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Ang (1–7) Has a Greater Contribution to the Blood Pressure Lowering Effects of AT1 Receptor Blockade in Female Spontaneously Hypertensive Rats (SHR) Compared to Males
Author(s) -
Zimmerman Margaret,
Sullivan Jennifer
Publication year - 2013
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.27.1_supplement.904.3
Subject(s) - candesartan , medicine , endocrinology , blood pressure , angiotensin ii , angiotensin ii receptor type 1 , basal (medicine) , renin–angiotensin system , antagonist , angiotensin receptor , receptor , insulin
Ang (1–7) contributes to the blood pressure (BP) lowering effects of renin angiotensin system inhibitors in male SHR. We have previously published that female SHR have greater Ang (1–7) levels than males, however, the functional implications of this with regards to BP control remains largely unknown. Therefore, the goal of this study was to test the hypothesis that female SHR have a larger Ang (1–7) contribution to the BP lowering effects of the angiotensin receptor blocker (ARB) candesartan than male SHR. BP was measured via telemetry in 12 week old male and female SHR (n=4–8). Animals were pre‐treated with either the Ang (1–7) antagonist A‐779 (4 days; 48 μg/kg/hr via osmotic minipump) or vehicle. Candesartan was then co‐administered (0.5 mg/kg/day via drinking water) for a week. A‐779 alone did not alter basal BP in either sex. In male SHR, candesartan‐mediated decreases in BP were comparable in vehicle (15% decrease: 143±2 to 122±3 mmHg; p<0.05) and A‐779 treated (12% decrease: 147±3 to 129±4 mmHg; p<0.05). In contrast, A‐779 attenuated candesartan‐mediated decreases in BP (5% decrease: 127±1 to 121±2 mmHg; NS) in female SHR compared to vehicle treatment (10% decrease: 128±1 to 115±1 mmHg; p<0.05). In conclusion, female SHR have a greater Ang (1–7) contribution to ARB‐mediated decreases in BP than males. This study was funded by National Institutes of Health grant 1R01 HL093271–01A1 to J.C.S.