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The involvement of central alpha-noradrenergic receptors in intracranial self-stimulation (ICSS) was studied. Dose-response curves were established for the blockade of ICSS by the antipsychotic drugs chlorpromazine, thioridazine, clozapine, and pimozide and the alpha-antagonist phenoxybenzamine. Antagonism of the facilitation, produced by the central alpha-agonist clonidine, of flexor withdrawal reflexes in the reserpinized spinal rat was used to assess the central alpha-blocking potency of the same drugs, and dose-response curves were established. No correlation was found between central alpha-blockade, as reflected by the ED50 for blockade of clonidine-facilated spinal reflexes, and the ED50 for blockade of ICSS. Pimozide blocked ICSS at doses virtually devoid of central alpha-blocking activity, while phenoxybenzamine was a potent alpha-antagonist and a weak blocker of ICSS. The lack of correlation between central alpha-blockade and decreased ICSS suggests that alpha-receptors are not critically involved in self-stimulation behavior.

This study was designed to determine if atriopeptin II (AP II) has any direct action on glomerular arterioles in vitro. Single superficial afferent or efferent arterioles were dissected from rabbit kidney, cannulated with micropipettes, and changes in lumen diameter were measured. The effect of AP II (10-(12)-10(-7) M) was tested alone or in arterioles precontracted with norepinephrine (3 X 10(-7) M, afferent) or angiotensin II (10(-10) M, efferent). By itself, AP II had no effect on lumen diameter in afferent or efferent arterioles, but both arterioles responded to 3 X 10(-7) M norepinephrine with 74 and 54% reductions in lumen diameter, respectively. Similarly, in norepinephrine-contracted afferent arterioles and angiotensin II-contracted efferent arterioles, AP II did not alter lumen diameter although acetylcholine (10(-6) M) produced near maximal relaxation of both arterioles. Furthermore, luminal addition of AP II (10(-7) M) had no effect on control lumen diameter or on the response to norepinephrine or angiotensin II. The preparation of AP II was biologically active since it caused dose-dependent increases in guanosine 3',5'-cyclic monophosphate levels in isolated rat glomeruli. These results suggest that the renal vascular effects of AP II observed in vivo are not due to a direct action on superficial glomerular arterioles but rather to an, as yet, unidentified indirect action of this peptide.