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SHR exhibit greater ANG II induced release of Neuropeptide Y (NPY) from mesenteric bed preparations than normotensive controls
Author(s) -
Byku Mirnela,
Macarthur Heather,
Westfall Thomas C
Publication year - 2008
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.22.1_supplement.912.17
Subject(s) - neuropeptide y receptor , endocrinology , medicine , angiotensin ii , mesenteric arteries , basal (medicine) , sympathetic nervous system , renin–angiotensin system , captopril , chemistry , receptor , neuropeptide , blood pressure , artery , insulin
NPY is a cotransmitter with NE and ATP in sympathetic nerves. There is evidence for increased activity of the sympathetic nervous system and the renin‐angiotensin system (RAS) as well as a role for NPY in the development and maintenance of hypertension in experimental animal models and in humans. Angiotensin II (Ang II) is known to facilitate sympathetic neurotransmission, and evoke the release of NE. This effect of Ang II is enhanced in blood vessels obtained from Spontaneously Hypertensive Rats (SHR). The objective of this study was to investigate the role of Ang II on the basal and nerve stimulated overflow of NPY from the perfused mesenteric arterial bed of SHR as hypertension develops. We observed that Ang II (0.01; 0.1 μM) facilitates basal and nerve stimulated overflow of NPY from the mesenteric arterial bed; an effect that is greater in preparations obtained from 4–6, 10–12 and 18–20 week old SHR than age matched normotensive Wistar‐Kyoto (WKY) or Sprague Dawley (SD) rats. Preparations obtained from prehypertensive (4–6 week old) SHR appear to behave similarly to those of 10–12 week old SHR with respect to Ang II induced changes in nerve stimulated NPY overflow. This facilitatory effect of Ang II appears to be mediated by the AT 1 receptor. In addition, Captopril administration resulted in decreased NE overflow from SHR preparations, suggesting that the local RAS is active in this model. (Sponsored by NIH HL60260 and AHA)