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Resistance arteries from normally‐reared and maternal separation rats display similar vascular reactivity (1087.3)
Author(s) -
Fox Brandon,
Loria Analia,
Pollock Jennifer
Publication year - 2014
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.28.1_supplement.1087.3
Subject(s) - phenylephrine , medicine , sodium nitroprusside , endocrinology , constriction , angiotensin ii , mesenteric arteries , vasoconstriction , vasodilation , vascular resistance , nitric oxide , artery , blood pressure
We previously reported that MatSep (3 hours/day from days 2‐14) induces exaggerated angiotensin II (AngII)‐induced vasoreactivity with decreased nitric oxide (NO) buffering capacity in aortae of adult rats compared to control rats (normally‐reared littermates). Also, chronic AngII infusion produced exaggerated hypertension in MatSep rats. The aim of this study was to investigate whether MatSep male and female rats display exaggerated vascular reactivity of resistance arteries. Third‐order mesenteric arteries from adult rats (n=5‐6 per group) were isolated and mounted on wire myographs. Concentration‐response curves were generated for phenylephrine or endothelin and normalized to maximal potassium chloride‐induced constriction. Additionally, we tested acetylcholine and sodium nitroprusside‐induced relaxation. No differences in EC50 or %maximum constriction/dilation were observed between MatSep and control rats. Curves in the presence of L‐NAME revealed similar NO buffering capacity in MatSep and control rats. No sex differences were observed across the study. These data suggest that the abnormal vascular phenotype due to MatSep involves large conduit arteries, sparing smaller resistance arteries. However, resistance arteries are known to play an important role in blood pressure control, and thus, further investigation of these arteries in response to chronic AngII infusion is warranted. Grant Funding Source : Supported by NIH Grants: P01 HL69999, K99 HL111354