Regular ArticleRole of cGMP-inhibited Phosphodiesterase and Sarcoplasmic Calcium in Mediating the Increase in Basal Heart Rate with Nitric Oxide Donors☆,☆☆
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Cited by (30)
Cardiovascular characterization of the novel organic mononitrate NDIBP in rats
2022, Nitric Oxide - Biology and ChemistryCitation Excerpt :Regarding the HR, tachycardia can be seen at first moment as the baroreceptors unloading in response to the fall in the blood pressure. However, several studies revealed that low concentrations of NO donors could also increase the spontaneous beating rate by the direct stimulation of the hyperpolarization-activated pacemaker current (If) in sinoatrial nodal cells through a NO-sGC-cGMP- dependent pathway which increase the repolarization and diastolic depolarization rates [84–86]. Our results of cardiovascular parameters are similar to the findings of França-Silva and colleagues (2012) [45] which studied the NO donor NDBP, an isomer of NDIBP.
Cyclic nucleotide signaling and pacemaker activity
2021, Progress in Biophysics and Molecular BiologyCitation Excerpt :In rabbit denervated hearts, NO donor increased HR by 10% (Hogan et al., 1999a), similar to what was observed in patients receiving intravenous infusion of NO donors, with blood pressure held constant (Hogan et al., 1999b). In SAN cells, NO-induced cGMP levels inhibit PDE3, increasing cAMP signaling and SR Ca2+ release, both responsible for the positive chronotropic response (Musialek et al., 2000). During β-AR stimulation, activation of the NO/cGMP pathway has a transient stimulatory effect that is If-dependent, and is limited in magnitude and duration by cGMP-stimulation of PDE2 (Herring et al., 2001).
Isoforms of cyclic nucleotide phosphodiesterase PDE3 and their contribution to cAMP hydrolytic activity in subcellular fractions of human myocardium
2005, Journal of Biological ChemistryCitation Excerpt :Effects of cGMP on cAMP Hydrolytic Activity—Our third objective was to examine the effect of cGMP on cAMP hydrolysis in subcellular fractions. Because cGMP is a competitive inhibitor of PDE3 activity, and because cGMP analogues and agents that raise cGMP content can raise intracellular cAMP content in cardiac myocytes (21, 28-30), our expectation was that cGMP would inhibit cAMP hydrolysis under different conditions to an extent that would reflect the contribution of PDE3 to total cAMP hydrolytic activity. We first examined the effects of 1.0 μm cGMP on rtPDE3A activity at different concentrations of cAMP in the absence or presence of Ca2+/calmodulin.
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Please address all correspondence to: Piotr Musialek, MD, DPhil or Barbara Casadei, MD, DPhil, MRCP, Department of Cardiovascular Medicine, John Radcliffe Hospital, Oxford OX3 9DU, UK. Fax: +44-1865-768844. E-mail: [email protected]; [email protected]
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Parts of this work have been previously published in abstract form (Circulation 1997 96: I–357Eur Heart J 1999 20: 123 Circulation 1999 100: I–281 Heart 2000 83: I–P38).