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Pathophysiology of Hypertension in the Absence of Nitric Oxide/Cyclic GMP Signaling

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2012

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Springer Science + Business Media
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Thoonen, Robrecht, Patrick Y. Sips, Kenneth D. Bloch, and Emmanuel S. Buys. 2012. “Pathophysiology of Hypertension in the Absence of Nitric Oxide/Cyclic GMP Signaling.” Curr Hypertens Rep 15 (1) (December 12): 47–58. doi:10.1007/s11906-012-0320-5.

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Abstract

The nitric oxide (NO)-cyclic guanosine monophosphate (cGMP) signaling system is a well-characterized modulator of cardiovascular function, in general, and blood pressure, in particular. The availability of mice mutant for key enzymes in the NO-cGMP signaling system facilitated the identification of interactions with other blood pressure modifying pathways (e.g. the renin-angiotensin-aldosterone system) and of gender-specific effects of impaired NO-cGMP signaling. In addition, recent genome-wide association studies identified blood pressure-modifying genetic variants in genes that modulate NO and cGMP levels. Together, these findings have advanced our understanding of how NO-cGMP signaling regulates blood pressure. In this review, we will summarize the results obtained in mice with disrupted NO-cGMP signaling and highlight the relevance of this pathway as a potential therapeutic target for the treatment of hypertension.

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Cyclic guanosine monophosphate, Blood pressure, Hypertension, Cardiovascular function, Soluble guanylate cyclase, Nitric oxide, Mutant mice, Genetic variants, Renin-angiotensin-aldosterone signaling, Gender, S-nitrosylation, Therapeutics

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