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Angiotensin II-induced calcium signaling in the afferent arteriole from rats with two-kidney, one-clip hypertension

Renal Research Group, Institute of Medicine, University of Bergen, and Haukeland University Hospital, Bergen, Norway

Submitted 7 July 2005 ; accepted in final form 27 January 2006

The aim of this study was to investigate ANG II-induced Ca²⁺ signaling in freshly isolated afferent arterioles (AA) from two-kidney, one-clip hypertensive (2K1C) rats, which have an elevated plasma and renal ANG II level, and different perfusion pressure and vascular tone in the clipped and nonclipped kidney. The Ca²⁺ responses in vessels from 2K1C and control rats were similar in all groups (P > 0.1). The intracellular Ca²⁺ (Ca_i²⁺) response in the afferent arteriole after 10^–8 M ANG II stimulation was 0.57 ± 0.10, 0.50 ± 0.07, 0.48 ± 0.04, and 0.36 ± 0.05 in the control, sham, nonclipped, and clipped kidney, respectively. These data were consistent with the finding of unchanged AT_1aR mRNA levels in AAs from all groups. Although the absolute values were similar, the dose-response curves to ANG II were different. In the control, sham, and nonclipped kidney from 2K1C, the dose-response curve leveled off between 10^–8 and 10^–6 M ANG II. In the clipped kidney, the dose-response curve was linear, with a significantly increased response at 10^–6 M compared with 10^–8 M ANG II (P < 0.05). Inhibition of cyclooxygenase-1 (COX-1) with indomethacin enhanced the ANG II response in the nonclipped (0.30 ± 0.09) and clipped (0.30 ± 0.09) kidneys from 2K1C (P < 0.005), but not in control rats (–0.02 ± 0.11, P > 0.8). Conclusively, the ANG II-induced Ca_i²⁺ response was reduced by COX-1-derived prostaglandins in 2K1C, in contrast to control animals, where the COX-1 inhibition had no effect. COX-2 inhibition with NS-398 did not increase the ANG II-mediated Ca_i²⁺ response in any of the groups.

calcium signaling/physiology; Fura-2; indomethacin; NS-398; cyclooxygenase inhibitors; receptors; AT_1aR

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