Plasma immunoreactive endothelin in essential hypertension

Kohno, Masakazu; Yasunari, Kenichi; Murakawa, Koh‐ichi; Yokokawa, Koji; Horio, Takeshi; Fukui, Toshiki; Takeda, Tadanao

doi:10.1016/0002-9343(90)90527-k

Cited by 291 publications

(113 citation statements)

References 22 publications

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“…In DOCA salt-sensitive models, bosentan, a nonselective receptor antagonist, was effective in lowering blood pressure. 10 In humans, early studies demonstrated an elevation in plasma ET-1 levels in hypertensive patients, 12 but a careful analysis of patient characteristics revealed that increased circulating levels were secondary to the impairment of renal clearance. 13 Schiffrin et al 14 reported increased PPET-1 expression in subcutaneous arteries of hypertensive patients, providing evidence of an upregulated ET system in a mainly white patient population.…”

Section: Discussionmentioning

confidence: 99%

“…First-strand cDNA synthesis was performed with 1 g total RNA and oligo(dT) [12][13][14][15][16][17][18] primers by using AMV reverse transcriptase (Promega). Polymerase chain reaction (PCR) was carried out in a reaction mixture containing 20 mmol/L Tris-HCl (pH 8.5), 50 mmol/L KCl, 1.5 mmol/L MgCl 2 , 0.2 mmol/L of each dNTP, 500 nmol/L of each sense and antisense primer, 3 L first-strand cDNA, and 2.5 U Taq DNA polymerase.…”

Section: Expression Studies By Reverse Transcription-pcrmentioning

confidence: 99%

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Saphenous Vein Endothelin System Expression and Activity in African American Patients

Grubbs

Anstadt

Ergul

2002

ATVB

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Objective-Plasma endothelin (ET)-1 levels are significantly higher in African American hypertensive patients than in white hypertensive patients. However, whether the molecular components of vascular ET-1 biosynthesis and function are altered in this population remains to be established. Accordingly, the overall goal of this study was to investigate the effects of race on vascular mRNA and protein levels of ET-converting enzyme (ECE)-1 subisoforms, ET-1, and ET receptor profiles in hypertension. Methods and Results-Saphenous vein samples were obtained from African American (nϭ13) and white (nϭ15) patients undergoing coronary artery grafting surgery. The expression of preproET-1 and of ECE-1a was upregulated Ϸ2-and 3-fold, respectively, in African Americans. In endothelium-intact vessels, the ET A expression was higher in whites. In endothelium-denuded vessels, the ET B mRNA was 3-fold higher in African Americans, suggesting that vasoconstriction-promoting ET B receptors are upregulated in this population. Vascular tissue ET-1 levels and ECE-1 activity were also augmented in African American patients. Conclusions-This study demonstrated that the biosynthetic pathway of ET-1 is activated to a higher degree and that the ET B receptor subtype expression is altered in the peripheral vasculature of African American hypertensive patients. The augmented synthesis and altered expression of ET B receptors may both contribute to the increased incidence of hypertension and related complications in this patient population. Key Words: endothelin-converting enzyme Ⅲ receptor subtype Ⅲ race Ⅲ hypertension Ⅲ gene expression T he prevalence of essential hypertension is significantly higher and the severity of cardiovascular complications is greater in the African American population than in whites. 1,2 These differences in the development and progression of hypertension in blacks have been proposed to be related to abnormal hemodynamic reactivity characterized by increased peripheral vascular resistance and diminished vasodilatation in response to environmental stress. 3 In a previous study, we found that plasma levels of the potent vasoconstrictor endothelin (ET)-1 were significantly higher in a black hypertensive group than in white hypertensive and white and black normotensive groups. 4 ET-1 acts locally in a paracrine/autocrine fashion and is predominantly secreted from the endothelial cells toward the underlying smooth muscle cells. 5 Local vascular ET-1 levels in this patient population remain unknown.The ET system consists of 3 major components: (1) ET-1, (2) ET-converting enzyme (ECE)-1, which is responsible for the biosynthesis of the active ET peptide, and (3) ET receptors, which mediate the biological effects of this peptide. Therefore, in addition to peptide levels, regulation of ECE-1 and regulation of ET receptor subtype expression in the vasculature in the setting of hypertension are equally critical. To date, there are 4 splice variants of ECE-1, with ECE-1a and ECE-1c being the most commonly expressed subisoforms...

