Contractions of rat uterine smooth muscle induced by acetylcholine and angiotensin II in Ca<sup>2+</sup>‐free medium

Lalanne, Catherine; Mironneau, C.; Mironneau, Jean; Savineau, J. P.

doi:10.1111/j.1476-5381.1984.tb10081.x

Cited by 60 publications

(35 citation statements)

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“…5). A similar mechanism has been demonstrated in renal proximal tubule cells (12, 23, 32, 44, 49) and is consistent with the accepted contractile effect of angiotensin II on the myometrium, which involves AT 1 receptor activation and elevation of [Ca 2ϩ ] i (23,28,32).…”

Section: C563 Angiotensin II Activates Intracellular At1 Receptors Insupporting

confidence: 57%

Intracellular angiotensin II activates rat myometrium

Deliu

Tica

Motoc

et al. 2011

American Journal of Physiology-Cell Physiology

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Deliu E, Tica AA, Motoc D, Brailoiu GC, Brailoiu E. Intracellular angiotensin II activates rat myometrium. Am J Physiol Cell Physiol 301: C559 -C565, 2011. First published May 22, 2011; doi:10.1152/ajpcell.00123.2011.-Angiotensin II is a modulator of myometrial activity; both AT1 and AT2 receptors are expressed in myometrium. Since in other tissues angiotensin II has been reported to activate intracellular receptors, we assessed the effects of intracellular administration of angiotensin II via microinjection on myometrium, using calcium imaging. Intracellular injection of angiotensin II increased cytosolic Ca 2ϩ concentration ([Ca 2ϩ ]i) in myometrial cells in a dose-dependent manner. The effect was abolished by the AT 1 receptor antagonist losartan but not by the AT2 receptor antagonist PD-123319. Disruption of the endo-lysosomal system, but not that of Golgi apparatus, prevented the angiotensin II-induced increase in [Ca 2ϩ ]i. Blockade of AT1 receptor internalization had no effect, whereas blockade of microautophagy abolished the increase in [Ca 2ϩ ]i produced by intracellular injection of angiotensin II; this indicates that microautophagy is a critical step in transporting the peptide into the endo-lysosomes lumenum. The response to angiotensin II was slightly reduced in Ca 2ϩ -free saline, indicating a major involvement of Ca 2ϩ release from internal stores. Blockade of inositol 1,4,5-trisphosphate (IP 3) receptors with heparin and xestospongin C or inhibition of phospholipase C (PLC) with U-73122 abolished the response to angiotensin II, supporting the involvement of PLC-IP 3 pathway. Angiotensin II-induced increase in [Ca 2ϩ ]i was slightly reduced by antagonism of ryanodine receptors. Taken together, our results indicate for the first time that in myometrial cells, intracellular angiotensin II activates AT 1-like receptors on lysosomes and activates PLC-IP 3-dependent Ca 2ϩ release from endoplasmic reticulum; the response is further augmented by a Ca 2ϩ -induced Ca 2ϩ release mechanism via ryanodine receptors activation. calcium imaging; cytosolic calcium concentration; endoplasmic reticulum; microinjection ANGIOTENSIN II is an eight amino acid peptide that exerts its actions by activation of G protein-coupled receptors, namely AT 1 and AT 2 receptors. Increasing evidence suggests that angiotensin II acts not only as an endocrine/paracrine factor, but also as an autacoid or intracrine peptide, with the ability to signal from within the cell, without stimulating plasma membrane receptors (21, 38). We previously reported that intracellular administration of angiotensin II via liposomes increases contractility of rat aorta via activation of intracellular receptors (7). Similarly, microinjection of angiotensin II increases cytosolic Ca 2ϩ concentration ([Ca 2ϩ ] i ) in vascular smooth muscle cells (13, 16) or kidney proximal tubule cells (49). The intracellular angiotensin II can result either via uptake from the interstitium or by intracellular synthesis. In the latter case, intracellular renin conver...

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Section: C563 Angiotensin II Activates Intracellular At1 Receptors Insupporting

confidence: 57%

Intracellular angiotensin II activates rat myometrium

Deliu

Tica

Motoc

et al. 2011

American Journal of Physiology-Cell Physiology

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“…Electrical activity was recorded with both conventional microelectrodes filled with 3 M KCI (resistance 40-50 MQ) and the double sucrose gap method (Mironneau, 1973 (Vassort & Rougier, 1972) and discussed in detail (Potreau & Raymond, 1983 (Lalanne et al, 1984). For longer applications of acetylcholine (2 min or more), the transient contraction was followed by a maintained response which lasted as long as the preparation was exposed to the agonist (Figure la (Figure 2).…”

