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Angiotensin II mediates renal blood flow reduction in chronic heart failure
Author(s) -
Clayton Sarah Christina,
Zucker Irving H
Publication year - 2007
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.21.6.lb92-b
Subject(s) - renal blood flow , losartan , medicine , angiotensin ii , renal circulation , cardiology , endocrinology , kidney , vascular resistance , angiotensin ii receptor type 1 , heart failure , hemodynamics , blood pressure
The cardio‐renal syndrome represents a major complication in the treatment of patients with heart failure (HF). To study this process, renal arterial flow probes were placed on the left kidney of New Zealand white rabbits. Rapid ventricular pacing was carried out for three weeks to induce HF. Renal blood flow (RBF) decreased significantly following induction of HF (49.9±5.1 ml/min normal vs. 34.8±3.2 ml/min HF, P<0.05). Losartan (los) (10 mg/kg), an angiotensin II (AngII) type 1 receptor antagonist, restored RBF to normal levels (48.6±3.0 ml/min, P<0.05). Similarly, as depicted in Table 1, renal vascular resistance (RVR) was significantly increased in HF and los decreased RVR in HF, but not in normal rabbits. The response to renal sympathetic nerve activation by nasopharyngeal smoke was augmented in HF, and los reduced this response. These data suggest AngII plays a role in the decrease in renal blood flow seen in HF. 1 Baseline and peak RVR response to renal sympathetic nerve activation by smoke. † P<0.05 from pre pace baseline value. ‡P<0.05 from post pace pre los value. ∗P<0.05 from pre pace peak response value. n P<0.05 from baseline. #P<0.05 from peak response pre los.