Key result
Hypertension and renal disease may reduce NO bioavailability via eNOS inactivation, endogenous inhibitors, or oxidation.
Why the study?
Recent advances have highlighted the role of endothelial-derived nitric oxide in regulating blood pressure and renal homeostasis, with mechanisms of its loss in hypertension and renal disease being elucidated.
Loss of nitric oxide bioavailability plays a key role in hypertension and renal disease, highlighting potential targets for novel cardiovascular diagnostics and treatments.
Endothelial NO loss in hypertension and renal disease identifies potential targets; extends mechanistic insights but leaves clinical translation open.
PURPOSE OF REVIEW: To highlight recent advances in the field of endothelial-derived nitric oxide regulation of blood pressure and renal homeostasis. RECENT FINDINGS: Many laboratories have dissected a role for nitric oxide in regulating blood pressure and renal function. In models of hypertension, and chronic and acute renal disease, the loss of nitric oxide bioavailability may occur due to inactivation of endothelial nitric oxide synthase, synthesis of endogenous inhibitors or oxidative inactivation of nitric oxide. SUMMARY: Understanding the molecular mechanisms of nitric oxide synthesis may lead to novel diagnostics and treatments for cardiovascular disorders.
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Marin et al. (2007) conducted a review in Hypertension and renal disease. Endothelial-derived nitric oxide was evaluated. Loss of nitric oxide bioavailability in hypertension and renal disease models may occur due to inactivation of endothelial nitric oxide synthase, endogenous inhibitors, or oxidative inactivation.
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