Vascular β-Adrenoceptor-mediated Relaxation and the Tone of the Tissue in Canine Arteries

Abstract

Abstract The aim of the present investigation was to study the influence of the tone in the response to β-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 μm, 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) μm, 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. We conclude that: the tone of the vessel represents a critical factor deciding the sense of the response (coronary artery; low concentrations of noradrenaline or adrenaline), the level at which the relaxant effect is triggered (mesenteric = 80% vs splenic = 65%), and the magnitude of the relaxant effect (always). β-Adrenoceptors predominate in the mesenteric, pulmonary and splenic arteries, while β1-adrenoceptors predominate in the coronary artery. It is unlikely that adrenaline is able to cause vasodilation in any of the vascular beds studied.