AN ALTERED β‐ADRENORECEPTOR‐MEDIATED MODULATION OF NORADRENALINE‐INDUCED VASOCONSTRICTION IN SPONTANEOUSLY HYPERTENSIVE RAT MESENTERIC ARTERIES

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Abstract
Pressor responses to bolus injections of noradrenaline (NA) [norepinephrine] were analyzed, 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 vasodilator .beta.-adrenoreceptor population. The suppressant effect of (-)isoprenaline (10-4 M) was antagonized 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. Although a vasodilator .beta.-adrenoreceptor population exists in the SHR mesenteric vasculature, its vasodilator function evidently is comprised when compared to that found in normotensive rats.