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Curr Hypertens Rep. 2013 Feb;15(1):47-58. doi: 10.1007/s11906-012-0320-5.

Pathophysiology of hypertension in the absence of nitric oxide/cyclic GMP signaling.

Author information

1
Molecular Cardiology Research Institute, Molecular Cardiology Research Center, Tufts Medical Center, Boston, MA 02111, USA. rthoonen@tuftsmedicalcenter.org

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.

PMID:
23233080
PMCID:
PMC3544991
DOI:
10.1007/s11906-012-0320-5
[Indexed for MEDLINE]
Free PMC Article

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