ArticleBritish journal of pharmacology2002
Effects of nitric oxide donors on cardiac contractility in wild-type and myoglobin-deficient mice.
Article in British journal of pharmacology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 26 citations in OpenAlex.
- An Exogenous NO Donor Provokes Mechanical Alternans in Normal Rat Atria and Impairs Sarcomere Contractility in Right Atrial Cardiomyocytes in Atrial Fibrillation.Biomolecules · 2025Article
- cGMP Signaling in the Cardiovascular System-The Role of Compartmentation and Its Live Cell Imaging.International journal of molecular sciences · 2018Review
- Physiologic, Pathologic, and Therapeutic Paracrine Modulation of Cardiac Excitation-Contraction Coupling.Circulation research · 2018Review
- Nitric oxide: what's new to NO?American journal of physiology. Cell physiology · 2017Review
- Recent insights in the paracrine modulation of cardiomyocyte contractility by cardiac endothelial cells.BioMed research international · 2014Review
- Nitric oxide effects depend on different mechanisms in different regions of the rat heart.Heart and vessels · 2012Article
- sGC{alpha}1 mediates the negative inotropic effects of NO in cardiac myocytes independent of changes in calcium handling.American journal of physiology. Heart and circulatory physiology · 2011Article
- Myocyte specific overexpression of myoglobin impairs angiogenesis after hind-limb ischemia.Arteriosclerosis, thrombosis, and vascular biology · 2008Article
- Modulation of cardiac contraction, relaxation and rate by the endothelial nitric oxide synthase (eNOS): lessons from genetically modified mice.The Journal of physiology · 2003Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. The effects of the nitric oxide (NO) donors S-nitroso-N-acetylpenicillamine (SNAP), sodium(Z)-1-(N,N-diethylamino)diazen-1-ium-1,2-diolate (DEA-NONOate), and (Z)-1-[N-(2-Aminoethyl)-N-(2-ammonioethyl)amino]diazen-1-ium-1,2-diolate (DETA-NONOate) on force of contraction (F(c)) were studied in atrial and ventricular muscle strips obtained from wild-type (WT) and myoglobin-deficient (myo(-/-)) mice. 2. SNAP slightly reduced F(c) in preparations from WT mice at concentrations above 100 microM; this effect was more pronounced in myo(-/-) mice. 3. DEA-NONOate reduced F(c) in preparations from myo(-/-) mice to a larger extent than those from WT mice. 4. DETA-NONOate reduced F(c) in preparations from myo(-/-) but not from WT mice. 5. Pre-incubation with an inhibitor of the soluble guanylyl cyclase (1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one; 100 microM) prevented the effects of SNAP, DEA-NONOate and DETA-NONOate on F(c) in myo(-/-) mice. 6. It is suggested that, in physiological conditions, myoglobin acts as intracellular scavenger preventing NO from reaching its intracellular receptors in cardiomyocytes, whereas, in myoglobin-deficient conditions, NO is able to reduce contractility via activation of the soluble guanylyl cyclase/cyclic GMP pathway.
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