Endothelin-1 and Vasopressin Activate Ca2+-permeable Non-selective Cation Channels in Aortic Smooth Muscle Cells: Mechanism of Receptor-mediated Ca2+Influx

Nakajima, Toshiaki; Hazama, Hisanori; Hamada, Eiji; Wu, Sheng‐Nan; Igarashi, Kazunori; Yamashita, Takeshi; Seyama, Yousuke; Omata, Masao; Kurachi, Yoshihisa

doi:10.1006/jmcc.1996.0066

Cited by 54 publications

(51 citation statements)

References 6 publications

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“…20 Earlier electrophysiological studies in A7r5 cells or freshly isolated rat aortic smooth muscle cells reported endothelin-or vasopressin-mediated activation of NSCCs, causing depolarization of the membrane potential and Ca 2ϩ influx; this was claimed to be attributable to the Ca 2ϩ permeability of NSCCs. 21 In the present study we found that the increase of [Ca 2ϩ ] i was attributed to depolarization-dependent opening of L-type Ca 2ϩ channels, because nifedipine completely blocked the LNP-induced increase of [Ca 2ϩ ] i , and the measured reversal potential of the LNP-activated NSCCs was close to the calculated reversal potential for monovalent cations, suggesting no or only low permeability to Ca 2ϩ . Because of the relatively slow on-kinetics of the LNPinduced response, we explored the potential involvement of principal intracellular signaling pathways, such as phosphatidylinositol 3-kinase and PKC, which are known to modulate L-type Ca 2ϩ channels in vessels.…”

Section: Discussionsupporting

confidence: 66%

Identification of a Novel Vasoconstrictor Peptide Specific for the Systemic Circulation

Wenzel

Koch²,

Matthey³

et al. 2012

Hypertension

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Abstract-Some small molecular weight peptides possess potent vasoactive properties. Herein we have identified the laminin nonapeptide (LNP) CDPGYIGSR as a novel vasoconstrictive agent. Isometric force measurements revealed that LNP induced vasoconstriction in small and large murine arteries in a dose-dependent fashion; LNP also increased vascular tone in human mammary arteries. The vasoactive response was specific for the nonapeptide, because neither scrambled nor very similar peptide sequences modulated vascular tone. As an underlying mechanism we found in [Ca 2ϩ ] i imaging experiments that the nonapeptide induced transmembrane [Ca 2ϩ ] i influx in vascular smooth muscle cells. Patch clamp experiments showed that LNP activated nonselective cation channels, causing depolarization of the membrane potential and opening of L-type Ca 2ϩ channels. The functional effect of LNP was also assessed with catheter measurements in mice in vivo and confirmed vasoconstriction. This effect was restricted to the systemic circulation, because measurements with the perfused lung system demonstrated that LNP did not alter vascular tone in pulmonary arteries. Thus, LNP is a vasoconstrictor in mouse and human arteries, and its vasoactivity is restricted to the systemic vasculature. (Hypertension. 2012;59:1256-1262.) • Online Data Supplement Key Words: cell signaling Ⅲ ion channels Ⅲ peptides Ⅲ smooth muscle Ⅲ vasoconstriction T he identification of vasoactive substances is of high interest for a better molecular understanding of the regulation of vascular tone and for the design of novel therapeutic agents. Different small peptides (eg, endothelin, angiotensin II, and bradykinin) have been found to exert potent vasomodulatory functions.1,2 Most of these peptides are derived from larger molecules that have no effect on vascular tone and are processed to vasoactive molecules via proteolytic cleavage. These can either have vasoconstrictive (endothelin or vasopressin) or vasorelaxant (bradykinin) properties and also exert other cell biological functions; for example, endothelin and angiotensin II stimulate proliferation of smooth muscle cells. 3The 9 amino acid peptide CDPGYIGSR, which is part of the LEb domain in the ␤1 chain of laminin, has been shown to affect vascular growth. 4 In addition, the peptide was also suggested to bind to the 67-kDa laminin receptor, 5 resulting in the inhibition of metastases formation. 6 The minimum sequence necessary for these effects was identified as the laminin pentapeptide YIGSR that also promoted vascular tube formation 5,7 and could inhibit shear stress-induced increase in endothelial NO expression. 8 In addition, laminin was also reported to modulate L-type Ca 2ϩ channels. 9 Because laminin and its ␤1 chain were shown to be in close contact with the endothelium and the smooth muscle layer of vessels 10 and a laminin fragment containing laminin nonapeptide (LNP) was found to be increased in blood of patients experiencing diabetes mellitus, 11 we explored whether LNP has direct impact on va...

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Section: Discussionsupporting

confidence: 66%

Identification of a Novel Vasoconstrictor Peptide Specific for the Systemic Circulation

Wenzel

Koch²,

Matthey³

et al. 2012

Hypertension

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“…In A7r5 cells, AVP was previously found to activate both CCE and NCCE (Byron and Taylor, 1995;Broad et al, 1999). Previous electrophysiological studies identified a nonselective cation current (I CAT ) in A7r5 cells activated by high [AVP] (100 nM; Van Renterghem et al, 1988;Krautwurst et al, 1994;Nakajima et al, 1996;Iwasawa et al, 1997;Jung et al, 2002), which may relate to AVP-activated NCCE. I CAT is clearly distinct from I SOC in several ways.…”

