Exaggerated sympathetic responses to bradykinin in spontaneously hypertensive rats.

Abstract

Possible defects in blood pressure (BP) regulation were studied by recording responses to centrally-administered bradykinin. Pressor effects accompanied by increased sympathetic nerve activity were elicited by intracerebroventricular injections in intact rats, but significant differences between Kyoto-Wistar normotensive (KNR) and spontaneously hypertensive rats (SHR) were not detected. By contrast, intracarotid injections into cross-perfused head preparations consistently produced more prominent systemic effects in SHR than in KNR, and these differences became even more pronounced following carotid denervation. After destruction of central noradrenergic neurons in KNR by intracerebroventricular injection of 6-hydroxydopamine (6-OHDA), responses to bradykinin became the same as those in SHR. These results are in accord with the interpretation that alpha-adrenergic mechanisms for blood pressure regulation in supramedullary brain areas no longer function normally in SHR and that a similar dysfunction can be induced in KNR by pretreatment with 6-OHDA.