The role of central nervous system α-adrenergic and β-adrenergic receptors in the increased renal sympathetic nerve activity and antinatriuresis resulting from environmental stress (air stress) in conscious spontaneously hypertensive rats (SHR) was examined. Intracerebroventrlcular administration of the α2-adrenergic receptor agonist clonidine (1, 5, and 15 μg) prevented the effects of air stress on renal sympathetic nerve activity and urinary sodium excretion. Clonidine, 5 and 15 μg, lowered baseline mean arterial pressure and renal sympathetic nerve activity and increased baseline urine flow rate and urinary sodium excretion; clonidine, 1 μg, had no effect on these baseline levels. Intravenous administration of 5 μg, but not 1 μg of clonidine, abolished the renal responses to air stress. Intracerebroventricular administration of α2-adrenergic receptor antagonists (yohimbine, rauwolscine) reversed the effects of clonidine. α2-adrenergic receptor blockade alone, α1-adrenergic receptor blockade (20 μg prazosin), or combined α1-adrenergic and α2-adrenergic receptor blockade (30 μg phenoxybenzamine) had no effect on the renal sympathetic nerve activity or antinatriuretic responses to air stress. Intracerebroventricular, but not Intravenous, administration of the β2-adrenergic receptor antagonist ICI 118551 (30 μg) prevented the Increased renal sympathetic nerve activity and antinatriuretic responses to air stress. In contrast, intracerebroventricular administration of the β1-adrenergic receptor antagonist atenolol (30 μg) had no effect on the renal responses to air stress. These results indicate that the increased renal sympathetic nerve activity and antinatriuresis resulting from environmental stress in conscious SHR can be prevented by pharmacological stimulation of central α1-adrenergic receptors or by blockade of central β2-adrenergic receptors.