Venous smooth muscle contains vasoconstrictor ETB-like receptors

Moreland, Suzanne; McMullen, Diane M.; Delaney, Carol; Lee, Ving G.; Hunt, John T.

doi:10.1016/0006-291x(92)91163-k

Cited by 251 publications

(124 citation statements)

References 15 publications

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“…It is present on endothelial cells [1,2] where its activation induces endothelium-dependent relaxation via release of prostacyclin or nitric oxide or both, and may be present on smooth muscle cells to mediate direct vasoconstriction [3,4]. ETB receptors present in certain nerve fibers might also indirectly contribute to constriction [5].…”

Section: Introductionmentioning

confidence: 99%

The role of ET_B receptors in normotensive and hypertensive rats as revealed by the non‐peptide selective ET_B receptor antagonist Ro 46‐8443

Clozel

Breu

1996

FEBS Letters

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We used Ro 46-8443, non-peptidic antagonist selective of endothelin ETB receptors, to study the role of ET8 receptors in rat hypertension models. In normotensive rats, Ro 46-8443 decreased blood pressure, but in SHR and DOCA rats, it induced a pressor effect, due to blockade of ETs-mediated release of nitric oxide since L-NAME prevented it. In rats rendered hypertensive by chronic L-NAME, Ro 46-8443 did not induce a pressor but depressor effect. Thus, in DOCA rats and SHR, Ro 46-8443 reveals a predominant influence of endothelial 'vasorelaxant' ETa receptors, while in normotensive rats the prevailing role of ETn receptors seems to be in mediating a vasoconstrictor tone.

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Section: Introductionmentioning

confidence: 99%

The role of ET_B receptors in normotensive and hypertensive rats as revealed by the non‐peptide selective ET_B receptor antagonist Ro 46‐8443

Clozel

Breu

1996

FEBS Letters

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show abstract

Section: Introductionmentioning

confidence: 99%

“…By use of these agonists and antagonists it has been demonstrated in arteries from several species that the contractile response to endothelin-l is mediated via ETA receptors (Moreland et al, 1992;Sumner et al, 1992;Cardell et al, 1993). In contrast, in certain veins, contractions to endothelin-I appear to be mediated by the ETB receptor (Moreland et al, 1992;Sumner et al, 1992). ETB receptors have also been found on endothelial cells (Sakurai et al, 1990;Sakamoto et al, 1991), and evidence is emerging to suggest that activation of ETB receptors is responsible for the transient endothelin-l induced vasodilatation in animal vessels in vitro (Clozel et al, 1992) and in vivo (Bigaud & Pelton, 1992).…”

Section: Introductionmentioning

confidence: 99%

Endothelin receptors mediating functional responses in human small arteries and veins

