An altered beta-adrenoreceptor-mediated modulation of noradrenaline-induced vasoconstriction in spontaneously hypertensive rat mesenteric arteries.

Pressor responses to bolus injections of noradrenaline (NA) were analysed, in the isolated perfused spontaneously hypertensive (SHR) rat mesenteric arterial bed, in an attempt to investigate the beta-adrenoreceptor-mediated modulation of catecholamine-induced vasoconstriction. NA-induced responses were potentiated in the presence of timolol (10(-7) M) and suppressed by (-)isoprenaline (10(-4) M), indicating the presence of a vasodilator beta-adrenoreceptor population. The suppressant effect of (-)isoprenaline (10(-4) M) was antagonised by timolol (10(-7) M). Lower doses of (-)isoprenaline (10(-7) M - 10(-5) M) potentiated the NA-induced pressor responses, while (+)isoprenaline (10(-5) M - 10(-4) M) suppressed the NA-induced responses. It is concluded that although a vasodilator beta-adrenoreceptor population exists in the SHR mesenteric vasculature, its vasodilator function is compromised when compared to that found in normotensive rats.