Direct regulation of smooth muscle contractile elements by second messengers

Nishimura, Junji; Breemen, Cornelis van

doi:10.1016/0006-291x(89)92311-5

Cited by 219 publications

(118 citation statements)

References 26 publications

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“…In permeabilized arterial muscles, it has also been reported that receptor agonists such as phenylephrine, noradrenaline and endothelin-l enhance Ca2"-induced contraction in the presence of GTP (Kitazawa et al, 1989;Nishimura et al, 1989;Anabuki et al, 1990;Hori et al, 1992). These receptor agonists induced contraction in the presence of the Ca2" channel blocker, verapamil, or in the absence of external Ca2" (with EGTA), and these contractions were not accompanied by an increase in MLC phosphorylation .…”

Section: Discussionmentioning

confidence: 99%

“…Activators of protein kinase C, phorbol esters, also induce contraction and increase Ca2+ sensitivity in intact and permeabilized smooth muscle preparations (Nishimura & van Breemen, 1989;Anabuki et al, 1990;Singer 1990;. Since various receptor agonists activate inositol phosphate metabolism to generate the endogenous activator of protein kinase C, diacylglycerol (Berridge, 1984;Nishizuka 1984), it is possible that activation of protein kinase C is…”

Section: Introductionmentioning

confidence: 99%

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Different pathways of calcium sensitization activated by receptor agonists and phorbol esters in vascular smooth muscle

Hori¹,

Sato

Miyamoto

et al. 1993

British J Pharmacology

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1 It has been shown that receptor agonists and activators of protein kinase C, phorbol esters, increase Ca2+ sensitivity of contractile elements in vascular smooth muscle. To discover if protein kinase C is involved in the agonist-mediated Ca2" sensitization, we examined the effects of receptor agonists in the rat isolated aorta in which protein kinase C activity had been diminished by pretreatment with phorbol 12-myristate 13-acetate for 24 h.2 In the aorta with protein kinase C activity, a high concentration (1 gM) of 12-deoxyphorbol 13-isobutyrate induced contraction and a low concentration (100 nM) potentiated high K+-induced contraction. In addition, prostaglandin F2. induced greater contractions than high K+ at a given cytosolic Ca2+ level. The maximally effective concentrations of noradrenaline and endothelin-1 also induced greater contraction than high K+. In the aorta without protein kinase C activity, the contraction induced by 12-deoxyphorbol 13-isobutyrate and its potentiation of the high K+-induced contraction were abolished. However, prostaglandin F2.., noradrenaline and endothelin-1 still induced a greater contraction than high K+.3 In the aorta without protein kinase C activity, noradrenaline, endothelin-l and prostaglandin F2,, but not 12-deoxyphorbol 13-isobutyrate, induced contractions in the presence of the Ca2+ channel blocker, verapamil, or in the absence of external Ca2+, by increasing Ca2+ sensitivify. 4 In the permeabilized preparations, inhibition of protein kinase C activity abolished the effect of potentiation of the Ca2'-induced contraction by 12-deoxyphorbol 13-isobutyrate although the potentiation of the contraction by prostaglandin F2C did not change.5 These results suggest that there are two pathways for Ca21 sensitization in rat aorta; a protein kinase C-dependent pathway which is activated by phorbol esters, and a protein kinase C-independent pathway which is activated by receptor agonists.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Different pathways of calcium sensitization activated by receptor agonists and phorbol esters in vascular smooth muscle

Hori¹,

Sato

Miyamoto

et al. 1993

British J Pharmacology

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“…NO activates guanlylate cyclase and increases cellular cyclic GMP level (Ignarro et al, 1987). The increase in cyclic GMP was reported to be associated with the decrease in the Ca 2+ -sensititivy (Abe et al, 1990;Nishimura & van Breemen, 1989). It is thus conceivable that the decrease in the Ca 2+ -sensitivity was mediated by NO.…”

Section: British Journal Of Pharmacology Vol 134 (4)mentioning

confidence: 99%

Mechanism of trypsin‐induced endothelium‐dependent vasorelaxation in the porcine coronary artery

