Cardiovascular effects of discrete intrahypothalamic and preoptic injections of bradykinin.

Blood pressure and heart rate were monitored during discrete injections of bradykinin (5 nmol; 100-300 nl) in the hypothalamus and preoptic area of halothane anesthetized rats. In the paraventricular nucleus, bradykinin produced bradycardia without effecting blood pressure. The decrease in heart rate was abolished by pretreatment with methylatropine (IP), suggesting that the parasympathetic nervous system mediates this response. In contrast, in the dorsomedial and posterior hypothalamic nuclei, bradykinin increased both heart rate and blood pressure; methylatropine pretreatment (but not adrenalectomy) blocked these responses, suggesting that inhibition of the parasympathetic nervous system is responsible for the actions of bradykinin in these nuclei. In the preoptic suprachiasmatic nucleus, bradykinin produced an increase in heart rate only, which was attenuated by either methylatropine or adrenalectomy, indicating that both inhibition of the parasympathetic nervous system and adrenal catecholamine release contribute to the actions of bradykinin at this site. The increase in heart rate observed with bradykinin in the medial preoptic and anterior hypothalamic (A6400-6001 region) nuclei was not effected by either methylatropine or adrenalectomy, therefore activation of the sympathetic nervous system may be involved in responses in these regions. Finally, a 5 nmol dose of bradykinin potentiating factor (converting enzyme inhibitor; CEI) had effects similar to bradykinin when injected into the posterior hypothalamus, but no effect at any other brain site. CEI administration into brain sites 15 min prior to bradykinin injections failed to alter the bradykinin response. In summary, the central cardiovascular responses to bradykinin depend upon the specific site of injection and these sites correspond with the localization of bradykinin-like immunoreactivity previously reported by others.