Endothelin-1- and endothelin-3-induced vasorelaxation via common generation of endothelium-derived nitric oxide

Namiki, Atsushi; Hirata, Yukio; Ishikawa, Mikiko; Moroi, Masao; Aikawa, Jo; Machii, Kiyoshi

doi:10.1016/0024-3205(92)90470-a

Cited by 80 publications

(42 citation statements)

References 12 publications

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“…Therefore, it is possible that cGMP accumulation is not equipotent among the three isopeptides in intact glomerulus. A similar result was also observed in a previous study ( 19), which showed that ET-3 had a more potent vasodilating action than ET-1, which seems to be mediated via ETB receptor.…”

Section: Effects Of Endothelins On Cgmp Generation In Rat Glomerulussupporting

confidence: 76%

Endothelin (ET)-3 stimulates cyclic guanosine 3',5'-monophosphate production via ETB receptor by producing nitric oxide in isolated rat glomerulus, and in cultured rat mesangial cells.

Owada

Tomita²,

Terada³

et al. 1994

J. Clin. Invest.

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We investigated the effects of endothelins on receptor-mediated cyclic nucleotide metabolism in rat glomerulus, inner medullary collecting duct (IMCD), and also in cultured rat glomerular mesangial cells. Endothelin (ET)-3 dose-dependently stimulated cGMP accumulation in glomerulus, which was higher than that of ET-1 or ET-2. ETB receptor agonist IRL 1620 produced cGMP in a dose-dependent manner, mimicking the effect of ET-3. ETA receptor antagonist BQ123-Na did not inhibit ET-3-or IRL 1620-stimulated cGMP generation. NG-monomethyl-L-arginine (L-NMMA) significantly inhibited ET-3-or IRL 1620-induced cGMP production, suggesting that ET-3-or IRL 1620-stimulated cGMP generation was mediated through nitric oxide (NO). Intracellular Ca chelator BAPTA /AM and calmodulin antagonist W-7, but not Ca channel blocker nicardipine, significantly inhibited ET-3-or IRL 1620-induced cGMP generation. In cultured rat mesangial cells, ET-3 stimulated cGMP generation through NO in the presence of fetal calf serum, which was not inhibited by addition of BQ123-Na. In IMCD, ET-3 had no stimulative effect on cGMP generation. We conclude that ET-3 stimulates NO-induced cGMP generation through ETB receptor in glomerulus. This effect seems to be mediated through intracellular Ca/calmodulin, but not through Ca influx via L-type Ca channel. Mesangial cells can be a source of NO coupled to ETB receptor activation in glomerulus. From these results, mesangial ETB receptor may work to counteract the vasoconstrictive effect of endothelin caused via ETA receptor in glomerulus. (J.

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Section: Effects Of Endothelins On Cgmp Generation In Rat Glomerulussupporting

confidence: 76%

Endothelin (ET)-3 stimulates cyclic guanosine 3',5'-monophosphate production via ETB receptor by producing nitric oxide in isolated rat glomerulus, and in cultured rat mesangial cells.

Owada

Tomita²,

Terada³

et al. 1994

J. Clin. Invest.

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“…A differential distribution of ET receptor subtypes has also been demonstrated in the human foetal heart and porcine pulmonary tissues (Nakamichi et al, 1991 (Hemsen et al, 1990;van Papendorp et al, 1991) (Takayanagi et al, 1991;Namiki et al, 1992 (Ihara et al, 1991;Fukurodoa et al, 1992;Moreland et al, 1992;Panek et al, 1992). Studies on mammalian isolated blood vessels indicate that ETA receptors mediate the ET-induced vasoconstriction of arterial smooth muscle whereas ETB receptors are responsible for the contractile response in veins (Moreland et al, 1992).…”

Section: Discussionmentioning

confidence: 97%

Differential localization of endothelin ET_a and ET_B binding sites in human placenta

Rutherford

Wharton

McCarthy

et al. 1993

British J Pharmacology

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1 The localization and differential distribution of endothelin (ET) receptor subtypes (ETA and ETB) was investigated in sections of human placenta by use of quantitative in vitro autoradiography and receptor selective ligands.2 Specific, high density ['251]-ET-1 binding sites were localized to the decidua and foetal membranes as well as to arteries and veins in the chorionic plate and throughout the villous tree. Moderate to low density binding was found in the extravillous and villous trophoblast respectively. 6 ET may have a local autocrine or paracrine role in the placenta, acting via specific receptors to influence foetoplacental blood flow and other aspects of placental function.