Nakayama

Hirano

Nishimura

et al. 2001

British J Pharmacology

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1 To investigate the mechanism underlying the trypsin-induced endothelium-dependent relaxation, cytosolic Ca 2+ concentration ([Ca 2+ ] i ) and tension development of smooth muscle were simultaneously monitored in the porcine coronary artery, and [Ca 2+ ] i of in situ endothelial cells were monitored in the porcine aortic valvular strips, using fura-2¯uorometry. 2 During the contraction induced by 30 nM U46619, a thromboxane A 2 analogue, 100 nM trypsin induced a rapid transient signi®cant decrease in both [Ca 2+ ] i (from 67.9+5.1 to 15.7+4.4%) and tension (from 97.5+9.2 to 16.8+3.5%) of smooth muscle only in the presence of endothelium (100% level was assigned to the level obtained with the 118 mM K + -induced contraction). [Ca 2+ ] i and the tension thus returned to the levels prior to the application of trypsin by 5 and 10 min, respectively. 3 The initial phase of this relaxation was partly inhibited by 100 mM N o -nitro-L-arginine (L-NOARG), and was completely inhibited by L-NOARG plus 40 mM K + or L-NOARG plus 100 nM charybdotoxin and 100 nM apamin, while the late phase of the relaxation was inhibited by L-NOARG alone. 4 Trypsin induced a transient [Ca 2+ ] i elevation in the endothelial cells mainly due to the Ca 2+ release from the intracellular stores, at the concentrations (1 ± 100 nM) similar to those required to induce relaxation. 5 In conclusion, trypsin induced an elevation in [Ca 2+ ] i mainly due to Ca 2+ release in endothelial cells, and thereby caused endothelium-dependent relaxation. The early phase of relaxation was due to nitric oxide and hyperpolarizing factors, while the late phase was mainly due to nitric oxide in the porcine coronary artery.

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“…6 Phospholipase C stimulation causes hydrolysis of inositol phospholipid (PI turnover) which generates inositol 1,4,5-triphosphate and diacylglycerol; the former releases Ca ++ from its intracellular Ca ++ stores, such as the sacroplasmic reticulum, and the latter activates protein kinase C to sensitize the contractile proteins. 7,8 Three types of vasoconstrictor agents were used in this study: (1) a high concentration of K +, which induces depolarization that results in Ca ++ influx from the extracellular fluid through voltage-dependent Ca ++ channels, (2) phenylephrine, a selective ai-adrenoceptor agonist and (3) prostanoids (STA2, a stable thromboxane A2 analogue, and PGF2~). Prostanoids, including thromboxane A2 and PGF2~, have been reported in common with phenylephrine, to exert their effects by binding to their specific receptors, resulting in Ca ++ influx via receptoroperated Ca ++ channels and release of Ca ++ from its intracellular stores by stimulating PI turnover in vascular smooth muscle cells.…”

Section: Discussionmentioning

confidence: 99%

Halothane and isoflurane preferentially inhibit prostanoid-induced vasoconstriction of rat aorta

et al. 1994

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The magnitude of the relaxant action of volatile anaesthetics on isolated vascular smooth muscle varies depending upon the contractile agonist. 1,2 Halothane has been shown to interfere selectively, with ct2-adrenoceptormediated vasoconstriction whilst having no effect on oqmediated responses of the rat aorta. 2 Halothane and isoflurane depress serotonin-evoked porcine coronary arterial contraction strongly, but have little effect upon that evoked by histamine, l Recently, we demonstrated that halothane and isoflurane reduce receptor binding of thromboxane A2 and abolish secondary aggregation of platelets, but have little CAN J ANAESTH 1994 / 41:10 / pp991-5

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Direct regulation of smooth muscle contractile elements by second messengers

Cited by 219 publications

References 26 publications

Different pathways of calcium sensitization activated by receptor agonists and phorbol esters in vascular smooth muscle

Different pathways of calcium sensitization activated by receptor agonists and phorbol esters in vascular smooth muscle

Mechanism of trypsin‐induced endothelium‐dependent vasorelaxation in the porcine coronary artery

Halothane and isoflurane preferentially inhibit prostanoid-induced vasoconstriction of rat aorta

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