Vascular beta-adrenoceptor-mediated relaxation and the tone of the tissue in canine arteries.

The aim of the present investigation was to study the influence of the tone in the response to beta-adrenoceptor activation of four different canine arteries: coronary pulmonary, mesenteric and splenic. Five different levels of tone were produced (of about 35, 50, 65, 80 and 95% of the maximum) by adding phenylephrine (0.6, 1.0, 2.0, 4.0, and 10 microM, respectively) to the bath. In the coronary artery at spontaneous tone, low concentrations of noradrenaline or adrenaline (1-3 nM) caused either relaxation or contraction, while after induced tone, both noradrenaline and adrenaline caused concentration-dependent relaxations, noradrenaline being more potent (EC50 of 0.16 (0.13-0.20) and 0.38 (0.28-0.67) microM, respectively; n = 6; P < 0.05). Only in the coronary artery did isoprenaline relax the tissue irrespective of the previous level of tone. In all the other arteries, isoprenaline was able to cause concentration-dependent relaxations only if the previous tone was submaximal. At 80% of the maximum, isoprenaline caused relaxation in the mesenteric and pulmonary arteries, but in the splenic artery it caused relaxation only when the tone was of about 65% of the maximum or less. While in the coronary artery atenolol and ICI-118,551 (erythro-DL 1(7-methylindan-4-yloxy)-3-isopropylaminobutan-2-ol) were equipotent in antagonizing isoprenaline, noradrenaline and adrenaline, in the other vessels ICI-118,551 was from 58 (splenic artery) to 525 (mesenteric artery) times more potent than atenolol against the isoprenaline relaxant effect.(ABSTRACT TRUNCATED AT 250 WORDS)