Endothelium-dependent contraction induced by acetylcholine in isolated rat renal arteries

Nishimura, Yoshitaka; Usui, Hachiro; Kurahashi, Kazuyoshi; Suzuki, Aritomo

doi:10.1016/0014-2999(95)00023-e

Cited by 20 publications

(27 citation statements)

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“…The production of endothelium-derived prostanoids is augmented in arteries with regenerated endothelium [36,37], and in normotensive aging and hypertensive arteries [5,7,9,38]. The endothelium of the renal arteries of healthy rats also releases EDCF, suggesting that it may play a role in the regulation of basal tone in this artery, and not only during agonist-induced stimulated release [39,40]. Studies in humans show that the acetylcholine-induced vasodilatation is diminished in conductance and resistance vessels of patients with hypertension.…”

Section: Cox-derived Edcfsmentioning

confidence: 98%

Endothelial dysfunction: a strategic target in the treatment of hypertension?

Tang

Vanhoutte

2010

Pflugers Arch - Eur J Physiol

146

121

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Endothelial dysfunction is a common feature of hypertension, and it results from the imbalanced release of endothelium-derived relaxing factors (EDRFs; in particular, nitric oxide) and endothelium-derived contracting factors (EDCFs; angiotensin II, endothelins, uridine adenosine tetraphosphate, and cyclooxygenase-derived EDCFs). Thus, drugs that increase EDRFs (using direct nitric oxide releasing compounds, tetrahydrobiopterin, or L-arginine supplementation) or decrease EDCF release or actions (using cyclooxygenase inhibitor or thromboxane A2/prostanoid receptor antagonists) would prevent the dysfunction. Many conventional antihypertensive drugs, including angiotensin-converting enzyme inhibitors, calcium channel blockers, and third-generation beta-blockers, possess the ability to reverse endothelial dysfunction. Their use is attractive, as they can address arterial blood pressure and vascular tone simultaneously. The severity of endothelial dysfunction correlates with the development of coronary artery disease and predicts future cardiovascular events. Thus, endothelial dysfunction needs to be considered as a strategic target in the treatment of hypertension.

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Section: Cox-derived Edcfsmentioning

confidence: 98%

Endothelial dysfunction: a strategic target in the treatment of hypertension?

Tang

Vanhoutte

2010

Pflugers Arch - Eur J Physiol

146

121

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“…Activation of a cytosolic PLA 2 , possibly followed by that of a cyclooxygenase, is another potential signaling mechanism of muscarinic receptors (Hunt et al, 1994;Felder, 1995;Nishimura et al, 1995). This could potentially also be involved in muscarinic receptor-mediated bladder contraction, since several cyclooxygenase products are known to contract the bladder (Andersson, 2000), and since it has recently been shown that rat bladder contraction elicited by protease-activated receptor-2 involves activation of a cyclooxygenase Nakahara et al, 2003).…”

Section: Phospholipases and Ca 2؉ In Muscarinic Bladder Contractionmentioning

confidence: 99%

“…Muscarinic stimulation of PLC has also been demonstrated in cultured smooth muscle cells from human bladder (Marsh et al, 1996) and in rat bladder slices (Kories et al, 2003), and the latter response was shown to be M 3 receptor mediated. However, muscarinic receptors can also activate a PLD or PLA 2 in a variety of cell types (Felder, 1995), the latter possibly leading to cyclooxygenase activation (Nishimura et al, 1995). Several cyclooxygenase products can contract isolated detrusor muscle (Andersson, 2000), and cyclooxygenase activation was shown to at least partly mediate rat urinary bladder contraction induced by proteaseactivated receptor-2 .…”

mentioning

confidence: 99%

Signal Transduction Underlying Carbachol-Induced Contraction of Rat Urinary Bladder. I. Phospholipases and Ca²⁺Sources