Riezebos

Watts

Vallance

1994

British J Pharmacology

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1 In the present study, responses of human omental small arteries and veins to endothelin-1 and endothelin-3 were characterized by use of the ETB receptor selective agonist, sarafotoxin S6c, the ETA receptor antagonist, BQ123, the ETB receptor antagonist, IRL1038, the NO-synthase inhibitor NGmonomethyl-L-arginine (L-NMMA, 300ELM) and indomethacin (10I1M).2 Small arteries (internal diameter 413 ± 22 Am) and parallel running veins (646 ± 35 Am) were mounted in a myograph under a normalized tension equivalent to 90% of a transmural pressure of 100 mmHg and 19 mmHg in vivo, respectively. 3 In small arteries and veins, endothelin-1 caused a concentration-dependent increase in wall tension (E.. = 3.90 ± 0.56 mN mm-' and 1.90 m ± 0.32 mN mm-' respectively, P < 0.05) and was equipotent (arteries: pD2 = 8.91 ± 0.11; veins: pD2 = 8.63 ± 0.08, NS). In endothelium intact arteries, L-NMMA significantly enhanced the sensitivity to endothelin-1 (pD2 control: 8.92 ± 0.16; pD2 L-NMMA: 9.37 ± 0.11; P<0.05). L-NMMA did not affect the sensitivity of veins to endothelin-1. Indomethacin was without effect in arteries and veins. In veins, endothelin-3 was about a hundred times less potent than endothelin-l and showed a biphasic response curve. Small arteries did not contract to endothelin-3. Neither small arteries nor veins contracted to sarafotoxin S6c. Furthermore, no relaxation to endothelin-1 or sarafotoxin S6c was seen in any precontracted vessels. 4 BQ123 (0.03-3 3LM) produced a concentration-dependent rightward parallel displacement of the endothelin-l concentration-response curve in small arteries and veins yielding pA2 values of 7.09 and 7.48 respectively. The slope of the Schild plot in arteries and veins was 1.26 ± 0.24 (NS from unity) and 0.61 ± 0.13 (P <0.05 compared to unity) respectively. IRL1038 (3 JLM) did not affect the potency of endothelin-1 in arteries and veins. In veins, the low sensitivity component (pD2 = 7.16 ± 0.08) of the biphasic response curve to endothelin-3 was completely blocked by BQ123 (31JM), whereas the high sensitivity component (pD2 = 8.66 ± 0.08) was resistant to BQ123 (3 JiM) and IRL1038 (3 JAM).5 These results indicate that contractions of human small vessels to endothelin-l are predominantly mediated by ETA receptors and that nitric oxide modulates the response to endothelin-l in small arteries but not in veins. The different antagonistic potency of BQ123 against endothelin-l and the differential endothelin-1/endothelin-3 potency ratios in arteries and veins provide evidence for the hypothesis that ETA receptors in human small arteries are different from ETA receptors in human small veins. There is no evidence of contractions mediated by 'classical' ETB receptors in these vessels, but small veins appear to contain a functional non ETA/non ETB receptor with a high affinity for endothelin-3.

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“…It has been demonstrated that not only ETA but also ETB receptors can mediate vaso-or bronchoconstriction [4][5][6]. Furthermore, the importance of ETB receptors in pathological situations may be reflected by enhanced receptor densities as recently described for the aorta of spontaneously hypertensive rats [9], the basilar artery of rabbits after subarachnoidal hemorrhage [11] and for the rabbit carotid artery after balloon denudation [29].…”

Section: Discussionmentioning

confidence: 89%

In vitro characterisation of Ro 46‐8443, the first non‐peptide antagonist selective for the endothelin ET_B receptor

Breu¹,

Clozel²,

Burri³

et al. 1996

FEBS Letters

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Venous smooth muscle contains vasoconstrictor ETB-like receptors

Cited by 251 publications

References 15 publications

The role of ET_B receptors in normotensive and hypertensive rats as revealed by the non‐peptide selective ET_B receptor antagonist Ro 46‐8443

The role of ET_B receptors in normotensive and hypertensive rats as revealed by the non‐peptide selective ET_B receptor antagonist Ro 46‐8443

Endothelin receptors mediating functional responses in human small arteries and veins

In vitro characterisation of Ro 46‐8443, the first non‐peptide antagonist selective for the endothelin ET_B receptor

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Venous smooth muscle contains vasoconstrictor ETB-like receptors

Cited by 251 publications

References 15 publications

The role of ETB receptors in normotensive and hypertensive rats as revealed by the non‐peptide selective ETB receptor antagonist Ro 46‐8443

The role of ETB receptors in normotensive and hypertensive rats as revealed by the non‐peptide selective ETB receptor antagonist Ro 46‐8443

Endothelin receptors mediating functional responses in human small arteries and veins

In vitro characterisation of Ro 46‐8443, the first non‐peptide antagonist selective for the endothelin ETB receptor

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The role of ET_B receptors in normotensive and hypertensive rats as revealed by the non‐peptide selective ET_B receptor antagonist Ro 46‐8443

The role of ET_B receptors in normotensive and hypertensive rats as revealed by the non‐peptide selective ET_B receptor antagonist Ro 46‐8443

In vitro characterisation of Ro 46‐8443, the first non‐peptide antagonist selective for the endothelin ET_B receptor