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Differences in resistance artery vasomotor responses in the hypertensive hamster
Author(s) -
Kurjiaka David T,
Preston Megan M,
Baer Canaan T,
Ward Sarah L,
Bender Shawn B
Publication year - 2006
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.20.4.a284-a
Subject(s) - losartan , medicine , endocrinology , angiotensin ii , vasoconstriction , hamster , bradykinin , vasodilation , sodium nitroprusside , blood pressure , renin–angiotensin system , vasomotor , receptor , nitric oxide
This study examined whether vasomotor responses in resistance arteries were different between normotensive (CHF‐148) and hypertensive hamsters (CHF‐H4). Resistance arteries were isolated, cannulated, and pressurized to 80 mm Hg. Thereafter, their concentration‐response relationship to endothelial‐dependent dilators, endothelial‐independent dilators and constrictors was determined. Maximal dilatory (Ca free PBS) and constrictor (65 mM KCl) responses were determined. Dilatory responses to endothelial‐dependent (acetylcholine and vasoactive intestinal peptide) and ‐independent (adenosine and sodium nitroprusside) agonists were not different between strains. However, endothelial‐independent responses was <50% of maximal dilation at mM doses. These submaximal responses reflected a diminished response downstream of cGMP (mM 8Br‐cGMP elicited ~25% dilation). With respect to constrictors, responses to KCl, norepinephrine, and endothelin‐1 were similar between strains. However, angiotensin II (AngII) constriction was amplified in the hypertensive hamster through the AT‐1 receptor (losartan 10 μM). At higher AngII concentrations (>3 nM), vessels relaxed via concentration‐dependent desensitization. The importance of AngII to the hypertension was evident when losartan infusion (60 mg/kg body weight) normalized blood pressure in the hypertensive hamster. As the hypertensive hamster is a high renin model of hypertension, the greater constriction of the resistance vasculature to AngII likely contributes to the elevated blood pressure in this model of hypertension.