Effects of prostaglandins on the cytosolic free calcium concentration in vascular smooth muscle cells

Fukuo, Keisuke; Morimoto, Shigeto; Koh, Eio; Yukawa, Satoshi; Tsuchiya, Hiroyasu; Imanaka, Shunji; Yamamoto, Hideki; Onishi, Toshio; Kumahara, Yuichi

doi:10.1016/0006-291x(86)90901-0

Cited by 69 publications

(20 citation statements)

References 11 publications

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“…VSMC were isolated from Wistar rat aortas by explant method as described previously (23) and grown in Dulbecco's modified Eagle's medium (DME) containing 10% FCS. The cells exhibited typical 'hill and valley' growth morphology and almost all cells reacted with the anti-a-actin monoclonal antibody (Boehringer Mannheim, Mannheim, Germany).…”

Section: Methodsmentioning

confidence: 99%

Nitric oxide mediates cytotoxicity and basic fibroblast growth factor release in cultured vascular smooth muscle cells. A possible mechanism of neovascularization in atherosclerotic plaques.

Fukuo

Inoue²,

Morimoto³

et al. 1995

J. Clin. Invest.

112

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To define the pathophysiological role of nitric oxide (NO) released from vascular smooth muscle cells (VSMC), we examined whether NO released from VSMC induces cytotoxicity in VSMC themselves and adjacent endothelial cells (EC) using a coculture system. Prolonged incubation with interleukin-1 (IL-1) induced large amounts of NO release and cytotoxicity in VSMC. NG-Monomethyl-L-arginine, an inhibitor of NO synthesis, inhibited both NO release and cytotoxicity induced by IL-1. In contrast, DNA synthesis in cocultured EC was not inhibited but rather stimulated by prolonged incubation with IL-1 or sodium nitroprusside (SNP), a NO donor. However, IL-1 and SNP did not stimulate but inhibited DNA synthesis in EC alone. On the other hand, conditioned medium from VSMC incubated for a long period with IL-1 or SNP stimulated DNA synthesis in EC alone. Furthermore, the concentration of basic fibroblast growth factor in the conditioned medium was increased and correlated with the degree of cytotoxicity in VSMC. These results indicate that NO released from VSMC induces VSMC death, which results in release of basic fibroblast growth factor, which then stimulates adjacent EC proliferation. Thus, NO released from VSMC may participate in the mechanism of neovascularization in atherosclerotic plaques. (J. Clin. Invest. 1995. 95:669-676.)

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Section: Methodsmentioning

confidence: 99%

Nitric oxide mediates cytotoxicity and basic fibroblast growth factor release in cultured vascular smooth muscle cells. A possible mechanism of neovascularization in atherosclerotic plaques.

Fukuo

Inoue²,

Morimoto³

et al. 1995

J. Clin. Invest.

112

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“…2 -adrenoceptor ( 2 AR) stimulation inhibits myometrial contractility in vivo (Caritis et al 1983) and in vitro (Fukuo et al 1986, Engstrøm et al 1997 and thus 2 -agonists are widely used as tocolytic agents (Gyetvai et al 1999). The effectiveness of these agents is, however, limited due to a relatively rapid development of tachyphylaxis (Lye et al 1992), and consequently the incidence of preterm delivery (Hemminki & Starfield 1978) as well as perinatal morbidity and mortality (The Canadian Preterm Labor Investigators Group 1992) has remained unchanged during several years.…”

Section: Introductionmentioning

confidence: 99%

Desensitization of beta2-adrenoceptor function in non-pregnant rat myometrium is modulated by sex steroids

