This study examined the alpha1-adrenoceptor subtypes involved in mediating adrenergically induced Na+ reabsorption in the kidney of pentobarbitone anaesthetised Wistar and stroke-prone spontaneously hypertensive rats (SHRSP). Close renal-arterial phenylephrine (50-100 mu g kg-1 h-1) administration in Wistars, with regulated renal perfusion pressure, caused small reductions in renal haemodynamics but large reductions, of 35%, 64% and 57% (all P < 0.05), in urine volume, absolute and fractional Na+ excretions. The magnitude of these excretory responses to phenylephrine were similar in the presence of the alpha1B-adrenoceptor alkylating agent, chloroethylclonidine (10 mu g kg-1 h-1), but were blocked during administration of the alpha1A-adrenoceptor antagonist, 5-methylurapidil (10 mu g kg-1 h-1). Phenylephrine infusion in the stroke-prone spontaneously hypertensive rats caused changes in renal haemodynamics and fluid excretion of comparable magnitude to that achieved in Wistars which was blocked by 5-methylurapidil but not chloroethylclonidine. These observations suggest that in Wistar and stroke-prone spontaneously hypertensive rats the adrenergically induced Na+ reabsorptive responses are mediated by alpha1A-adrenoceptors.