The control of endothelin-1 secretion

Tasaka, Kenjí; Kitazumi, Kazuhiro

doi:10.1016/0306-3623(94)90120-1

Cited by 46 publications

(24 citation statements)

References 98 publications

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“…Furthermore bosentan has shown promising results in prevention of ischemic skeletal muscle necrosis [12,15,26] and tissue protection in different organs (liver, kidney, lung, heart, brain) in case of infection and sepsis [22,31,35,8]. As a result of the low incidence, larger study groups are necessary for determining specific ET-1 release kinetics in patients with wound healing disorders and early infections to indicate a prophylactic effect of ET-1 antagonists, bosentan being the most promising candidate.…”

Section: Discussionmentioning

confidence: 99%

Endothelin‐1 is secreted after total knee arthroplasty regardless of the use of a tourniquet

Matziolis

Drahn

Schröder

et al. 2005

Journal Orthopaedic Research

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Early infections and wound healing disorders after implantation of a total knee replacement occur regardless of the intraoperative use of a tourniquet. The biochemical regulatory processes responsible for the disturbances in microcirculation and thus the potential therapeutic options have yet to be elucidated. The hypothesis of the present paper was that endothelin-1 (ET-l), a mediator of microcirculation disturbances in parenchymatous organs, also is released after major operations on peripheral joints.The concentration of ET-1 in the plasma was determined preoperatively and at 10 postoperative time points (5min43h) with (group A, n = 10) and without the use of a tourniquet (group B, n = 10). The ET-1 concentration achieved its maximum 6h after opening the tourniquet, which corresponded to 3.3 times the preoperative value. Without a tourniquet, the concentration maximum (2.9 times the baseline value) was achieved already 1.5 h after the end of the operation. However, the total amount of ET-1 secreted over 24h was identical in both groups (p > 0.5).We conclude that the tissue hypoxia resulting from the use of a tourniquet modulates ET-I secretion, but that traumatization during the operation has a much stronger influence on the total amount secreted.ET-I antagonists thus should be discussed for the drug prophylaxis of wound healing disorders, regardless of the use of a tourniquet.

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Section: Discussionmentioning

confidence: 99%

Endothelin‐1 is secreted after total knee arthroplasty regardless of the use of a tourniquet

Matziolis

Drahn

Schröder

et al. 2005

Journal Orthopaedic Research

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“…The most likely explanation for these experimental observations is that vasopressin-induced arterial superoxide production depends on the newly synthesized ET-1 peptide from preproET-1, a process that requires a period of longer than 4 hours. 29,30 Alternatively, the cellular source for new ET-1 synthesis could be smooth muscle cells instead of endothelial cells, because agonists such as cytokines have been shown to stimulate ET-1 release quite rapidly from endothelial cells. 31 However, it is important to point out that although we observed that arterial vasopressin levels are Ϸ3-fold higher in DOCA-salt rats than in sham rats (7.1Ϯ1.4 versus 1.9Ϯ04 pg/mg protein), previously published studies showed that the normal plasma vasopressin levels (1 to 30 pmol/L) are generally elevated by 3-to 5-fold in the benign phase of hypertension in this model.…”

Section: Discussionmentioning

confidence: 99%

Vasopressin Induces Vascular Superoxide Via Endothelin-1 in Mineralocorticoid Hypertension

Galligan

Fink

et al. 2003

Hypertension

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Abstract-We have recently reported that endothelin-1 (ET-1), which is increased in the arteries of deoxycorticosterone acetate (DOCA)-salt hypertensive rats, stimulates superoxide production. However, the humoral mechanisms responsible for ET-1-induced superoxide formation in low-renin models of hypertension, such as DOCA-salt hypertension, remain undefined. Vasopressin is known to upregulate vascular preproET-1 gene expression in DOCA-salt rats, an effect that is absent in vasopressin-deficient Brattleboro rats treated with DOCA-salt. The present study tested the hypothesis that vasopressin contributes to ET-1-induced vascular superoxide production in DOCA-salt hypertensive rats. Carotid arterial segments of DOCA, sham (uninephrectomized), or normal (untreated) rats were used for the study. In vitro vasopressin treatment of carotid arteries from normal rats for 24 hours, but not 4 hours, increased both ET-1 and superoxide levels. The increase of vasopressin-induced superoxide was reduced by pretreatment of the vessels with ABT627, a selective ET A receptor antagonist ABT627. Vasopressin, ET-1, and superoxide levels were significant elevated in carotid arteries of DOCA-salt rats compared with sham controls. The selective V1-vasopressin receptor antagonist (␤-Mercapto-␤, ␤-cyclopentamethylenepropiony 1 , O-Me-Tyr 2 , Arg 8 vasopressin, ME-AVP), decreased superoxide both in vasopressin-treated vessels of normal rats and in vessels of DOCA-salt rats, with a concomitant reduction of ET-1 content. These results suggest that vasopressin increases vascular superoxide levels by stimulating ET-1 formation in mineralocorticoid hypertension, and that V1-vasopressin receptors play an important role in this process. Ϫ is produced in activated endothelial cells, 4 smooth muscle cells, 5 and adventitial fibroblasts. 6 Vascular dysfunction is manifested as impaired endothelium-dependent NO-mediated relaxation, 1-3 adhesion molecule expression, 7 low-density lipoprotein oxidation, 8 and cell proliferation. 9 However, the detailed mechanisms responsible for O 2 Ϫ production under different pathophysiological circumstances remain to be defined.We have recently shown that arterial endothelin-1 (ET-1) levels are elevated in deoxycorticosterone acetate (DOCA)-salt hypertension, 10 and that this resulted in increased O 2 Ϫ production 7,10 via ET A receptor activation 10 in this low-renin hypertension model. 11 However, the mechanisms contributing to increased ET-1 are unknown. The peptide hormone 8-argininevasopressin (AVP) is able to stimulate preproendothenlin-1 mRNA expression in arteries and cultured endothelial cells. [12][13][14] Furthermore, the enhanced endothelin gene expression observed in DOCA-salt rats was absent in vasopressin-deficient Brattleboro rats treated with DOCA-salt, 13 suggesting a functional link between vasopressin and ET-1 gene expression.The biological effects of vasopressin are mediated through 2 AVP receptor subtypes, the V 1 and V 2 receptors. 15-17 V 1 receptors mediate vasoconstriction, proliferation, ...

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“…There is evidence that vascular smooth muscle cells are also capable to produce endothelin [48,49]. Apart being a potent vasoconstrictor, ET-1 also exhibits hypertrophic, mitogenic and anti-apoptotic effects on vascular smooth muscle cells [50][51][52]. EТ-1 induces strong and prolonged contractile responses in vascular smooth muscle cells in different systems, with a special effect on the renal vascular bed [48,[53][54][55][56].…”

Section: Endothelinmentioning

confidence: 99%

Structure and Function of Smooth Muscle with Special Reference to Mast Cells

Vodenicharov¹

2012

Current Basic and Pathological Approaches to the Function of Muscle Cells and Tissues - From Molecules to Humans

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The control of endothelin-1 secretion

Cited by 46 publications

References 98 publications

Endothelin‐1 is secreted after total knee arthroplasty regardless of the use of a tourniquet

Endothelin‐1 is secreted after total knee arthroplasty regardless of the use of a tourniquet

Vasopressin Induces Vascular Superoxide Via Endothelin-1 in Mineralocorticoid Hypertension

Structure and Function of Smooth Muscle with Special Reference to Mast Cells

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