Down-regulation of endothelin B receptors in autogenous saphenous veins grafted into the arterial circulation

Eguchi, Daihiko; Nishimura, Junji; Kobayashi, Sei; Komori, Kimihiro; Sugimachi, Keizō; Kobayashi, Hideo

doi:10.1016/s0008-6363(97)00103-x

Cited by 10 publications

(7 citation statements)

References 31 publications

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“…However, there are other reports of an increased ET A -R expression in porcine saphenous vein-carotid artery interposition grafts 1 month after surgery, 30 a downregulation of ET B -R in rabbit saphenous vein-carotid artery interposition grafts 1 month after surgery, 31 and no apparent change in ET A -R and ET B -R distribution but an enhanced ET A -Rmediated sensitivity to ET-1 in human aortocoronary saphenous vein grafts several years after surgery. 32 In a related setting of pressure-induced gene expression (ie, angioplasty), on the other hand, evidence has been provided that points to an important role for the ET B -R or a non-ET A -R/non-ET B -R in the rabbit 33 and rat carotid artery 34 -36 in restenosis.…”

Section: Discussionmentioning

confidence: 92%

Pressure-Induced Upregulation of Preproendothelin-1 and Endothelin B Receptor Expression in Rabbit Jugular Vein In Situ

Lauth

Berger

Cattaruzza

et al. 2000

ATVB

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Abstract-Upregulation of endothelin-1 (ET-1) synthesis in venous bypass grafts in response to arterial levels of blood pressure may play a major role in graft failure. To investigate this hypothesis, isolated segments of the rabbit jugular vein were perfused at physiological (0 to 5 mm Hg) and nonphysiological (20 mm Hg) levels of intraluminal pressure.As judged by reverse transcription-polymerase chain reaction analysis (mRNA level), neither endothelin-converting enzyme nor endothelin A receptor expression appeared to be pressure sensitive. In contrast, there was a profound and time-dependent increase in endothelial prepro-ET-1 mRNA and intravascular ET-1 abundance (by ELISA) as well as in smooth muscle endothelin B receptor mRNA and functional protein (by superfusion bioassay) on raising the perfusion pressure from 5 to 20 mm Hg, but not from 0 to 5 mm Hg, for up to 12 hours. Video microscopy analysis revealed that the segments were distended by 75% at 5 mm

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Section: Discussionmentioning

confidence: 92%

Pressure-Induced Upregulation of Preproendothelin-1 and Endothelin B Receptor Expression in Rabbit Jugular Vein In Situ

Lauth

Berger

Cattaruzza

et al. 2000

ATVB

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“…The predominant receptor present in arterial tissue appears to be the ET A receptor. This is supported by functional studies in multiple different arteries from several species (rat thoracic aorta (White et al ., 1993), rat mesenteric artery, rabbit carotid artery (Calo et al ., 1996), human coronary artery, human pulmonary artery, rabbit femoral artery (Eguchi et al ., 1997) and human pial artery (Pierre & Davenport, 1998). ET‐1 causes a contraction with greater potency than ET‐3 and the ET B receptor agonist S6c is virtually inactive in these arteries.…”

Section: Discussionmentioning

confidence: 99%

Endothelin‐1‐induced venous contraction is maintained in DOCA‐salt hypertension; studies with receptor agonists

