BETA-ADRENERGIC RELAXATION IN MESENTERIC RESISTANCE ARTERIES OF SPONTANEOUSLY HYPERTENSIVE AND WISTAR-KYOTO RATS - THE ROLE OF PRECONTRACTION AND INTRACELLULAR CA2+

An attenuated beta-adrenergic vasodilation of small arteries may help explain the increased peripheral resistance in hypertension. To invest igate this, we compared the isoprenaline-induced relaxation of mesente ric resistance arteries of spontaneously hypertensive rats (SHR) and W istar-Kyoto rats (WKY) using a small vessel myograph. The arteries had similar diameters, but the contractile force induced by cumulative ad dition of KC (10-130 mM) was 1.3-fold higher for the SHR. The beta-adr enoceptor-mediated relaxation of arteries, precontracted with 40 mM K, was significantly less in SHR (41 +/- 3%, n = 11) than in WKY (56 +/ - 3%, n = 15, p = 0.003), and the pD(2) value for isoprenaline was sig nificantly lower in SHR (7.13 +/- 0.09 vs. 7.41 +/- 0.07, p = 0.02). I n contrast, when precontracted with phenylephrine (PE, alpha(1)-adreno ceptor agonist, 3-10 mu M), isoprenaline relaxation was almost complet e in both SHR and WKY, and the pD(2) value for isoprenaline did not di ffer between strains. Forskolin induced complete relaxation of both pr econtractions. Because the beta-adrenergic relax ation of the mesenter ic resistance arteries was attenuated only after K+-precontraction, we conclude that alterations in this precontracting mechanism in SHR rat her than a defect in the beta-adrenoceptor system may provide an expla nation for the decreased relaxation in these vessels. Intracellular Ca 2+ measurements and a review of the literature support this conclusion .