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- W3197227 abstract "In cultured vascular muscle cells, nitric oxide (NO) has been shown to inhibit voltage-dependent Ca 2+ channels, which are involved in renal blood flow (RBF) autoregulation. Therefore, our purpose was to specify in vivo the effects of this interaction on RBF autoregulation. To do so, hemodynamics were investigated in anesthetized rats during Ca 2+ channel blockade before or after acute NO synthesis inhibition. Rats were treated intravenously with vehicle ( n = 10), 0.3 mg/kg body wt N G -nitro-l-arginine-methyl ester (l-NAME; n = 7), 4.5 μg ⋅ kg body wt −1 ⋅ min −1 nifedipine ( n = 8) alone, or with nifedipine infused before ( n = 8), after ( n = 8), or coadministered with l-NAME ( n = 10). Baseline renal vascular resistance (RVR) averaged 14.0 ± 1.2 resistance units and did not change after vehicle. RVR increased or decreased significantly by 27 and 29% afterl-NAME or nifedipine, respectively. Nifedipine reversed, but did not prevent, RVR increase after or coadministered withl-NAME. RBF autoregulation was maintained afterl-NAME, but the autoregulatory pressure limit (P A ) was significantly lowered by 15 mmHg. Nifedipine pretreatment or coadministration with l-NAME limited P A resetting or suppressed autoregulation at higher doses. Results were similar with verapamil. Intrarenal blockade of Ca 2+ -activated K + channels also prevented autoregulatory resetting by l-NAME ( n = 8). These findings suggest NO inhibits voltage-dependent Ca 2+ channels and thereby modulates RBF autoregulatory efficiency." @default.
- W3197227 created "2016-06-24" @default.
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- W3197227 date "2000-04-01" @default.
- W3197227 modified "2023-10-14" @default.
- W3197227 title "Effects of Ca<sup>2+</sup>channel activity on renal hemodynamics during acute attenuation of NO synthesis in the rat" @default.
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- W3197227 doi "https://doi.org/10.1152/ajprenal.2000.278.4.f561" @default.
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