Increased vascular reactivity is a common observation in human and experimental hypertension. In this study, reactivity of the perfused mesenteric arterial/arteriolar vascular bed was examined during the development of renal and renal/salt hypertension in the rat. Increased reactivity to noradrenaline was observed in tissues from rats 1-12 weeks after the induction of renal/salt hypertension. In the early (1-2 week) stages, preparations were supersensitive to noradrenaline but not to KCl. In the later (4-6 week) stages, the increase in noradrenaline reactivity was due to supersensitivity and another factor which increased KCl reactivity and was characterized by an elevated maximum response. The noradrenaline response potentiating effects of exogenous angiotensin II were attenuated in the early but not the later stages of hypertension. Vascular reactivity to noradrenaline in tissues from renal hypertensive rats was similar to that in renal/salt hypertensive rats, but with a slower time course. The decay of noradrenaline responses in calcium-free conditions was slower in tissues from early renal/salt hypertensive rats, indicating that an increased availability of activator calcium was the mechanism of supersensitivity. The characteristics of the α-adrenoceptor did not appear to differ in the renal/salt hypertensive rat as the pA(2) value for phentolamine did not change. Differences in the pA(2) value for indorarin were observed in tissues from hypertensive rats but probably resulted from the unusual properties of this drug. The early supersensitivity to noradrenaline was partially attributable to the effects of a positive sodium balance.