Role of glutamate receptors in the lateral parabrachial nucleus in regulation of cardiac sympathoexcitatory reflexes

Abstract

Stimulation of cardiac sympathetic afferents by ischemic metabolites like bradykinin (BK) evokes sympathoexcitatory reflex responses and activates neurons in the external lateral parabrachial nucleus (elPBN). The present study tested the hypothesis that the elPBN processes these reflexes through a glutamatergic mechanism. BK (0.1–1 μg) was injected into pericardial sack of anesthetized and bilateral vagotomized cats. Hemodynamic and renal sympathetic nerve activity (RSNA) responses to repeated intrapericardial BK before and after microinjection of kynurenic acid (Kyn, 25 mM, 50 nl) into the elPBN were recorded. Intrapericardial BK application evoked significant increases in mean blood pressure (MAP, 50 ± 6 mmHg) and RSNA (59 ± 8.6 %) in six cats. Kyn in the elPBN reduced BK-evoked reflex responses including MAP (50 ± 6 vs. 29 ± 2 mmHg, before vs. after) and RSNA (59 ± 8.6 vs. 29 ± 4.7 %, before vs. after). In contrast, inadvertent microinjection into areas surrounding the elPBN did not alter the responses to intrapericardial BK (MAP, 49 ± 3 vs. 51 ± 4 mmHg; RSNA, 64 ± 4 vs. 62 ± 2%, before vs. after). These data suggest that glutamate receptors in the elPBN play an important role in processing cardiac sympathoexcitatory reflex responses (supported by NIH HL-66217).