Section: Methodsmentioning

confidence: 99%

“…(ii) a Ca2+-influx through receptor-operated channels (Bolton & Kitamura, 1983); (iii) a release of Ca2+ ions from a limited intracellular Ca2+ store producing only one transient contraction (Casteels & Raeymaekers, 1979;Lalanne et al, 1984). However, it has also been reported that, during the same Ca2+-free perfusion, maintained contractions of myometrium can be repeatedly produced by different stimulant substances without diminution in size for 1 h or longer (Sakai et al, 1982;Lalanne et al, 1984).…”

Section: Introductionmentioning

confidence: 99%

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Maintained contractions of rat uterine smooth muscle incubated in a Ca²⁺‐free solution

Mironneau¹,

Mironneau²,

Savineau³

1984

British J Pharmacology

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1The effects of acetylcholine (10-4 M), prostaglandin E2 (10-6 M), vanadate (5 x 10-4M) and fluoride (10-2 M) have been studied on the mechanical and electrical activities of rat myometrial strips perfused in Ca2+-free EGTA-containing solutions. (fluoride) or Ca2+ release from an intracellular store. This latter mechanism would include both pharmacomechanical (prostaglandin E2, vanadate) and electromechanical (acetylcholine) coupling.

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“…NA was applied after 1.5 min in Ca2+-free solutions. Lalanne et al, 1984). Decreasing the temperature of the perfusing solution to 20C suppressed both electrical activity and calcium influx through voltagedependent channels.…”

Section: Diussionmentioning

confidence: 99%

Effects of calcium entry blockers on calcium‐dependent contractions of rat portal vein

Dacquet

Mironneau

1987

British J Pharmacology

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1 The effects of six calcium entry blockers belonging to the dihydropyridine (isradipine or PN 200-110, nifedipine, nicardipine), verapamil (D888 or desmethoxyverapamil, D600 or gallopamil) and diltiazem classes were investigated on isometric spontaneous contractions and contractions induced by high-K+ solutions, noradrenaline, acetylcholine and caffeine. 2 The rank order of potency was PN 200-110>nicardipine=nifedipine=D888>D600>diltiaz-em from experiments on spontaneous contractions and high-K+ induced contractions. With depolarized preparations, the concentration-response curves for nicardipine, PN 200-1 10, nifedipine and D600 were significantly shifted to the left indicating that the calcium entry blockers show voltagedependent inhibitory properties. This effect was not significant with D888 and diltiazem. 3 All the calcium entry blockers strongly reduced the noradrenaline (NA)-and acetylcholine (ACh)-induced contractions at concentrations which produced complete inhibition of spontaneous contractions. They had a slight effect on caffeine-induced contractions. 4 In Ca2+-free, EGTA-containing solutions, both ACh, NA and caffeine produced transient contractions, the amplitude of which could be taken as a measurement of the amount of internal calcium present in a drug-sensitive calcium store. The filling ofthe calcium store was maximal after 10-12 min ofcalcium loading in 2.1 mM Ca2", while the depletion was complete after 4-6 min ofperfusion in Ca2"-free solution.5 At concentrations which abolished spontaneous contractions, PN 200-110, nifedipine, D888 and D600 had no appreciable effect on contractions evoked in Ca2"-free solutions by ACh, NA and caffeine. When added in Ca2+-containing solutions diltiazem and, to a lesser extent, nicardipine strongly reduced the contractions evoked in Ca2 -free solutions, suggesting that they inhibited the filling of the internal calcium store. 6 These results indicate that the six calcium entry blockers are potent inhibitors of calcium influx through voltage-dependent calcium channels. Two of them (diltiazem and nicardipine) may exert an additional effect to depress contractions dependent on intracellular calcium release.

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Contractions of rat uterine smooth muscle induced by acetylcholine and angiotensin II in Ca²⁺‐free medium

Abstract: 1The effects of acetylcholine (ACh,10-M) and angiotensin II (Ang II,

Cited by 60 publications

References 34 publications

Intracellular angiotensin II activates rat myometrium

Intracellular angiotensin II activates rat myometrium

Maintained contractions of rat uterine smooth muscle incubated in a Ca²⁺‐free solution

Effects of calcium entry blockers on calcium‐dependent contractions of rat portal vein

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Contractions of rat uterine smooth muscle induced by acetylcholine and angiotensin II in Ca2+‐free medium

Abstract: 1The effects of acetylcholine (ACh,10-M) and angiotensin II (Ang II,

Cited by 60 publications

References 34 publications

Intracellular angiotensin II activates rat myometrium

Intracellular angiotensin II activates rat myometrium

Maintained contractions of rat uterine smooth muscle incubated in a Ca2+‐free solution

Effects of calcium entry blockers on calcium‐dependent contractions of rat portal vein

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Contractions of rat uterine smooth muscle induced by acetylcholine and angiotensin II in Ca²⁺‐free medium

Maintained contractions of rat uterine smooth muscle incubated in a Ca²⁺‐free solution