1. Experiments were undertaken in groups of pentobarbitone anaesthetized normotensive, spontaneously hypertensive or stroke-prone spontaneously hypertensive rats to determine the alpha-adrenoceptor subtype mediating renal nerve-stimulated tubular sodium readsorption at the level of the nephron. 2. In normotensive rats, stimulation of the renal nerves at low frequencies, which caused small changes in renal blood flow and glomerular filtration rate, caused significant reductions in urine volume, absolute sodium excretion and fractional sodium excretion of between 35 and 55% (P less than 0.01) respectively. The renal nerve-mediated antidiuresis and antinatriuresis were inhibited by the administration of doses of prazosin which selectively blocked alpha 1-adrenoceptor vascular responses. The magnitude of the renal nerve-induced excretory responses was unaffected by the presence of idazoxan at a dose which selectively blocked alpha 2-adrenoceptor blood pressure and renal vasoconstrictor responses. 3. Renal nerve stimulation in spontaneously hypertensive rats caused small falls in renal blood flow and glomerular filtration rate but larger significant reductions in urine flow, absolute and fractional sodium excretions of between 40 and 50%, which were of similar magnitude to those observed in the normotensive rats. The renal nerve-induced reductions in urine flow, absolute and fractional sodium were abolished in the presence of prazosin but were unaffected by idazoxan. 4. In the stroke-prone spontaneously hypertensive rat, low level renal nerve stimulation had small effects on renal haemodynamics but reduced urine flow, absolute and fractional sodium excretions by similar magnitudes to those in the other groups of rats, by between 45 and 55%. These renal nerve-induced reductions in water and sodium excretion were abolished by prazosin but not by idazoxan. 5. Together, these data show that in both normotensive rats and the two models of genetic hypertension, the renal nerves have important actions on the renal tubules to increase sodium and water reabsorption while having little effect on renal haemodynamics. In all these groups of rats this tubular action of the renal nerves was mediated by alpha 1- but not alpha 2-adrenoceptors.

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