Effects of prolactin-releasing peptide microinjection into the ventrolateral medulla on arterial pressure and sympathetic activity in rats.

Prolactin-releasing peptide (PrRP), originally isolated from the hypothalamus, is highly localized in the cardiovascular regions of the medulla, and intracerebroventricular administration of PrRP causes a pressor response. In the present study we investigated the cardiovascular effects of PrRP applied to functionally different areas of the ventrolateral medulla (VLM), and to the nucleus tractus solitarius (NTS) and the area postrema (AP). In urethane-anesthetized rats, microinjection of PrRP into the pressor area of the most caudal VLM, recognized as the caudal pressor area in the rat, elicited dose-dependent increases in mean arterial pressure, heart rate, and renal sympathetic nerve activity. In the same injection area, neither thyrotropin-releasing hormone, corticotropin-releasing hormone nor angiotensin II affected these baseline cardiovascular variables. On the other hand, microinjection of PrRP into more rostral parts of the VLM, i.e. the depressor area of the caudal VLM and the pressor area of the rostral VLM, as well as the NTS and the AP, had no effect on these cardiovascular variables. Immunohistochemical analysis in the medulla revealed that the cardiovascularly PrRP-responsive region contained PrRP-immunoreactive cell bodies and nerve fibers. These results suggest that the most caudal VLM is an action site of PrRP to induce a pressor response, which is mediated, at least partly, by the increase in sympathetic outflow.