CommentaryControl of the ductus arteriosus—A new function for cytochrome P450, Endothelin and nitric oxide
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Cited by (46)
Carbon monoxide signaling and soluble guanylyl cyclase: Facts, myths, and intriguing possibilities
2022, Biochemical PharmacologyCitation Excerpt :Overall, the question of whether sGC is a key target for NO and CO to intersect under a given set of conditions still needs much more work. On a related note, the effect of CO on vasodilation is supported by results from many studies, though the proposed mechanism(s) of actions go beyond sGC and may include modulation of ROS-related responses, ion channels, p-450 actions, and expression of endothelin and growth factors.[7,56,57,61,67,84-88,159,160,165-168]. With the above examples and analyses, several points are clear.
Transcriptional profiling of the ductus arteriosus: Comparison of rodent microarrays and human RNA sequencing
2018, Seminars in PerinatologyCitation Excerpt :PDE1C catalyzes hydrolysis of the second messengers, cAMP and cGMP. Given the importance of both EP4 and nitric oxide signaling via cAMP and cGMP, respectively, in regulating DA tone,60,63–65 PDE1C’s involvement in the DA is logical. PDE1C activity has been shown to affect DA tone66–68 and is thought to do this by attenuating the dilatory effects of EP4 stimulation and downstream cAMP production in the DA.20
Mutations in the Histone Modifier PRDM6 Are Associated with Isolated Nonsyndromic Patent Ductus Arteriosus
2016, American Journal of Human GeneticsCitation Excerpt :According to results from animal studies, the remodeling of the DA is a complex process involving the migration of neural-crest-derived cells into the subendothelial space and their transformation to vascular smooth muscle cells (VSMCs), as well as extracellular-matrix accumulation and formation of subintimal cushions. Subsequently, an increase in vasoactive peptides such as endothelin A1, a decrease in prostaglandin E2 levels,3,4 and ultimately VSMC contraction result in closure of the vessel.5,6 Experimental in vivo and in vitro studies have shown that failure in any step of this process can result in persistent patency of the DA and thus lead to pulmonary arterial hypertension, pulmonary edema, and congestive heart failure in humans.7
Effect of PGE2 on DA tone by EP4 modulating Kv channels with different oxygen tension between preterm and term
2011, International Journal of CardiologyCitation Excerpt :The previous studies believe that this vasodilator role of PGE2, mainly via its E-prostanoid receptor 4 (EP4), one of a G-protein-coupled receptors (GPCRs), is to remodel DA in fetal. The duct functionally close shortly after birth caused from circulation PGE2 drop and systemic PO2 raise by constricted leading DA smooth muscle cells (DASMCs) [9]. O2 sensitivity of K+ channels have been described in various specialized O2-sensing tissues like chemoreceptors in the carotid body, pulmonary smooth muscle cells (SMCs), neuroepithelial bodies, placenta, and adrenal chromaffin cells [10].
The role of endothelins and their receptors in heart failure
2001, Pharmacological Research