Faculty Opinions recommendation of Neural peptidase endothelin-converting enzyme 1 regulates endothelin 1-induced pruritus.

Endothelin (ET-1) is a potent renal and systemic vasoconstrictor and sodium regulating peptide. Endothelin synthesis in the kidney have been reported in glomerulus endothelial, epithelial and mesangial cells as well as in inner medullary collecting duct. Factors stimulating the production of endothelin include shear stress, hypoxia, vasoactive agents and cytokines. Endothelin binding to ET-A receptor in vascular smooth muscle cells stimulates vasoconstriction.Renal graft rejection is a major problem after kidney transplantation with severe renal damage and renal vasoconstriction. We hypothesized that renal tissue level of endothelin-1, endothelin receptors and endothelin converting enzyme (ECE) may increase in renal tissue with rejection after kidney transplantation. Therefore, the current study was designed to determine the endothelin-1 and endothelin receptors (ET-A and ET-B) as well as endothelin converting enzyme level by immunohistochemical staining (IHCS) in human renal tissue with rejection after kidney transplantation.

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Expression of endothelin-1, ETA and ETB receptors, and ECE and distribution of endothelin-1 in failing rat heart

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1999.276.4.h1197 ◽

1999 ◽

Vol 276 (4) ◽

pp. H1197-H1206 ◽

Cited By ~ 21

Author(s):

Tsutomu Kobayashi ◽

Takashi Miyauchi ◽

Satoshi Sakai ◽

Masahiko Kobayashi ◽

Iwao Yamaguchi ◽

...

Keyword(s):

Positive Inotropic Effect ◽

Chronic Myocardial Infarction ◽

Converting Enzyme ◽

Endothelin 1 ◽

Protein Levels ◽

Failing Heart ◽

Precise Analysis ◽

Endothelin Converting Enzyme ◽

Peptide Level ◽

And Control

Endothelin (ET)-1 has a positive inotropic effect and induces hypertrophy in cardiomyocytes. We previously reported that the peptide level of ET-1 is increased in the failing heart of rats with chronic heart failure (CHF) and that treatment with an ETA-receptor antagonist greatly improves survival in rats with CHF. However, precise analysis for alteration of the myocardial ET system in the failing heart is not known. In this study, we used rats with CHF due to chronic myocardial infarction. Sham-operated rats served as a control. The results showed that the level of preproendothelin (preproET)-1 mRNA and the peptide level of ET-1 were markedly increased in the heart of rats with CHF, whereas the expression of endothelin-converting enzyme (ECE)-1 mRNA in the heart did not differ between CHF and control rats. The intensity of ET-1 staining (ET-1-like immunoreactivity) in cardiomyocytes was markedly stronger in rats with CHF than in control rats, and the fibrotic tissues of the infarcted area were not stained. The mRNA and protein levels of both ETA and ETB receptors in the heart were significantly higher in rats with CHF than in control rats. The present study suggests that the increase in ET-1 peptide level in the heart of the rats with CHF originated from upregulation of preproET-1 mRNA, which was not attendant with the alteration of ECE-1 mRNA expression, and that both the ETA- and ETB-receptor systems are greatly accelerated in the failing heart.

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