To identify a physiological role for renal A2adrenergic receptors, renal vascular and tubular responses to administration of graded frequencies of renal nerve stimulation or graded doses of adrenergic agonists were determined in anesthetized spontaneously hypertensive, Wistar-Kyoto, and Sprague-Dawley rats. Renal vasoconstrictor responses to renal nerve stimulation and α1-adrenergk receptor agonists (norepinephrine, phenylephrine) were inhibited by an α1-adrenergic receptor antagonist (prazosin) but not by an aradrenergic receptor antagonist (rauwolscine). A semilog plot of renal vasoconstrictor responses as fraction of control renal blood flow versus agonist dose (in nanograms) was linear with the slope, k, taken as the fractional decrease in renal blood flow per nanogram. The α1-adrenergic receptor agonists (clonidine, guanabenz) produced minimal renal vasoconstrictor responses (fractional decrease in renal blood flow per nanogram: norepinephrine, 0.011; phenylephrine, 0.003; clonidine, 0.00087; guanabenz, 0.000037). The small renal vasoconstrictor responses to clonidine and guanabenz were more inhibited by rauwolscine than by prazosin. Low frequency renal nerve stimulation produced antidiuresis and antinatriuresis without decreasing giomenilar filtration rate or renal blood flow. The antidiuretic and antlnatriuretic responses were inhibited by prazosin but unaffected by rauwolscine. The magnitude of the renal vascular and tubular responses and their adrenergic receptor mediation were not different between spontaneously hypertensive, Wistar-Kyoto, and Sprague-Dawley rats. Although increased numbers of renal α2-adrenergic receptors have been described in spontaneously hypertensive rats, these results indicate that the renal vascular and tubular responses to renal nerve stimulation and adrenergic agonists are dependent on renal α1-adrenergic receptors; renal α2-adrenergic receptors are not involved.