Engstrøm

Vilhardt²,

Bratholm³

et al. 2001

Journal of Endocrinology

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The effects of in vivo treatment with estrogen and progesterone on isoproterenol-induced uterine relaxation and 2 -adrenoceptor ( 2 AR) mRNA production in nonpregnant rat myometrium were investigated. Whether homologous myometrial desensitization of 2 AR function was dependent on or modulated by the two steroids was also examined.Estrogen treatment alone or in combination with progesterone reduced maximal relaxation (E max ) of isolated uterine strips subsequently challenged with isoproterenol whereas progesterone alone had no effect on this parameter. The reduction was accompanied by an enhanced 2 AR mRNA concentration. The concentration of isoproterenol giving half-maximal relaxing response (EC 50 ) increased following estrogen treatment and this effect was curbed by progesterone.Isoproterenol had no effect on 2 AR transcription irrespective of the steroid regimes employed. E max of isolated uterine strips was reduced following prolonged in vivo treatment with isoproterenol but the effect was found only when estrogen alone was administered concomitantly. Finally, in vivo treatment with isoproterenol increased EC 50 of uterine strips subsequently stimulated with isoproterenol in vitro. This effect was independent of steroid treatment.We conclude that homologous desensitization of 2 AR function in non-pregnant rat myometrium in terms of sensitivity (EC 50 ) is independent of sex steroids but in terms of maximal response (E max ) occurs only in the presence of estrogen. We speculate whether progesterone withdrawal in connection with the well-known estrogen dominance at rat parturition may strengthen the desensitization induced by 2 AR activation and thus contribute to the transformation of the uterus from a quiescent to a highly contractile organ.

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“…Interest-ingly, 5,6-EET increased [Ca2+]i in pituitary and parotid cells (15,16) and was implicated to mediate secretory responses (17)(18)(19)(20)(21). The mechanism whereby 5,6-EET increases [Ca2i] has not been investigated; other eicosanoids, such as PGF2,, PGE2, 5-hydroxyeicosatetraenoic acid (5-HETE), and leukotriene B4, are known to induce rises in [Ca2+i primarily from intracellular stores through IP3-dependent mechanisms and, to a lesser extent, through influx of extracellular Ca (22)(23)(24)(25)(26) …”

Section: Introductionmentioning

confidence: 99%

An epoxygenase metabolite of arachidonic acid mediates angiotensin II-induced rises in cytosolic calcium in rabbit proximal tubule epithelial cells.

Madhun¹,

Goldthwait²,

McKay³

et al. 1991

J. Clin. Invest.

116

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Previous studies from this and other laboratories have shown that angiotensin II (AII) induces [Ca2"j transients in proximal tubular epithelium independent of phospholipase C. AII also stimulates formation of 5,6-epoxyeicosatrienoic acid (5,6-EET) from arachidonic acid by a cytochrome P450 epoxygenase and decreases Na' transport in the same concentration range. Because 5,6-EET mimics AII with regard to Na' transport, its effects on calcium mobilization were evaluated. ICa2i, was measured by video microscopy with the fluorescent indicator fura-2 employing cultured rabbit proximal tubule. AII-induced ICa2+i transients were enhanced by arachidonic acid and attenuated by ketoconazole, an inhibitor of cytochrome P450 epoxygenases. Arachidonic acid also elicited a ICa2i1, transient that was attenuated by ketoconazole. 5,6-EET augmented (Ca2'], similar to that seen with AII, but was unaffected by ketoconazole. By contrast, the other regioisomers (8,9-, 11,12-, and 14,15-EET) were much less potent. ICa2+i, transients resulted from influx through verapamil-and nifedipine-sensitive channels. These results suggest a novel mechanism for AII-induced Ca mobilization in proximal tubule involving cytochrome P450-dependent arachidonic asid metabolism and Ca influx through voltage-sensitive channels. (J. Clin. Invest. 1991.

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Effects of prostaglandins on the cytosolic free calcium concentration in vascular smooth muscle cells

Cited by 69 publications

References 11 publications

Nitric oxide mediates cytotoxicity and basic fibroblast growth factor release in cultured vascular smooth muscle cells. A possible mechanism of neovascularization in atherosclerotic plaques.

Nitric oxide mediates cytotoxicity and basic fibroblast growth factor release in cultured vascular smooth muscle cells. A possible mechanism of neovascularization in atherosclerotic plaques.

Desensitization of beta2-adrenoceptor function in non-pregnant rat myometrium is modulated by sex steroids

An epoxygenase metabolite of arachidonic acid mediates angiotensin II-induced rises in cytosolic calcium in rabbit proximal tubule epithelial cells.

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