Basal production of nitric oxide is required to maintain normal renal blood flow and glomerular filtration, highlighting endothelium-derived NO as a key regulator of renal vascular resistance.
Supports basal NO in renal perfusion preclinically; leaves open translation to human cardiorenal therapy.
Summary: This study tested the effects on renal hemodynamics of blockade of nitric oxide (NO) synthesis from l-arginine with NG-methyl-l-arginine (l-NMA) using both intact and isolated perfused rat kidneys. Infusion of l-NMA into anesthetized rats increased the mean arterial pressure and reduced the glomerular filtration rate and renal plasma flow only when the renal perfusion pressure was maintained at control levels. In isolated kidneys, l-NMA increased vascular resistance; this was attenuated by coadministration of l-arginine. l-NMA selectively inhibited acetylcholine-induced renal vasodilation without attenuating that elicited by sodium nitroprusside. We conclude that basal production of NO within both the intact and isolated kidney is required to maintain the normally high levels of renal blood flow and glomerular filtration and that endothelium-derived NO is an important regulator of renal vascular resistance.
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Welch et al. (1991) studied this question.
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