ArticleThe Journal of clinical investigation2006
Spare guanylyl cyclase NO receptors ensure high NO sensitivity in the vascular system.
Article in The Journal of clinical investigation, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
97 citing papers in PubMed, 194 citations in OpenAlex.
- Hypoxic erythrocytes mediate cardioprotection through activation of soluble guanylate cyclase and release of cyclic GMP.The Journal of clinical investigation · 2023Trial
- Endothelial nitric oxide signaling in cellular and systemic metabolism.Redox biology · 2026Review
- Carbon dioxide is a triple vasodilator.Cardiovascular research · 2026Article
- Proteomic surveys of the mouse heart unveil cardiovascular responses to nitric oxide/cGMP signaling deficiencies.Communications biology · 2025Article
- Challenging the Norm: The Unrecognized Impact of Soluble Guanylyl Cyclase Subunits in Cancer.International journal of molecular sciences · 2024Review
- Functional polymorphisms ofFrontiers in genetics · 2024Article
- It takes two to tango: cardiac fibroblast-derived NO-induced cGMP enters cardiac myocytes and increases cAMP by inhibiting PDE3.Communications biology · 2023Article
- Cellular Factors That Shape the Activity or Function of Nitric Oxide-Stimulated Soluble Guanylyl Cyclase.Cells · 2023Review
- Acute deletion of the central MR/GR steroid receptor correlates with changes in LTP, auditory neural gain, and GC-A cGMP signaling.Frontiers in molecular neuroscience · 2023Article
- Review
- The differential roles of the two NO-GC isoforms in adjusting airway reactivity.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- PDGF regulates guanylate cyclase expression and cGMP signaling in vascular smooth muscle.Communications biology · 2022Article
- FoxO4 controls sGCβ transcription in vascular smooth muscle.American journal of physiology. Heart and circulatory physiology · 2022Article
- Violet LED induces vasodilation in rat aortic rings by soluble guanylate cyclase-dependent mechanism and increases SOD activity.Lasers in medical science · 2022Article
- Age Impairs Soluble Guanylyl Cyclase Function in Mouse Mesenteric Arteries.International journal of molecular sciences · 2021Article
- Involvement of 3',5'-cyclic inosine monophosphate in cystathionine γ-lyase-dependent regulation of the vascular tone.British journal of pharmacology · 2021Article
- Current Modulation of Guanylate Cyclase Pathway Activity-Mechanism and Clinical Implications.Molecules (Basel, Switzerland) · 2021Review
- Loss of PKGIβ/IRAG1 Signaling Causes Anemia-Associated Splenomegaly.International journal of molecular sciences · 2021Article
- Higher susceptibility to heme oxidation and lower protein stability of the rare αBiochemical pharmacology · 2021Article
- Angiotensin II-Induced Cardiovascular Fibrosis Is Attenuated by NO-Sensitive Guanylyl Cyclase1.Cells · 2020Article
37 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the vascular system, the receptor for the signaling molecule NO, guanylyl cyclase (GC), mediates smooth muscle relaxation and inhibition of platelet aggregation by increasing intracellular cyclic GMP (cGMP) concentration. The heterodimeric GC exists in 2 isoforms (alpha1-GC, alpha2-GC) with indistinguishable regulatory properties. Here, we used mice deficient in either alpha1- or alpha2-GC to dissect their biological functions. In platelets, alpha1-GC, the only isoform present, was responsible for NO-induced inhibition of aggregation. In aortic tissue, alpha1-GC, as the major isoform (94%), mediated vasodilation. Unexpectedly, alpha2-GC, representing only 6% of the total GC content in WT, also completely relaxed alpha1-deficient vessels albeit higher NO concentrations were needed. The functional impact of the low cGMP levels produced by alpha2-GC in vivo was underlined by pronounced blood pressure increases upon NO synthase inhibition. As a fractional amount of GC was sufficient to mediate vasorelaxation at higher NO concentrations, we conclude that the majority of NO-sensitive GC is not required for cGMP-forming activity but as NO receptor reserve to increase sensitivity toward the labile messenger NO in vivo.
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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.