ArticleProceedings of the National Academy of Sciences of the United States of America2008
High blood pressure arising from a defect in vascular function.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.
What it found
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Who cites it
75 citing papers in PubMed.
- Genes involved in vasoconstriction and vasodilation system affect salt-sensitive hypertension.PloS one · 2011Trial
- Gut microbiome drives glycodeoxycholic acid-mediated attenuation of hypertension.Gut microbes · 2026Article
- Sex Differences and Oxidative Stress in Cardiovascular Disease.Physiology (Bethesda, Md.) · 2026Review
- Myocardial PKG1α dysregulation contributes to ventricular tachycardia pathogenesis in type 2 diabetes and metabolic syndrome.Heart rhythm · 2026Article
- Renal TRPM3 Channels Regulate Blood Pressure via Tubuloglomerular Feedback and Plasma Volume Control.Hypertension (Dallas, Tex. : 1979) · 2025Article
- Blockade of AGeroScience · 2025Article
- Facilitating Nitrite-Derived S-Nitrosothiol Formation in the Upper Gastrointestinal Tract in the Therapy of Cardiovascular Diseases.Antioxidants (Basel, Switzerland) · 2024Review
- Dissociation of sodium-chloride cotransporter expression and blood pressure during chronic high dietary potassium supplementation.JCI insight · 2023Article
- Oxidative Regulation of Vascular CaAntioxidants (Basel, Switzerland) · 2022Review
- Single-Cell Chromatin Accessibility Data Combined with GWAS Improves Detection of Relevant Cell Types in 59 Complex Phenotypes.International journal of molecular sciences · 2022Article
- Constitutive protein kinase G activation exacerbates stress-induced cardiomyopathy.British journal of pharmacology · 2022Article
- Role of smooth muscle activation in the static and dynamic mechanical characterization of human aortas.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- GJD Modulates Cardiac/Vascular Inflammation and Decreases Blood Pressure in Hypertensive Rats.Mediators of inflammation · 2022Article
- RNO3 QTL regulates vascular structure and arterial stiffness in the spontaneously hypertensive rat.Physiological genomics · 2021Article
- MLK3 mediates impact of PKG1α on cardiac function and controls blood pressure through separate mechanisms.JCI insight · 2021Article
- Cyclic GMP-Dependent Regulation of Vascular Tone and Blood Pressure Involves Cysteine-Rich LIM-Only Protein 4 (CRP4).International journal of molecular sciences · 2021Article
- Loss of PKGIβ/IRAG1 Signaling Causes Anemia-Associated Splenomegaly.International journal of molecular sciences · 2021Article
- Editing of the myosin phosphatase regulatory subunit suppresses angiotensin II induced hypertension via sensitization to nitric oxide mediated vasodilation.Pflugers Archiv : European journal of physiology · 2021Article
- Sacubitril/Valsartan Improves Left Ventricular Function in Chronic Pressure Overload Independent of Intact Cyclic Guanosine Monophosphate-dependent Protein Kinase I Alpha Signaling.Journal of cardiac failure · 2020Article
- cGMP Signaling and Modulation in Heart Failure.Journal of cardiovascular pharmacology · 2020Review
15 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
Hypertension, a major cardiovascular risk factor and cause of mortality worldwide, is thought to arise from primary renal abnormalities. However, the etiology of most cases of hypertension remains unexplained. Vascular tone, an important determinant of blood pressure, is regulated by nitric oxide, which causes vascular relaxation by increasing intracellular cGMP and activating cGMP-dependent protein kinase I (PKGI). Here we show that mice with a selective mutation in the N-terminal protein interaction domain of PKGIalpha display inherited vascular smooth muscle cell abnormalities of contraction, abnormal relaxation of large and resistance blood vessels, and increased systemic blood pressure. Renal function studies and responses to changes in dietary sodium in the PKGIalpha mutant mice are normal. These data reveal that PKGIalpha is required for normal VSMC physiology and support the idea that high blood pressure can arise from a primary abnormality of vascular smooth muscle cell contractile regulation, suggesting a new approach to the diagnosis and therapy of hypertension and cardiovascular diseases.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.