Oxytocin-induced endothelial nitric oxide dependent vasorelaxation and ERK1/2-mediated vasoconstriction in the rat aorta

Qian Xu; Kunping Zhuo; Xiaotian Zhang; Yaoxia Zhang; Jiaojiao Xue; Ming-Sheng Zhou

doi:10.4196/kjpp.2022.26.4.255

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자료유형: 학술저널

저자정보: Qian Xu (Department of Physiology Shenyang Medical University Shenyang 110034 P.R. China) Kunping Zhuo (Department of Physiology Shenyang Medical University Shenyang 110034 P.R. China) Xiaotian Zhang (Department of Physiology Shenyang Medical University Shenyang 110034 P.R. China) Yaoxia Zhang (Department of Physiology Shenyang Medical University Shenyang 110034 P.R. China) Jiaojiao Xue (Department of Physiology Shenyang Medical University Shenyang 110034 P.R. China) Ming-Sheng Zhou (Department of Physiology Shenyang Medical University Shenyang 110034 P.R. China)

저널정보: 대한약리학회 The Korean Journal of Physiology & Pharmacology The Korean Journal of Physiology & Pharmacology 제26권 제4호

발행연도: 2022.7

수록면: 255 - 262 (8page)

DOI: 10.4196/kjpp.2022.26.4.255

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Oxytocin is a neuropeptide produced primarily in the hypothalamus and plays an important role in the regulation of mammalian birth and lactation. It has been shown that oxytocin has important cardiovascular protective effects. Here we investigated the effects of oxytocin on vascular reactivity and underlying the mechanisms in human umbilical vein endothelial cells (HUVECs) in vitro and in rat aorta ex vivo. Oxytocin increased phospho-eNOS (Ser 1177) and phospho-Akt (Ser 473) expression in HUVECs in vitro and the aorta of rat ex vivo. Wortmannin, a specific inhibitor of phosphatidylinositol 3-kinase (PI3K), inhibited oxytocin-induced Akt and eNOS phosphorylation. In the rat aortic rings, oxytocin induced a biphasic vascular reactivity: oxytocin at low dose (10-9?10-8 M) initiated a vasorelaxation followed by a vasoconstriction at high dose (10-7 M). L-NAME (a nitric oxide synthase inhibitor), endothelium removal or wortmannin abolished oxytocin-induced vasorelaxation, and slightly enhanced oxytocin-induced vasoconstriction. Atosiban, an oxytocin/ vasopressin 1a receptor inhibitor, totally blocked oxytocin-induced relaxation and vasoconstriction. PD98059 (ERK1/2 inhibitor) partially inhibited oxytocin-induced vasoconstriction. Oxytocin also increased aortic phospho-ERK1/2 expression, which was reduced by either atosiban or PD98059, suggesting that oxytocin-induced vasoconstriction was partially mediated by oxytocin/V1aR activation of ERK1/2. The present study demonstrates that oxytocin can activate different signaling pathways to cause vasorelaxation or vasoconstriction. Oxytocin stimulation of PI3K/eNOS-derived nitric oxide may participate in maintenance of cardiovascular homeostasis, and different vascular reactivities to low or high dose of oxytocin suggest that oxytocin may have different regulatory effects on vascular tone under physiological or pathophysiological conditions.

#Endothelial nitric oxide synthase #Oxytocin #Phosphatidylinositol 3-kinase #Vascular reactivity

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