Watts

Fink

Northcott

et al. 2002

British J Pharmacology

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1 Deoxycorticosterone acetate (DOCA) salt hypertension is associated with an endothelin-1 (ET-1)-dependent increase in arterial resistance and mean circulatory ®lling pressure. Contraction of endothelium-intact arteries and veins from sham and DOCA-salt hypertensive rats to agonists of the ET A (ET-1 (1 ± 31) ) and ET B receptor (sarafotoxin 6c; S6c) was investigated in tissue baths as was expression of mRNA for ET-1 and mRNA and protein for the ET A and ET B receptor. 2 ET-1 (1 ± 31) contracted aorta and vena cava from sham rats with a 30 fold lower potency than ET-1. Contraction was not altered by the ET B receptor antagonist BQ788 (100 nM) but was abolished by the ET A receptor antagonist ABT-627 (30 nM). 3 In DOCA-salt thoracic aorta, maximum contraction to ET-1 and ET-1 (1 ± 31) was reduced (36.6+6.3 and 13.3+4.4% of sham response, respectively); aorta did not contract to S6c. 4 In vena cava from DOCA-salt rats, contraction to ET-1 and ET-1 (1 ± 31) was not reduced compared to sham contraction; vena cava from sham and DOCA-salt rats contracted to S6c with a similar potency. 5 Real time RT ± PCR revealed that prepro ET-1 mRNA was increased 6.6+3.3 fold and 8.7+3.9 fold greater in DOCA-salt aorta and vena cava, respectively, compared to sham. Vena cava expressed a higher content of ET A and ET B receptor mRNA than aorta (P50.05), but no dierences were observed between sham and DOCA-salt tissues. ET A and ET B receptor protein was identi®ed in all tissues. Immunoreactive ET A receptor, observed as a 65, 30 and 28 kDa bands, was expressed 400% greater in DOCA-salt aorta compared to sham, but was not altered in vena cava. Immunoreactive ET B receptor, observed as 120, 45 and 30 kDa bands, tended to be higher in vena cava compared to aorta, but was not dierent in sham and DOCA-salt vena cava. 6 These results suggest that ET A receptor function is impaired in aorta but not vena cava of DOCA-salt rats. The ET B receptor was present in the aorta but, unlike in veins, does not mediate contraction directly. A sustained response to ET-1 in the venous circulation may contribute to the elevated blood pressure in the DOCA-salt model.

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“…This was consistent with findings in the atherosclerotic human coronary artery ( Bacon et al ., 1996 ; Russell et al ., 1997 ) which showed no evidence for up‐regulation of smooth muscle ET B receptors in disease. In a rabbit model, both ET B mRNA and S6c‐mediated contractile responses were actually reduced in saphenous vein grafts compared to native veins ( Eguchi et al ., 1997 ). Our data were from grafts that had failed after a number of years, however, alterations in receptor expression in the earlier stages of the disease process may have contributed to earlier graft failure.…”

Section: Discussionmentioning

confidence: 99%

Endothelin receptor expression and pharmacology in human saphenous vein graft

Maguire

Davenport

1999

British J Pharmacology

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3 The ratio of medial ET A :ET B receptors was 75% : 25% in both graft and control saphenous vein. 4 ET-1 contracted control (EC 50 2.9 nM) and graft (EC 50 4.5 nM) saphenous vein more potently than diseased coronary artery (EC 50 25.5 nM). 5 In all three blood vessels ET-1 was 100 times more potent than ET-3 and three times more potent than sarafotoxin 6b (S6b). Little or no response was obtained in any vessel with the ET B agonist sarafotoxin 6c (S6c). 6 The ET A antagonist PD156707 (100 nM) blocked ET-1 responses in all three vessels with pK b values of approximately 8.0. 7 For individual graft veins the EC 50 value for ET-1 and`age' of graft in years showed a signi®cant negative correlation. 8 In conclusion there is no alteration in ET receptor expression in the media of saphenous veins grafted into the coronary circulation compared to control veins. ET A receptors predominantly mediate the vasoconstrictor response to ET-1 in graft vein, with no apparent up-regulation of ET B receptors. The sensitivity of the graft vein to ET-1 increased with graft`age', suggesting that these vessels may be particularly vulnerable to the increased plasma ET levels that are detected in patients with cardiovascular disease.

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Down-regulation of endothelin B receptors in autogenous saphenous veins grafted into the arterial circulation

Abstract: Functioning ETB receptors and their mRNA are down-regulated when veins are grafted into the arterial circulation. All these changes in gene expression and function are part of adaptive responses known as 'arterialization'.

Cited by 10 publications

References 31 publications

Pressure-Induced Upregulation of Preproendothelin-1 and Endothelin B Receptor Expression in Rabbit Jugular Vein In Situ

Pressure-Induced Upregulation of Preproendothelin-1 and Endothelin B Receptor Expression in Rabbit Jugular Vein In Situ

Endothelin‐1‐induced venous contraction is maintained in DOCA‐salt hypertension; studies with receptor agonists

Endothelin receptor expression and pharmacology in human saphenous vein graft

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