Contractile responses of the human umbilical artery to KCl and serotonin in Ca-free medium and the effects of levcromakalim

Tufan, Hale; Ayan-Polat, Belgin; Tecder-Ünal, Müge; Polat, G.; Kayhan, Zeynep; Öğüş, Ersin

doi:10.1016/s0024-3205(02)02382-2

Cited by 29 publications

(35 citation statements)

References 29 publications

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“…logical modulation. These results agree with previous studies in intestine (33), aorta (34), coronary artery (35), human umbilical artery (36), and portal vein (37), in which contraction of smooth muscle cells by a Ca 2ϩ -free depolarizing solution was reported. Contraction of the basilar artery elicited upon Ca 2ϩ channel activation does not necessarily require membrane depolarization, because FPL, a Ca 2ϩ channel agonist that directly modifies Ca 2ϩ channel gating, (20)(21)(22) also produced contraction of arterial rings bathed in Ca 2ϩ -free solution.…”

Section: Discussionsupporting

confidence: 93%

Metabotropic Ca ²⁺ channel-induced Ca ²⁺ release and ATP-dependent facilitation of arterial myocyte contraction

Valle‐Rodríguez

Calderón

Ruiz

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

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Voltage-gated Ca 2؉ channels in arterial myocytes can mediate Ca 2؉ release from the sarcoplasmic reticulum and, thus, induce contraction without the need of extracellular Ca 2؉ influx. This metabotropic action of Ca 2؉ channels (denoted as calcium-channelinduced calcium release or CCICR) involves activation of G proteins and the phospholipase C-inositol 1,4,5-trisphosphate pathway. Here, we show a form of vascular tone regulation by extracellular ATP that depends on the modulation of CCICR. In isolated arterial myocytes, ATP produced facilitation of Ca 2؉ -channel activation and, subsequently, a strong potentiation of CCICR. The facilitation of L-type channel still occurred after full blockade of purinergic receptors and inhibition of G proteins with GDP␤S, thus suggesting that ATP directly interacts with Ca 2؉ channels. The effects of ATP appear to be highly selective, because they were not mimicked by other nucleotides (ADP or UTP) or vasoactive agents, such as norepinephrine, acetylcholine, or endothelin-1. We have also shown that CCICR can trigger arterial cerebral vasoconstriction in the absence of extracellular calcium and that this phenomenon is greatly facilitated by extracellular ATP. Although, at low concentrations, ATP does not induce arterial contraction per se, this agent markedly potentiates contractility of partially depolarized or primed arteries. Hence, the metabotropic action of L-type Ca 2؉ channels could have a high impact on vascular pathophysiology, because, even in the absence of Ca 2؉ channel opening, it might mediate elevations of cytosolic Ca 2؉ and contraction in partially depolarized vascular smooth muscle cells exposed to small concentrations of agonists.L-type Ca 2ϩ channel ͉ vascular contractility ͉ excitation-contraction coupling C ontraction of vascular smooth muscle cells (VSMCs) determines vessel diameter and, thus, regulates blood flow and pressure. VSMC contraction is triggered by a rise of cytosolic calcium ion concentration ([Ca 2ϩ ]) due to either transmembrane Ca 2ϩ influx or Ca 2ϩ release from the sarcoplasmic reticulum (SR). Extracellular Ca 2ϩ entry normally occurs through L-type voltagedependent Ca 2ϩ channels, although there are numerous ligandgated membrane channels that are also Ca 2ϩ permeable (1). Ca 2ϩ release from the SR is mediated by inositol trisphosphate (InsP 3 ) and ryanodine receptors. Vasoactive agents acting on the different vascular territories induce VSMC contraction by binding to membrane receptors and the subsequent activation of one or more of the Ca 2ϩ -entry and͞or Ca 2ϩ -release channels (2-5).We have described a previously unnoticed metabotropic effect of vascular L-type Ca 2ϩ channels, denoted as calcium-channelinduced Ca 2ϩ release (CCICR), which requires Ca 2ϩ channel activation but is independent of extracellular Ca 2ϩ influx (6). This new Ca 2ϩ -release mechanism depends on the conformational change of L-type Ca 2ϩ channels and the downstream activation of the G protein͞phospholipase C (PLC) cascade, leading to synthesis of InsP 3 and C...