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“…However, in terms of systemic and glomerular inflammation, ET B receptor antagonism seems to counteract the benefit of ET A blockade. ET B receptors are involved in the synthesis of the vasodilator NO by endothelial cells, through activation by either ET-1 or ET-3 (Namiki et al, 1992). Inhibition of NO has also been associated with an increase in leukocyte adhesion to mesenteric venules, reflecting that the increases in monocyte/macrophage infiltration are caused by decreases in NO production (Dubey et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

Distinct Actions of Endothelin A-Selective Versus Combined Endothelin A/B Receptor Antagonists in Early Diabetic Kidney Disease

Saleh

Pollock²,

Pollock³

2011

J Pharmacol Exp Ther

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Selective endothelin A (ET A ) and combined ET A and ET B receptor antagonists are being investigated for use in treating diabetic nephropathy. However, the receptor-specific mechanisms responsible for producing the potential benefits have not been discerned. Thus, we determined the actions of ET A and ET B receptors on measures of glomerular function and renal inflammation in the early stages of diabetic renal injury in rats through the use of selective and combined antagonists. Six weeks after streptozotocin (STZ)-induced hyperglycemia, rats were given 2R-(4-pyrrolidine-3-carboxylic acid hydrochloride (A-182086) (10 mg/kg/day), a combined ET A/B antagonist; or vehicle for 1 week. Sham controls received STZ vehicle (saline). Hyperglycemia led to significant proteinuria, increased glomerular permeability to albumin (P alb ), nephrinuria, and an increase in total matrix metalloprotease (MMP) and transforming growth factor-␤1 (TGF-␤1) activities in glomeruli. Plasma and glomerular soluble intercellular adhesion molecule-1 (sICAM-1) and monocyte chemoattractant protein-1 (MCP-1) were elevated after 7 weeks of hyperglycemia. Daily administration of both ABT-627 and A-182086 for 1 week significantly attenuated proteinuria, the increase in P alb , nephrinuria, and total MMP and TGF-␤1 activity. However, glomerular sICAM-1 and MCP-1 expression was attenuated with ABT-627, but not A-182086, treatment. In summary, both selective ET A and combined ET A/B antagonists reduced proteinuria and glomerular permeability and restored glomerular filtration barrier component integrity, but only ET A -selective blockade had antiinflammatory and antifibrotic effects. We conclude that selective ET A antagonists are more likely to be preferred for the treatment of diabetic kidney disease.

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Endothelin-1- and endothelin-3-induced vasorelaxation via common generation of endothelium-derived nitric oxide

Cited by 80 publications

References 12 publications

Endothelin (ET)-3 stimulates cyclic guanosine 3',5'-monophosphate production via ETB receptor by producing nitric oxide in isolated rat glomerulus, and in cultured rat mesangial cells.

Endothelin (ET)-3 stimulates cyclic guanosine 3',5'-monophosphate production via ETB receptor by producing nitric oxide in isolated rat glomerulus, and in cultured rat mesangial cells.

Differential localization of endothelin ET_a and ET_B binding sites in human placenta

Distinct Actions of Endothelin A-Selective Versus Combined Endothelin A/B Receptor Antagonists in Early Diabetic Kidney Disease

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Endothelin-1- and endothelin-3-induced vasorelaxation via common generation of endothelium-derived nitric oxide

Cited by 80 publications

References 12 publications

Endothelin (ET)-3 stimulates cyclic guanosine 3',5'-monophosphate production via ETB receptor by producing nitric oxide in isolated rat glomerulus, and in cultured rat mesangial cells.

Endothelin (ET)-3 stimulates cyclic guanosine 3',5'-monophosphate production via ETB receptor by producing nitric oxide in isolated rat glomerulus, and in cultured rat mesangial cells.

Differential localization of endothelin ETa and ETB binding sites in human placenta

Distinct Actions of Endothelin A-Selective Versus Combined Endothelin A/B Receptor Antagonists in Early Diabetic Kidney Disease

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Differential localization of endothelin ET_a and ET_B binding sites in human placenta