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- W1489741583 abstract "Overall, it appears that perfusion of the kidney is particularly sensitive to the tonic vasodilator tone of endothelium-derived NO. Basal renal vascular resistance is highly dependent on NO synthesis, and the arterioles are particularly sensitive to the influence of NO. Of the various constricting factors which oppose the dilator effect of NO, angiotensin II can become a particularly important antagonist with a seemingly unique renal interaction with NO under conditions which elevate angiotensin II above normal levels. While endothelium-derived NO does not seem to participate in renal blood flow autoregulation, it does control the basal level of renal blood flow around which autoregulation operates. The neuronal isoform of NOS in the macula densa appears to have a negative influence on TGF, and under certain conditions its absence or suppression allows TGF to exert an even greater influence on renal blood flow. While NO synthesis may be impaired in some conditions or models of hypertension, endothelial dysfunction and diminished NO synthesis in resistance arterioles do not seem to be generalized predisposing conditions for hypertension. Overall, NO not only contributes to basal vascular tone and regulates renal vascular resistance, but also acts as an important regulatory vasodilating buffer against factors or conditions which would acutely or chronically increase renal resistance beyond the homeostatic state." @default.
- W1489741583 created "2016-06-24" @default.
- W1489741583 creator A5043754683 @default.
- W1489741583 date "2000-01-01" @default.
- W1489741583 modified "2023-10-18" @default.
- W1489741583 title "Endothelial factors in the regulation of the renal circulation: Nitric oxide" @default.
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- W1489741583 doi "https://doi.org/10.1016/s1569-2590(00)09064-9" @default.
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