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Section: Discussionsupporting

confidence: 93%

Metabotropic Ca ²⁺ channel-induced Ca ²⁺ release and ATP-dependent facilitation of arterial myocyte contraction

Valle‐Rodríguez

Calderón

Ruiz

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

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“…The main difference between this artery and the systemic vessels is the lack of nerve fibers, and since it is a local physiological regulation of muscle contraction and relaxation, it is independent of nerve regulation. The vascular tonus of HUA depends entirely on vasoactive substances released locally or existing in the circulation, such as serotonin (5‐HT), histamine (His) and thromboxane, and of some ions such as calcium (Ca 2+ ) and potassium (K + ) . So, the HUA tonus is modulated by endocrine and paracrine mechanisms that regulate the contractile response of SMC .…”

Section: Introductionmentioning

confidence: 99%

How is the human umbilical artery regulated?

Lorigo

Mariana

Feiteiro

2018

J of Obstet and Gynaecol

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The purpose of this review is to present an update of the main mechanisms involved in the physiological regulation of contraction and relaxation of the human umbilical artery (HUA) smooth muscle cells. A literature review was performed based on the analysis of papers available on PubMed. The most important and relevant studies regarding the regulation of the HUA are presented in this article. The vascular smooth muscle is a highly specialized structure, whose main function is to regulate the vascular tonus. This is controlled by a balance between the cellular signaling pathways that mediate contraction and relaxation. The cells responsible for the contractile property of this muscle are the smooth muscle cells (SMC), and an excellent source of these cells is the HUA, involved in fetoplacental circulation. Since the umbilical blood vessels are not innervated, the HUA tonus is modulated by vasoactive substances that regulate the contractile process. The main vasoactive substances that induce contraction are serotonin, histamine, thromboxane, bradykinin, endothelin 1 and prostaglandin F2α, that are linked to the activation of proteins G and G . On the other hand, the main vasorelaxation mechanisms are the activation of adenyl and guanil cyclases, potassium channels and the inhibition of calcium channels. The SMC from the HUA allow the study of different cellular mechanisms and their functions. Therefore, these cells are an important tool to study the mechanisms regulating the contractility of this artery, allowing to detect potential therapeutic targets to treat HUA disorders (gestational hypertension and pre-eclampsia).

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“…Immediately after dissection, rings were suspended in 5-ml organ baths and stretched with an optimal resting tension of 2 to 4 g (Tufan et al, 2003). Changes in tension were measured with Grass isometric force transducers (FT-03C; Grass Instruments, Quincy, MA) and displayed on Grass polygraphs (model 7D).…”

Section: Methodsmentioning

confidence: 99%

Neutral Endopeptidase Up-Regulation in Isolated Human Umbilical Artery: Involvement in Desensitization of Bradykinin-Induced Vasoconstrictor Effects

Pelorosso¹,

Halperin²,

Palma³

et al. 2006

J Pharmacol Exp Ther

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Contractile responses of the human umbilical artery to KCl and serotonin in Ca-free medium and the effects of levcromakalim

Cited by 29 publications

References 29 publications

Metabotropic Ca ²⁺ channel-induced Ca ²⁺ release and ATP-dependent facilitation of arterial myocyte contraction

Metabotropic Ca ²⁺ channel-induced Ca ²⁺ release and ATP-dependent facilitation of arterial myocyte contraction

How is the human umbilical artery regulated?

Neutral Endopeptidase Up-Regulation in Isolated Human Umbilical Artery: Involvement in Desensitization of Bradykinin-Induced Vasoconstrictor Effects

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Contractile responses of the human umbilical artery to KCl and serotonin in Ca-free medium and the effects of levcromakalim

Cited by 29 publications

References 29 publications

Metabotropic Ca 2+ channel-induced Ca 2+ release and ATP-dependent facilitation of arterial myocyte contraction

Metabotropic Ca 2+ channel-induced Ca 2+ release and ATP-dependent facilitation of arterial myocyte contraction

How is the human umbilical artery regulated?

Neutral Endopeptidase Up-Regulation in Isolated Human Umbilical Artery: Involvement in Desensitization of Bradykinin-Induced Vasoconstrictor Effects

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Metabotropic Ca ²⁺ channel-induced Ca ²⁺ release and ATP-dependent facilitation of arterial myocyte contraction

Metabotropic Ca ²⁺ channel-induced Ca ²⁺ release and ATP-dependent facilitation of arterial myocyte contraction