Abstract
Ang‐(1–7) produces a significant decreasein the nerve stimulation (NS)‐induced release of both NE andNPY as well as perfusion pressure of the perfused mesentericarterial bed of the rat. This effect is greater in mesenteric beds obtained from Spontaneously Hypertensive Rats (SHR) compared to normotensive control. Two hypotheses were examined; 1. The Ang‐(1–7) induced inhibition of sympatheticneurotransmission is mediated at least in part by prostacyclin(PGI2) and 2. Ang‐(1–7) elicits greater effects in mesenteric beds of SHR because there is decreased Ang‐(1–7) present in the mesenteric artery and plasma of SHR. Experiments were carried out using mesenteric beds and plasmaobtained from 10–12 week old SHR and Wistar‐Kyoto (WKY) rats. The effect of Ang‐(1–7) on the NS‐evokedrelease of NPY was determined before and after the administrationof the COX inhibitor Indomethacin (to prevent PGI2 synthesis) and the PGI2 receptor blocker CAY 10441. A reversal in the attenuation of perfusion pressure by Ang‐(1–7) was observed in the presence of Indomethacin and CAY10441. The attenuation of NPY release by Ang‐(1‐7) also appears to be reversed by Indomethacin and CAY10441. Additionally, plasma and tissue concentration of Ang‐(1–7) were significantly lower in SHR, while those of Ang II were significantly higher. (Supported by HL60260 and NIGMS008306)
Published Version
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