Light-induced vs. bradykinin-induced relaxation of coronary arteries: do S-nitrosothiols act as endothelium-derived hyperpolarizing factors?

Batenburg, Wendy W.; Kappers, Mariëtte H.W.; Eikmann, Melissa J; Ramzan, Serge N A; Vries, René de; Danser, A.H. Jan

doi:10.1097/hjh.0b013e32832bff54

Cited by 34 publications

(37 citation statements)

References 37 publications

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“…This initially suggested a role for nonendothelial NO synthase-derived NO-like factors like S-nitrosothiols. 31 However, an alternative explanation is that the cobalt group of hydroxocobalamin inactivated C21 through interaction with its imidazole ring. Indeed, spectral analysis subsequently confirmed this concept.…”

Section: Discussionmentioning

confidence: 99%

Compound 21 Induces Vasorelaxation via an Endothelium- and Angiotensin II Type 2 Receptor-Independent Mechanism

et al. 2012

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Abstract-Angiotensin II type 2 (AT 2 ) receptor stimulation has been linked to vasodilation. Yet, AT 2 receptor-independent hypertension and hypotension (or no effect on blood pressure) have been observed in vivo after application of the AT 2 receptor agonist compound 21 (C21). We, therefore, studied its effects in vitro, using preparations known to display AT 2 receptor-mediated responses. Hearts of Wistar rats, spontaneously hypertensive rats (SHRs), C57Bl/6 mice, and AT 2 receptor knockout mice were perfused according to Langendorff. Mesenteric and iliac arteries of these animals, as well as coronary microarteries from human donor hearts, were mounted in Mulvany myographs. In the coronary vascular bed of Wistar rats, C57Bl/6 mice, and AT 2 receptor knockout mice, C21 induced constriction followed by dilation. SHR hearts displayed enhanced constriction and no dilation. Irbesartan (angiotensin II type 1 receptor blocker) abolished the constriction and enhanced or (in SHRs) reintroduced dilation, and PD123319 (AT 2 receptor blocker) did not block the latter. C21 relaxed preconstricted vessels of all species, and this did not depend on angiotensin II receptors, the endothelium, or the NO-guanylyl cyclase-cGMP pathway. C21 constricted SHR iliac arteries but none of the other vessels, and irbesartan prevented this. C21 shifted the concentration-response curves to U46619 (thromboxane A 2 analog) and phenylephrine (␣-adrenoceptor agonist) but not ionomycine (calcium ionophore) to the right. In conclusion, C21 did not cause AT 2 receptor-mediated vasodilation. Yet, it did induce vasodilation by blocking calcium transport into the cell and constriction via angiotensin II type 1 receptor stimulation. The latter effect is enhanced in SHRs. These data may explain the varying effects of C21 on blood pressure in vivo. (Hypertension. 2012;60:722-729.)

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Section: Discussionmentioning

confidence: 99%

Compound 21 Induces Vasorelaxation via an Endothelium- and Angiotensin II Type 2 Receptor-Independent Mechanism

et al. 2012

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“…Hence, a difference in cGMP action may contribute to the heterogeneous responses of the different sized coronary arteries. We also tested the effect of endothelium-derived NO in the presence of indomethacin, an inhibitor of cyclooxygenase, and apamin plus TRAM-34, the inhibitors of EDHF [1,11]. Under these conditions, bradykinin caused a greater relaxation of large arteries vs. small arteries, suggesting that endotheliumderived NO is also more potent in dilating large than small coronary arteries.…”

Section: Discussionmentioning

confidence: 98%

“…1). In the presence of indomethacin (10 −5 M), apamin (5×10 −7 M), and TRAM-34 (10 −5 M) but in the absence of nitro-Larginine (10 −4 M) to eliminate the involvement of endogenous prostanoids and endothelium-derived hyperpolorizing factor (EDHF) [1,11], bradykinin (10 −7 M) caused a greater relaxation in large coronary arteries (55.24±4.96%) than in small arteries (19.23±5.38%; n=6, P<0.05).…”

Section: Vessel Tension Studiesmentioning

confidence: 99%

Heterogeneity in relaxation of different sized porcine coronary arteries to nitrovasodilators: role of PKG and MYPT1

Lei

Liu

et al. 2011

Pflugers Arch - Eur J Physiol

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The present study was to determine the role of the type I isoform of cGMP-dependent protein kinase (PKG I) and its downstream effector myosin phosphatase target subunit 1 (MYPT1) in the responses of different sized coronary arteries to nitrovasodilators. Relaxations of isolated porcine coronary arteries were determined by isometric tension recording technique. Protein levels of PKG I and its effectors were analyzed by Western blotting. The activities of PKG I and MYPT1 were studied by analyzing phosphorylation of vasodilator-stimulated phosphoprotein (VASP) and MYPT1, respectively. Nitroglycerin, DETA NONOate, and 8-Br-cGMP caused greater relaxations in large than in small coronary arteries. Relaxations were attenuated to a greater extent by Rp-8-Br-PET-cGMPS (a PKG inhibitor) in large vs. small arteries. The expressions of PKG I and MYPT1 in large arteries were more abundant than in small arteries. DETA NONOate stimulated phosphorylation of VASP at Ser239 and inhibited phosphorylation of MYPT1 at Thr853 to a greater extent in large than in small arteries. A suppressed phosphorylation of MYPT1 at Thr853 was caused by 8-Br-cGMP in large but not small arteries, which was inhibited by Rp-8-Br-PET-cGMPS. These results suggest that the greater responsiveness of large coronary arteries to nitrovasodilators result in part from greater activities of PKG I and MYPT1. Dysfunction in nitric oxide signaling is implicated in the vulnerability of large coronary arteries to certain disorders such as atherosclerosis and spasm. Augmentation of PKG I-MYPT1 signaling may be of therapeutic benefit for combating these events.

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“…This penetration is enhanced while neonates are being exposed to a higher spectral irradiance of NNPT [87]. The light photon causes the relaxation of aortic smooth muscle [91] through the activation of the nitric oxide-cyclic GMP pathway and Ca 2+ -dependent K + ion channels [17]. Therefore, NNPT exerts a relaxing effect on the smooth muscles of the ductus arteriosus in neonates, thus reopening the ductus arteriosus [19].…”

Section: Nnpt and Patent Ductus Arteriosusmentioning

confidence: 99%

The side effects of phototherapy for neonatal jaundice: what do we know? What should we do?

et al. 2011

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Neonatal phototherapy (NNPT), a noninvasive, easily available therapy, has been widely used for the treatment of neonatal jaundice for more than half a century. Its efficiency in decreasing plasma bilirubin concentration is well documented, and NNPT leads to greatly reduced exchange transfusion rates for neonates with hyperbilirubinemia. It is generally accepted that the side effects of NNPT are not serious and seem to be well controlled. This review will focus on these possible side effects as well as the approaches to minimize them.

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Light-induced vs. bradykinin-induced relaxation of coronary arteries: do S-nitrosothiols act as endothelium-derived hyperpolarizing factors?

Cited by 34 publications

References 37 publications

Compound 21 Induces Vasorelaxation via an Endothelium- and Angiotensin II Type 2 Receptor-Independent Mechanism

Compound 21 Induces Vasorelaxation via an Endothelium- and Angiotensin II Type 2 Receptor-Independent Mechanism

Heterogeneity in relaxation of different sized porcine coronary arteries to nitrovasodilators: role of PKG and MYPT1

The side effects of phototherapy for neonatal jaundice: what do we know? What should we do?

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