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Baylis C, Davison J: The normal renal physiological changes which occur during pregnancy. In The Oxford Textbook of Clinical Nephrology 2nd Edition. Edited by Cameron JS, Davison AM, Grunfeld JP, Kerr DNS, Ritz E. Oxford: Oxford University Press; (in press).
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NOXV) do not predict renal vascular NO production
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NOXV) do not predict renal vascular NO production. Kidney Int 1995, 48:1272-1277.
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24
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Determinants of aortic cyclic guanosine monophosphate in hypertension induced by chronic Inhibition of nitric oxide synthase
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Nitric oxide directly activates calcium-dependent potassium channels in vascular smooth muscle
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Bolotina VM, Najibi S, Palacino JJ, Pagano PJ, Cohen RA: Nitric oxide directly activates calcium-dependent potassium channels in vascular smooth muscle. Nature 1994, 368:850-853. This study defines the mechanism by which NO causes hyperpolarization of vascular smooth muscle.
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Morton JJ, Beattie EC, Speirs A, Gulliver F: Persistent hypertension following inhibition of nitric oxide formation in the young Wistar rat: role of renin and vascular hypertrophy. J Hypertens 1993, 11:1083-1088.
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G-nitro-L-arginine methyl ester treatment in conscious rats. Hypertension 1994, 23:982-986.
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Effect of nitric oxide on renin secretion: Studies in the perfused juxtaglomerular apparatus
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••] represent the most extensive evaluation of the complex interactions between NO and renin release and help to explain earlier conflicts in the literature
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••] represent the most extensive evaluation of the complex interactions between NO and renin release and help to explain earlier conflicts in the literature.
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Stoos BA, Garcia NH, Garvin JF: Nitric oxide inhibits sodium reabsorption in the isolated perfused cortical collecting duct. J Am Soc Nephrol 1995, 6:89-94. This study reports that NO directly inhibits sodium transport in the isolated perfused collecting duct.
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This study demonstrates that the normal, normotensive response to increased dietary salt intake involves a stimulus to NO production
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Tolins JP, Shultz PJ: Endogenous nitric oxide synthesis determines sensitivity to the pressor effect of salt. Kidney Int 1994, 46:230-236. This study demonstrates that the normal, normotensive response to increased dietary salt intake involves a stimulus to NO production.
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