations from stroke-prone spontaneously hypertensive rats (SHRSP) or weight-matched normotensive Wistar-Kyoto (WKY) rats in the presence of chloroethylclonidine (CEC, alpha(1B)-adrenoceptor antagonist) or WB4101 (WB, alpha(1B)-adrenoceptor antagonist), with or without the addition of nifedipine, were studied. NA caused a greater maximum increase in the perfusion pressure of the SHRSP mesenteric bed than that of the WKY, and the EC(50) for NA was lower in the SHRSP. There was no difference between the normotensive or hypertensive beds in the reduction of responses to NA produced by WB or CEC. Nifedipine, in the presence of either CEC or WB, further reduced responses to NA, but to a significantly greater extent in the SHRSP than in the WKY. There was no difference within either group between the additional inhibitory effect of nifedipine in combination with CEC or WB. These results confirm that following alpha(1)-adrenoceptor subtype blockade, the response to NA by the mesenteric bed of the SHRSP is more sensitive to inhibition by nifedipine than its WKY counterpart. However, the increased sensitivity to the inhibitory effects of nifedipine on responses to NA is not a result of preferential linkage of Ca2+ entry mechanisms to one or other of the alpha(1)-adrenoceptor subtypes.