Schneider¹,

Hein²,

Michel³

2003

J Pharmacol Exp Ther

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We have reexamined the muscarinic receptor subtype mediating carbachol-induced contraction of rat urinary bladder and investigated the role of phospholipase (PL)C, D, and A 2 and of intra-and extracellular Ca 2ϩ sources in this effect. Based on the nonsubtype-selective tolterodine, the highly M 2 receptorselective (R)-4-{2-[3-(4-methoxy-benzoylamino)-benzyl]-piperidin-1-ylmethyl}-piperidine-1-carboxylic acid amide , and the highly M 3 receptor-selective darifenacin and 3-(1-carbamoyl-1,1-diphenylmethyl)-1-(4-methoxyphenylethyl)pyrrolidine (APP), contraction occurs via M 3 receptors. Carbachol stimulated inositol phosphate formation in rat bladder slices, and this was abolished by the phospholipase C inhibitor 1- Carbachol had only little effect on PLD activity in bladder slices, but the PLD inhibitor butan-1-ol, relative to its negative control butan-2-ol (0.3% each), caused detectable inhibition of carbachol-induced bladder contraction. The cytosolic PLA 2 inhibitor arachidonyltrifluoromethyl ketone weakly inhibited carbacholinduced contraction at a concentration of 300 M, but the cyclooxygenase inhibitor indomethacin (1-10 M) remained without effect. The Ca 2ϩ entry blocker nifedipine (10 -100 nM) almost completely inhibited carbachol-induced bladder contraction. In contrast, 1-[␤-[3-(4-methoxyphenyl)propoxy]-4-methoxyphenethyl]-1H-imidazole HCl (SKF 96,365; 10 M), an inhibitor of storeoperated Ca 2ϩ channels, caused little inhibition. We conclude that carbachol-induced contraction of rat bladder largely depends on Ca 2ϩ entry through nifedipine-sensitive channels and, perhaps, PLD, PLA 2 , and store-operated Ca 2ϩ channels, whereas cyclooxygenase and, surprisingly, also PLC are not involved to a relevant extent.Muscarinic acetylcholine receptors are the physiologically most important mechanisms to elicit contraction of the urinary bladder (Andersson, 1993). In the bladder of various mammalian species, including humans, M 2 and M 3 muscarinic receptors coexist, but the expression of M 2 receptors is much greater than that of the M 3 receptors (Wang et al., 1995;Goepel et al., 1998;Yamanishi et al., 2000;Kories et al., 2003). Nevertheless, the contractile response to the exogenous agonist carbachol and to endogenous agonists released by field stimulation have been attributed predominantly, if not exclusively, to M 3 receptors in rats (Longhurst et al., 1995;Hegde et al., 1997;Tong et al., 1997;Braverman et al., 1998;Choppin et al., 1998;Longhurst and Levendusky, 2000;Kories et al., 2003), mice (Choppin and Eglen, 2001b), pigs (Yamanishi et al., 2000), dogs (Choppin and Eglen, 2001a), and humans (Chess-Williams et al., 2001;Fetscher et al., 2002). Moreover, at least male M 3 (but not M 2 ) receptorknockout mice exhibit bladder distension and develop urinary retention (Matsui et al., 2000). On the other hand, it should be considered that hitherto available antagonists have only modest subtype selectivity and/or do not act in a purely competitive manner; hence, they were not well suited for detecting a pot...

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“…1 The main component of EDRF has been identified to be nitric oxide. 2 Increased production of EDCF has been reported in anoxia, 1 hypertension, 3 aging, 4 and diabetes. 5 Thromboxane A 2 (TXA 2 ) and prostaglandin H 2 (PGH 2 ) have been reported to be EDCF in spontaneously hypertensive rats (SHR).…”

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confidence: 99%

Endothelium-Derived Contracting Factor in Carotid Artery of Hypertensive Dahl Rats

et al. 1999

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Abstract-The present study is designed to investigate whether acetylcholine (ACh) elicits an endothelium-derived contracting factor (EDCF) and whether it contributes to decreased relaxant response induced by ACh in Dahl rats. Dahl salt-sensitive (DS) and -resistant (DR) rats were fed a 0.4% NaCl or an 8% NaCl diet for 4 weeks. High sodium intake significantly increased blood pressure in DS rats but not in DR rats. The carotid rings were suspended for isometric tension recording. ACh caused an endothelium-dependent contraction in carotid rings from hypertensive DS rats but not from normotensive Dahl rats.

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Endothelium-dependent contraction induced by acetylcholine in isolated rat renal arteries

Cited by 20 publications

References 10 publications

Endothelial dysfunction: a strategic target in the treatment of hypertension?

Endothelial dysfunction: a strategic target in the treatment of hypertension?

Signal Transduction Underlying Carbachol-Induced Contraction of Rat Urinary Bladder. I. Phospholipases and Ca²⁺Sources

Endothelium-Derived Contracting Factor in Carotid Artery of Hypertensive Dahl Rats

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Endothelium-dependent contraction induced by acetylcholine in isolated rat renal arteries

Cited by 20 publications

References 10 publications

Endothelial dysfunction: a strategic target in the treatment of hypertension?

Endothelial dysfunction: a strategic target in the treatment of hypertension?

Signal Transduction Underlying Carbachol-Induced Contraction of Rat Urinary Bladder. I. Phospholipases and Ca2+Sources

Endothelium-Derived Contracting Factor in Carotid Artery of Hypertensive Dahl Rats

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Signal Transduction Underlying Carbachol-Induced Contraction of Rat Urinary Bladder. I. Phospholipases and Ca²⁺Sources