INCREASED SENSITIVITY TO INHIBITION BY NIFEDIPINE OF RESPONSES OF THEMESENTERIC-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 mesente ric vascular bed preparations from stroke-prone spontaneously hyperten sive rats (SHRSP) or weight-matched normotensive Wistar-Kyoto (WKY) ra ts in the presence of chloroethylclonidine (CEC, alpha(1B)-adrenocepto r antagonist) or WB4101 (WB, alpha(1B)-adrenoceptor antagonist), with or without the addition of nifedipine, were studied. NA caused a great er 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 bed s in the reduction of responses to NA produced by WB or CEC. Nifedipin e, in the presence of either CEC or WB, further reduced responses to N A, but to a significantly greater extent in the SHRSP than in the WKY. There was no difference within either group between the additional in hibitory effect of nifedipine in combination with CEC or WB. These res ults confirm that following alpha(1)-adrenoceptor subtype blockade, th e response to NA by the mesenteric bed of the SHRSP is more sensitive to inhibition by nifedipine than its WKY counterpart. However, the inc reased sensitivity to the inhibitory effects of nifedipine on response s to NA is not a result of preferential linkage of Ca2+ entry mechanis ms to one or other of the alpha(1)-adrenoceptor subtypes.