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Section: Discussionmentioning

confidence: 99%

Section: Expression Studies By Reverse Transcription-pcrmentioning

confidence: 99%

Saphenous Vein Endothelin System Expression and Activity in African American Patients

Grubbs

Anstadt

Ergul

2002

ATVB

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“…54 Analogously, in patients with endothelinsecreting malignant haemoangioendotheliomas, removal of the tumour led to resolution of the hypertension. 79 Reports on plasma endothelin in essential hypertension have been controversial, with increased levels published by some, 80,81 but not all investigators. 82,83 It has now become evident that two reasons account for this apparent controversy.…”

Section: Endothelin and Hypertension In Humansmentioning

confidence: 99%

Participation of renal and circulating endothelin in salt-sensitive essential hypertension

Elijovich

Laffer

2002

J Hum Hypertens

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Salt sensitivity of blood pressure is a cardiovascular risk factor, independent of and in addition to hypertension. In essential hypertension, a conglomerate of clinical and biochemical characteristics defines a salt-sensitive phenotype. Despite extensive research on multiple natriuretic and antinatriuretic systems, there is no definitive answer yet about the major causes of salt-sensitivity, probably reflecting the complexity of saltbalance regulation. The endothelins, ubiquitous peptides first described as potent vasoconstrictors, also have vasodilator, natriuretic and antinatriuretic actions,

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“…"-" columns (C 18) for which extraction efficiency is frequently only 60-70% for free peptide [23]. Therefore, standardized extraction and assay procedures need to be established for a meaningful interpretation of ET-1 and big ET-1 plasma levels.…”

Section: 5mentioning

confidence: 99%

Binding of endothelin to plasma proteins and tissue receptors: effects on endothelin determination, vasoactivity, and tissue kinetics

Brünner

Stessel

Watzinger³

et al. 1995

FEBS Letters

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In vitro binding of (3-[lZSllTyr)-endothelin-1 ([12SllET-1) and -hig ET-1(1-38) ([~ZSlIhig ET-1) to plasma proteins of healthy humans, cardiac patients and normotensive and hypertensive rats was investigated by equilibrium dialysis. Binding of both tracers was similar in plasma from healthy humans, patients with congestive heart failure, and following myocardial infarction (-60%), and marginally higher in rat plasmas (~70%). Binding of [~ZSlIET-1 to human plasma could be explained by binding to human serum albumin. Endogenous plasma ET-1 levels were ~9 pg/ml in healthy humans, and ~ 12-16 pg/ml in cardiac patients; big ET-1 concentrations were approximately two-to threefold higher. ET-1 bound to plasma protein was partly lost in column extraction. In rat isolated perfnsed hearts, the coronary dilator and constrictor potency of exogenous free and albumin-bound ET-1 was similar, whereas the kinetics of endogenous ET-1 was impeded by tight binding to ET receptors. The data indicate that binding of ET-I to plasma proteins is without effect on peptide vasoactivity, but binding to tissue receptors greatly impedes its tissue kinetics.

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Plasma immunoreactive endothelin in essential hypertension

Cited by 291 publications

References 22 publications

Saphenous Vein Endothelin System Expression and Activity in African American Patients

Saphenous Vein Endothelin System Expression and Activity in African American Patients

Participation of renal and circulating endothelin in salt-sensitive essential hypertension

Binding of endothelin to plasma proteins and tissue receptors: effects on endothelin determination, vasoactivity, and tissue kinetics

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