Rostral Ventrolateral Medulla mediate the Sympathoexcitatory influence from Caudal Pressor Area in Spontaneously Hypertensive Rats

Abstract

The caudal pressor area (CPA), located in the caudal extent of ventrolateral medulla, tonically activates sympathoexcitatory outflow via the rostral ventrolateral medulla (RVLM) vasomotor neurons and regulates the blood pressure in normotensive animals. However, sympathoexcitatory influence from CPA in the hypertensive status have not been well examined. The sympathoexcitation from the CPA is independent of excitatory amino acid (EAA)-sensitive RVLM neurons in normotensive rats, thus other than EAA receptors may mediate these pathway. It has been reported that, in spontaneously hypertensive rats (SHR), one of the reason for maintaining high blood pressure is over-expression of AT1 receptor in RVLM. Moreover, previously we have reported that sympathoexcitatory input from CPA is enhanced in SHR (EB2003). On the basis of these findings, we hypothesized that the sympathoexcitatory influence from CPA is mediated by AT1 receptors in SHR. In chloralose-anesthetized male SHR, injection of glutamate into the CPA elicited a pressor response (27±2 mm Hg) that was substantially larger than that of WKY. Preinjection of Valsaltan into bilateral RVLM significantly attenuated the response of CPA (7±4 mmHg). In contrast, preinjection of aCSF did not change the response. These results indicate that the sympathoexcitatory influence evoked from CPA is mediated by AT1 receptor in RVLM. According to these results, enhancement of non-EAA dependent sympathoexcitatory influence from CPA and over-expression of AT1 receptor in RVLM may participate in maintenance of high blood pressure in SHR.