ArticleAmerican journal of physiology. Heart and circulatory physiology2012
Soluble guanylyl cyclase is a target of angiotensin II-induced nitrosative stress in a hypertensive rat model.
Article in American journal of physiology. Heart and circulatory physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 54 citations in OpenAlex.
- Loss of erythrocyte arginase-1 impairs vasorelaxation due to endothelial GSNOR overexpression and denitrosylation of G protein subunits.Redox biology · 2026Article
- Soluble guanylyl cyclase, the NO receptor, drives vasorelaxation via endothelial S-nitrosation.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The Renin-Angiotensin-Aldosterone System (RAAS): Beyond Cardiovascular Regulation.Veterinary sciences · 2025Review
- Potential Beneficial Role of Nitric Oxide in SARS-CoV-2 Infection: Beyond Spike-Binding Inhibition.Antioxidants (Basel, Switzerland) · 2024Article
- Protective effects of limb remote ischemic per-conditioning on the heart injury induced by renal ischemic-reperfusion through the interaction of the apelin with the RAS/iNOS pathway.BioImpacts : BI · 2024Article
- Celiac ganglia neurolysis suppresses high blood pressure in rats.Hypertension research : official journal of the Japanese Society of Hypertension · 2023Article
- Evidence for Angiotensin II as a Naturally Existing Suppressor for the Guanylyl Cyclase A Receptor and Cyclic GMP Generation.International journal of molecular sciences · 2023Article
- Inhibitory Peptide of Soluble Guanylyl Cyclase/Trx1 Interface Blunts the Dual Redox Signaling Functions of the Complex.Antioxidants (Basel, Switzerland) · 2023Article
- Cellular Factors That Shape the Activity or Function of Nitric Oxide-Stimulated Soluble Guanylyl Cyclase.Cells · 2023Review
- The Renin-Angiotensin-Aldosterone System, Nitric Oxide, and Hydrogen Sulfide at the Crossroads of Hypertension and COVID-19: Racial Disparities and Outcomes.International journal of molecular sciences · 2022Review
- Angiotensin II augments renal vascular smooth muscle soluble GC expression via an ATBritish journal of pharmacology · 2022Article
- Soluble guanylyl cyclase: Molecular basis for ligand selectivity and actionFrontiers in molecular biosciences · 2022Review
- Higher susceptibility to heme oxidation and lower protein stability of the rare αBiochemical pharmacology · 2021Article
- RNF213 and GUCY1A3 in Moyamoya Disease: Key Regulators of Metabolism, Inflammation, and Vascular Stability.Frontiers in neurology · 2021Review
- Nitrosative Stress and Its Association with Cardiometabolic Disorders.Molecules (Basel, Switzerland) · 2020Review
- Regulation of Vascular Function and Inflammation via Cross Talk of Reactive Oxygen and Nitrogen Species from Mitochondria or NADPH Oxidase-Implications for Diabetes Progression.International journal of molecular sciences · 2020Review
- Structure/function of the soluble guanylyl cyclase catalytic domain.Nitric oxide : biology and chemistry · 2018Review
- Angiotensin II Signal Transduction: An Update on Mechanisms of Physiology and Pathophysiology.Physiological reviews · 2018Review
- Differential effects of long-term slow-pressor and subpressor angiotensin II on contractile and relaxant reactivity of resistance versus conductance arteries.Physiological reports · 2018Article
- Role of Thioredoxin in Age-Related Hypertension.Current hypertension reports · 2018Review
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
Nitric oxide (NO) by activating soluble guanylyl cyclase (sGC) is involved in vascular homeostasis via induction of smooth muscle relaxation. In cardiovascular diseases (CVDs), endothelial dysfunction with altered vascular reactivity is mostly attributed to decreased NO bioavailability via oxidative stress. However, in several studies, relaxation to NO is only partially restored by exogenous NO donors, suggesting sGC impairment. Conflicting results have been reported regarding the nature of this impairment, ranging from decreased expression of one or both subunits of sGC to heme oxidation. We showed that sGC activity is impaired by thiol S-nitrosation. Recently, angiotensin II (ANG II) chronic treatment, which induces hypertension, was shown to generate nitrosative stress in addition to oxidative stress. We hypothesized that S-nitrosation of sGC occurs in ANG II-induced hypertension, thereby leading to desensitization of sGC to NO hence vascular dysfunction. As expected, ANG II infusion increases blood pressure, aorta remodeling, and protein S-nitrosation. Intravital microscopy indicated that cremaster arterioles are resistant to NO-induced vasodilation in vivo in anesthetized ANG II-treated rats. Concomitantly, NO-induced cGMP production decreases, which correlated with S-nitrosation of sGC in hypertensive rats. This study suggests that S-nitrosation of sGC by ANG II contributes to vascular dysfunction. This was confirmed in vitro by using A7r5 smooth muscle cells infected with adenoviruses expressing sGC or cysteine mutants: ANG II decreases NO-stimulated activity in the wild-type but not in one mutant, C516A. This result indicates that cysteine 516 of sGC mediates ANG II-induced desensitization to NO in cells.
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Registered trials
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.