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Angiotensin (1–7) Induced Inhibition of the Nerve‐Stimulation Induced Release of Norepinephrine (NE) and Neuropeptide Y (NPY) from the Rat Mesenteric Arterial Bed: Role of Prostacyclin
Author(s) -
Murray Jessica M.,
Macarthur Heather,
Westfall Thomas C.
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.956.2
Subject(s) - endocrinology , prostacyclin , medicine , neuropeptide y receptor , vasodilation , stimulation , norepinephrine , mesenteric arteries , neurotransmission , angiotensin ii , perfusion , sympathetic nerve , chemistry , blood pressure , receptor , neuropeptide , dopamine , artery
We have observed that Ang‐(1‐7) produces a significant decrease in the nerve stimulation (NS)‐induced release of both NE and NPY as well as perfusion pressure of the perfused mesenteric arterial bed of the rat. In the present study we examined the hypothesis that the Ang‐(1‐7) induced inhibition of sympathetic neurotransmission is mediated at least in part by prostacyclin (PGI 2 ), which is well known to inhibit sympathetic neurotransmission and to mediate part of the vasodilator action of Ang‐(1‐7). Experiments were carried out using the mesenteric arterial bed obtained from 10–12 week old Sprague Dawley and Spontaneously Hypertensive Rats (SHR). The effect of Ang‐(1‐7) on the NS‐evoked release of NE and NPY was determined before and after the administration of indomethacin to block PGI 2 synthesis and before and after the administration of the PGI 2 receptor blocker CAY 10441. Results obtained to date support our hypothesis that PGI 2 mediates the actions of Ang‐(1‐7). (Supported by HL60260 and NIGMS008306)