HYPERTENSION AND ENHANCED BETA-ADRENOCEPTOR-MEDIATED FACILITATION OF NORADRENALINE RELEASE PRODUCED BY CHRONIC BLOCKADE OF ADENOSINE RECEPTORS

1 The study was undertaken to compare the beta-adrenoceptor-mediated f acilitation of noradrenaline release in the tail artery of vehicle-tre ated rats and of rats rendered hypertensive by chronic administration of 1,3-dipropyl-8-sulphophenylxanthine (DPSPX). Artery rings were load ed with [H-3]-noradrenaline, and five periods of electrical stimulatio n (1 Hz for 2 min) were applied. To eliminate the influence of prejunc tional alpha(2)-adrenoceptors, the tissues were pre-exposed to 1 mu M phenoxybenzamine. 2 Isoprenaline caused a concentration-dependent incr ease of tritium overflow elicited by electrical stimulation. It was mo re effective in arteries from DPSPX-treated than in those from vehicle -treated rats; isoprenaline (27.8 nM) increased by 30% tritium overflo w in vessels from vehicle-treated rats whereas isoprenaline (7.0 nM) p roduced a 30% increase in vessels from DPSPX-treated animals. Furtherm ore, the maximal effect of isoprenaline was a 32.6% increase in contro l rats but a 48.6% increase in DPSPX-treated rats. 3 These results sho w that the sympathetic nerve endings of the rat tail artery are endowe d with prejunctional beta-adrenoceptors which mediate facilitation of noradrenaline release elicited by electrical stimulation. They also su ggest that adenosine receptors and beta-adrenoceptors interact at the prejunctional level and that impairment of this 'talk' may lead to the development of a hypertensive state.