In normotensive rats, microinjections of neuropeptide Y (2.5 to 25 ptnol) into the unilateral nucleus tractus solitarius elicited dose-dependent vasodepressor and bradycardic responses accompanied by an inhibition of sympathetic nerve firing. After microinjections of the a 2 -adrenergic receptor antagonist yohimbine (100 ng) into the nucleus tractus solitarius, the depressor and bradycardic responses to the injection of neuropeptide Y (25 pmol) into the nucleus tractus solitarius were significantly attenuated. In contrast, pretreatment with the a,-adrenergic receptor antagonist doxazosin (200 ng) injected into the nucleus tractus solitarius did not alter these responses. In spontaneously hypertensive rats, microinjections of neuropeptide Y (25 pmol) into the nucleus tractus solitarius also elicited depressor and bradycardic responses that were significantly less than those of normotensive Wistar-Kyoto rats. However, pretreatment with yohimbine (100 ng) in the nucleus tractus solitarius did not diminish these depressor responses in spontaneously hypertensive rats. Depressor responses to neuropeptide Y, which was administered after yohimbine pretreatment, were also less in Wistar-Kyoto rats than in spontaneously hypertensive rats. The results suggest that the depressor and bradycardic responses elicited by neuropeptide Y were accompanied by the inhibition of sympathetic nerve activity. These responses may be mediated in part by a 2 -adrenergic receptor in the nucleus tractus solitarius. The impairment of a 2 -adrenergic receptor-mediated responses to neuropeptide Y in spontaneously hypertensive rats may contribute to the development of hypertension. 4 Thus, these findings suggest that NPY is involved in the central regulation of blood pressure. In in vitro studies, it has been demonstrated that NPY could interact with the a 2 -adrenergic receptor in the medulla oblongata and that this interaction could be impaired in spontaneously hypertensive rats (SHR).
5However, the underlying mechanism of action of NPY in the brain area has not been clarified.The present study was designed to determine the role of the a-adrenergic receptor in cardiovascular responses to NPY injected into the NTS in normotensive rats and SHR.