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1 Renal Research Group, Institute of Medicine, University of Bergen and Department of Medicine, Haukeland University Hospital, Bergen, Norway
* To whom correspondence should be addressed. E-mail: Monica.Bivol{at}med.uib.no.
The ANG II receptor 1 (AT1R) level in the non-clipped kidney of two kidney, one clip hypertension (2K1C) has shown to be unchanged in spite of high circulating angiotensin (ANG ) II level. To examine vasoreactive response to ANG II in this kidney, injections of ANG II into renal artery were performed six weeks after clipping and compared with normotensive controls. The renal blood flow (RBF) response to 2.5 ng ANG II was measured by a transonic transit-time flowmeter, before and after indomethacin and candesartan treatment and analyzed by a computer program. The RBF response to 5 ng arginine-vasopressin (AVP) was examined for comparison to ANG II. The mRNA for AT1A and AT1B as well as Western blot for AT1R in renal resistance vessels were determined, and plasma renin activity (PRA) was measured. Systolic blood pressure was 183±4 mmHg in 2K1C compared to 113±1 mmHg in controls (p<0.001). PRA was significantly increased in 2K1C animals (p<0.05). Injection of ANG II reduced RBF with 10±2% in the non-clipped kidney and 24±3% in controls (p<0.001). After indomethacin, the RBF response increased from 10±2% to 20 ±3% (p<0.02) in 2K1C, and from 24±3% to 34±6% in controls (p<0.01). The doses of candesartan needed to completely inhibit RBF response to ANG II were 30 µg/kg and in the non-clipped kidney and 100 µg/kg in controls (p<0.001). Western blot and mRNA for AT1A and AT1B in the non-clipped kidney were similar to the controls. The results indicate that in spite of no difference in total AT1R levels; the functional AT1R is down-regulated in the non-clipped kidney of 2K1C.
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