ETA Receptors Predominate in the Human Vasculature and Mediate Constriction

Davenport, Anthony P.; Kuc, Rhoda E.; Maguire, Janet J.; Harland, Spencer P.

doi:10.1097/00005344-199506263-00080

Cited by 29 publications

(24 citation statements)

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“…Previous studies of cerebral arteries from man (Adner et al 1994;Davenport et al 1995), goat (Salom et al 1993), rat (Feger et al 1994) and guinea-pig (Adner et al 1993) have indicated the presence of ETA receptors mediating vasoconstriction in these vessels. In the present study, the order of potency of the endothelins (ET-1 > ET-3) was in accordance with the properties of an ETA receptor (Masaki et al 1994).…”

Section: Discussionmentioning

confidence: 94%

Contractile effect of big endothelin-1 and its conversion to endothelin-1 in rabbit cerebral arteries

Petersson¹,

Hanson

Lindberg

et al. 1996

Naunyn-Schmiedeberg's Arch Pharmacol

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The effect of big endothelin-1 (big ET-1) and its conversion to endothelin-1 (ET-1) in rabbit cerebral arteries were examined. Big ET-1 and ET-1 induced concentration-dependent contractions in the basilar artery; ET-1 was approximately 8 times more potent than big ET-1. The metalloprotease inhibitor phosphoramidon (30 mumol/l) almost abolished the contractile response to big ET-1, whereas the ET-1-induced contraction was unaffected. Removal of the endothelium did not attenuate the big ET-1-induced contraction. ET-1 was approximately 14 times more potent than endothelin-3 (ET-3) to elicit contraction. The contractions induced by big ET-1, ET-1 and ET-3 were all inhibited by ET(A) receptor antagonist BQ 123 (3 mumol/l). The ET(B) receptor antagonist IRL 1038 (3 mumol/l) had no effect on the contractile responses to big ET-1 and ET-1, but produced a small inhibition of the ET-3-induced contraction. Formation of ET-1 was demonstrated in membrane fractions of cerebral arteries incubated with big ET-1 as measured by high pressure liquid chromatography followed by radioimmunoassay. These results suggest that externally applied big ET-1 is converted to ET-1 by a phosphoramidon-sensitive "endothelin converting enzyme" present in the vascular smooth muscle cells. The ET-1 formed subsequently mediates the big ET-1-induced contraction by activation of mainly ET(A) receptors, although a small contribution of ET(B) receptors cannot be excluded.

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Section: Discussionmentioning

confidence: 94%

Contractile effect of big endothelin-1 and its conversion to endothelin-1 in rabbit cerebral arteries

Petersson¹,

Hanson

Lindberg

et al. 1996

Naunyn-Schmiedeberg's Arch Pharmacol

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“…Renal proximal tubule cells were treated with vehicle (dH 2 O), an ETB agonist (BQ3020) [29,30] (Sigma Chemical Co., St. Louis, MO, USA), and/or an ETB receptor antagonist (BQ788) [29,30] (Sigma Chemical Co.), at the indicated concentrations and times. BQ3020 is 1000-fold selective to the ETB receptor relative to the ETA receptor in human kidney and other tissues [31][32][33]. Immunoblotting was performed as reported [22][23][24][25][26][27], except that the transblots were probed with ETB (1:300) or AT 1 receptor antibodies (1:400).…”

Section: Immunoblottingmentioning

confidence: 99%

Aberrant ETB receptor regulation of AT1 receptors in immortalized renal proximal tubule cells of spontaneously hypertensive rats

Zeng¹,

Wang²,

Asico³

et al. 2005

Kidney International

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“…The ratio of ET A to ET B is approximately 90:10 in the renal artery and about 92:8 in the renal vein, suggesting an important role for ET A in regulating renal vascular reactivity. 33 Similar to human kidney, ET A are the predominant receptors present in rat renal vascular smooth muscle. ET B however, are detected largely in endothelial cells of renal vessels and glomeruli.…”

Section: Introductionmentioning

confidence: 96%

“…33-37 Radioligand binding studies show that the proportion of ET A and ET B in membranes of preglomerular vessels averages 40:60 in rabbits 34 and approximately 50:50 in rats. 35 Studies using ligand binding and autoradiography by Kuc and Davenport 36 suggest that the human kidney contains 70% ET B .…”

Section: Introductionmentioning

confidence: 99%

Endothelin and the Renal Microcirculation

Guan¹,

VanBeusecum²,

Inscho³

2015

Seminars in Nephrology

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Endothelin is one of the most potent renal vasoconstrictors. Endothelin plays an essential role in the regulation of renal blood flow, glomerular filtration, sodium and water transport, and acid-base balance. ET-1, ET-2 and ET-3 are the three distinct endothelin isoforms comprising the endothelin family. ET-1 is the major physiologically relevant peptide and exerts its biological activity through two G-protein coupled receptors, ET A and ET B . Both ET A and ET B are expressed by the renal vasculature. While ET A are mainly expressed by vascular smooth muscle cells, ET B are expressed by both renal endothelial and vascular smooth muscle cells. Activation of the endothelin system, or over-expression of downstream endothelin signaling pathways, has been implicated in several pathophysiological conditions including hypertension, acute kidney injury, diabetic nephropathy and immune nephritis. In the current review, we will focus on the effects of endothelin on the renal microvasculature, and update recent findings on endothelin in the regulation of renal hemodynamics.

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ETA Receptors Predominate in the Human Vasculature and Mediate Constriction

Cited by 29 publications

References 0 publications

Contractile effect of big endothelin-1 and its conversion to endothelin-1 in rabbit cerebral arteries

Contractile effect of big endothelin-1 and its conversion to endothelin-1 in rabbit cerebral arteries

Aberrant ETB receptor regulation of AT1 receptors in immortalized renal proximal tubule cells of spontaneously hypertensive rats

Endothelin and the Renal Microcirculation

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