Section: Discussionmentioning

confidence: 97%

“…A number of earlier electrophysiological studies (Nakajima et al, 1996;Iwasawa et al, 1997;Iwamuro et al, 1999;Jung et al, 2002) failed to detect store-operated currents in A7r5 cells despite evidence from fura-2 fluorescence studies that Ca 2ϩ influx is stimulated following depletion of Ca 2ϩ stores. In a recent study (Brueggemann et al, 2005), we reported conditions under which store-operated currents can be detected in A7r5 cells, but the resulting current differs in its apparent cation selectivity and voltage dependence from I SOC recorded from other vascular smooth muscle preparations.…”

Section: ]-Vasopressin (Avp) Wasmentioning

confidence: 99%

Pharmacological and Electrophysiological Characterization of Store-Operated Currents and Capacitative Ca²⁺Entry in Vascular Smooth Muscle Cells

Brueggemann

Markun²,

Henderson³

et al. 2006

J Pharmacol Exp Ther

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Capacitative Ca2ϩ entry (CCE) in vascular smooth muscle cells contributes to vasoconstrictor and mitogenic effects of vasoactive hormones. In A7r5 rat aortic smooth muscle cells, measurements of cytosolic free Ca 2ϩ concentration ([Ca 2ϩ ] i ) have demonstrated that depletion of intracellular Ca 2ϩ stores activates CCE. However, there is disagreement in published studies regarding the regulation of this mechanism by the vasoconstrictor hormone [Arg 8 ]-vasopressin (AVP). We have employed electrophysiological methods to characterize the membrane currents activated by store depletion [store-operated current (I SOC )]. Because of different recording conditions, it has not been previously determined whether I SOC corresponds to CCE measured using fura-2; nor has the channel protein responsible for CCE been identified. In the present study, the pharmacological characteristics of I SOC , including its sensitivity to blockade by 2-aminoethoxydiphenylborane, diethylstilbestrol, or micromolar Gd 3ϩ , were found to parallel the effects of these drugs on thapsigargin-or AVP-activated CCE measured under identical external ionic conditions using fura-2. Thapsigargin-stimulated I SOC was also measured in freshly isolated rat mesenteric artery smooth muscle cells (MASMC). Members of the transient receptor potential (TRP) family of nonselective cation channels, TRPC1, TRPC4, and TRPC6, were detected by reverse transcription-polymerase chain reaction and Western blot in both A7r5 cells and MASMC. TRPC1 expression was reduced in a stable A7r5 cell line expressing a small interfering RNA (siRNA) or by infection of A7r5 cells with an adenovirus expressing a TRPC1 antisense nucleotide sequence. Thapsigargin-stimulated I SOC was reduced in both the TRPC1 siRNAand TRPC1 antisense-expressing cells, suggesting that the TRPC1 channel contributes to the I SOC /CCE pathway. Article, publication date, and citation information can be found at

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“…However, calphostin C requires light for activation (12), which is inconvenient for experimental drug application. PKC pseudosubstrate inhibitory oligopeptide (e.g., [19][20][21][22][23][24][25][26][27][28][29][30][31][32][33][34][35][36][19][20][21][22][23][24][25][26][27][28][29][30][31], which is derived from the PKC regulatory C1 domain, inhibits PKC activity with high affinity, as the oligopeptide is Invited Mini Review http://bmbreports.org recognized by specific amino acid sequences. It consists of arginine-rich and lysine-rich sequences with non-phosphorylatable alanine instead of serine in the protein substrates (5,13).…”

Section: Pkc Inhibitorsmentioning

confidence: 99%

“…Ion channel modulation by PKC activation is relatively well characterized. For example, PKC activation leads to the activation of L-type Ca 2+ channels, Cl − channels, and nonselective cation channels in vascular smooth muscle (20)(21)(22). Generally, K + channels in vascular smooth muscle, including voltage-dependent K + (Kv), ATP-sensitive K + (KATP), and inward rectifier K + (Kir), are inhibited by PKC activation (18,23,24).…”

Section: Biological Actions Of Pkc Inhibitors On Ion Channelsmentioning

confidence: 99%

Direct effect of protein kinase C inhibitors on cardiovascular ion channels

Son

Hong²,

Kim³

et al. 2011

BMB Reports

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Endothelin-1 and Vasopressin Activate Ca2+-permeable Non-selective Cation Channels in Aortic Smooth Muscle Cells: Mechanism of Receptor-mediated Ca2+Influx

Cited by 54 publications

References 6 publications

Identification of a Novel Vasoconstrictor Peptide Specific for the Systemic Circulation

Identification of a Novel Vasoconstrictor Peptide Specific for the Systemic Circulation

Pharmacological and Electrophysiological Characterization of Store-Operated Currents and Capacitative Ca²⁺Entry in Vascular Smooth Muscle Cells

Direct effect of protein kinase C inhibitors on cardiovascular ion channels

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Endothelin-1 and Vasopressin Activate Ca2+-permeable Non-selective Cation Channels in Aortic Smooth Muscle Cells: Mechanism of Receptor-mediated Ca2+Influx

Cited by 54 publications

References 6 publications

Identification of a Novel Vasoconstrictor Peptide Specific for the Systemic Circulation

Identification of a Novel Vasoconstrictor Peptide Specific for the Systemic Circulation

Pharmacological and Electrophysiological Characterization of Store-Operated Currents and Capacitative Ca2+Entry in Vascular Smooth Muscle Cells

Direct effect of protein kinase C inhibitors on cardiovascular ion channels

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Product

Resources

About

Pharmacological and Electrophysiological Characterization of Store-Operated Currents and Capacitative Ca²⁺Entry in Vascular Smooth Muscle Cells