dc.contributor.author | Thoonen, Robrecht | |
dc.contributor.author | Sips, Patrick | |
dc.contributor.author | Bloch, Kenneth Daniel | |
dc.contributor.author | Buys, Emmanuel | |
dc.date.accessioned | 2015-03-18T18:17:24Z | |
dc.date.issued | 2012 | |
dc.identifier.citation | 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. | en_US |
dc.identifier.issn | 1522-6417 | en_US |
dc.identifier.issn | 1534-3111 | en_US |
dc.identifier.uri | http://nrs.harvard.edu/urn-3:HUL.InstRepos:14229236 | |
dc.description.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. | en_US |
dc.language.iso | en_US | en_US |
dc.publisher | Springer Science + Business Media | en_US |
dc.relation.isversionof | doi:10.1007/s11906-012-0320-5 | en_US |
dc.relation.hasversion | http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3544991/ | en_US |
dash.license | LAA | |
dc.subject | Cyclic guanosine monophosphate | en_US |
dc.subject | Blood pressure | en_US |
dc.subject | Hypertension | en_US |
dc.subject | Cardiovascular function | en_US |
dc.subject | Soluble guanylate cyclase | en_US |
dc.subject | Nitric oxide | en_US |
dc.subject | Mutant mice | en_US |
dc.subject | Genetic variants | en_US |
dc.subject | Renin-angiotensin-aldosterone signaling | en_US |
dc.subject | Gender | en_US |
dc.subject | S-nitrosylation | en_US |
dc.subject | Therapeutics | en_US |
dc.title | Pathophysiology of Hypertension in the Absence of Nitric Oxide/Cyclic GMP Signaling | en_US |
dc.type | Journal Article | en_US |
dc.description.version | Accepted Manuscript | en_US |
dc.relation.journal | Current Hypertension Reports | en_US |
dash.depositing.author | Buys, Emmanuel | |
dc.date.available | 2015-03-18T18:17:24Z | |
dc.identifier.doi | 10.1007/s11906-012-0320-5 | * |
dash.contributor.affiliated | Thoonen, Robrecht | |
dash.contributor.affiliated | Sips, Patrick | |
dash.contributor.affiliated | Buys, Emmanuel | |
dash.contributor.affiliated | Bloch, Kenneth | |