Key result
Nitric oxide promotes natriuresis and diuresis to maintain normal blood pressure, and its reduced production in chronic kidney disease is associated with elevated arterial pressure.
This review highlights the critical role of nitric oxide in renal physiology, blood pressure regulation, and its pathophysiological implications in chronic kidney disease.
NO pathway merits targeted study in CKD hypertension; leaves open whether modulation improves outcomes.
Nitric oxide has been implicated in many physiologic processes that influence both acute and long-term control of kidney function. Its net effect in the kidney is to promote natriuresis and diuresis, contributing to adaptation to variations of dietary salt intake and maintenance of normal blood pressure. A pretreatment with nitric oxide donors or L-arginine may prevent the ischemic acute renal injury. In chronic kidney diseases, the systolic blood pressure is correlated with the plasma level of asymmetric dimethylarginine, an endogenous inhibitor of nitric oxide synthase. A reduced production and biological action of nitric oxide is associated with an elevation of arterial pressure, and conversely, an exaggerated activity may represent a compensatory mechanism to mitigate the hypertension.
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Jong‐Un Lee (2008) conducted a review in Kidney function and diseases. Nitric oxide was evaluated. Nitric oxide promotes natriuresis and diuresis to maintain normal blood pressure, and its reduced production in chronic kidney disease is associated with elevated arterial pressure.
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