Endothelin-1-Like Immunoreactivity in Human Urine

Ando, Kenji; Hirata, Yukio; Takei, Yoshio; Kawakami, M; Marumo, Fumiaki

doi:10.1159/000186212

Cited by 52 publications

(21 citation statements)

References 8 publications

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“…The minimum detectable quantity in the present ET-1 RIA was 0.3 pg/tube, and the 50% intercept was 9 pg/ tube. The antibody was specific for ET-1 because it crossreacted 100% with ET-1, but less than 0.01 % with ET-2 and ET-3, and 1 % with human big ET-1 and porcine big ET-1, respectively, on a molar basis (16). The intra-and interassay coefficients of variance were both less than 10%.…”

Section: Methodsmentioning

confidence: 96%

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Plasma Immunoreactive Endothelin-1 Concentration in Human Fetal Blood: Its Relation to Asphyxia

et al. 1991

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ABSTRACT. To elucidate the effects of birth stress on immunoreactive endothelin-1 (irET-1) concentrations in fetal blood, we determined irET-1 levels in cord plasma in different modes of delivery associated with or without complications such as asphyxia. The irET-1 concentrations in both the umbilical artery and vein were significantly higher than those found in maternal venous blood at delivery, although there was no significant difference between preterm and full-term infants. When plasma irET-1 concentrations of healthy infants born by vaginal delivery and by cesarean section without labor were compared, the former had significantly ( p < 0.05) higher levels than the latter (15.4 f 4.9 pg/mL versus 11.1 f 3.1 pg/mL). Furthermore, umbilical venous plasma obtained from vaginally delivered infants complicated by asphyxia showed significantly ( p < 0.001) higher irET-1 levels (28.2 f 9.4 pg/ mL) than those of nonasphyxiated infants (14.2 f 4.5 pg/ mL). These data suggest that birth stress, especially asphyxia, may contribute to the increase in fetal circulating irET-1 levels. (Pediatr Res 30: 244-247, 1991) Abbreviations CPK, creatine phosphokinase ET-1, endothelin-1 GOT, aspartate aminotransferase irET-1, immunoreactive ET-1 LDH, lactic acid dehydrogenase TFA, trifluoroacetic acid Endothelin-1 is a potent vasoconstrictor peptide with 2 1 amino acid residues, originally isolated and sequenced from the supernatant of cultured porcine aortic endothelial cells, and the first member of the mammalian endothelin family (1-4). Since ET-1 produces very potent vasoconstriction and an extremely longlasting pressor response, ET-1 may play an important role in the control of blood pressure and/or local blood flow (1, 3, 4). Recently, low concentrations of ET-1 have been detected in plasma from healthy subjects (5-7). Raised plasma concentrations of ET-1 have been observed in certain pathophysiologic conditions, such as uremia (8), acute renal failure (9), acute

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Section: Methodsmentioning

confidence: 96%

“…ET-1 RIA was performed essentially in the same manner as reported (5) using a new polyclonal antibody specific for ET-1 (16). Samples were reconstituted with the assay buffer (50 mM phosphate buffer, pH 6.8, containing 0.9% NaCl, 1 mM EDTA, 0.005% Triton X-100,0.05% NaN3 and 0.3% bovine yglobulin).…”

Section: Methodsmentioning

confidence: 99%

Plasma Immunoreactive Endothelin-1 Concentration in Human Fetal Blood: Its Relation to Asphyxia

et al. 1991

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“…Endothelin probably acts primarily in a paracrine fashion, especially in the vasculature, but also has been shown to circulate in blood 16 and to be excreted in urine. 17 A hormonal function for ET-1 is therefore a possibility as significantly altered circulating concentrations of endothelin have been reported in both clinical 18 and experimental 19 hypertension. Furthermore, two patients with an endothelin-secreting hemangioendothelioma exhibited hypertension in association with increased circulating concentrations of endothelin 20 ; blood pressure and plasma endothelin concentrations both fell after excision of the rumor.…”

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confidence: 99%

Salt-dependency of endothelin-induced, chronic hypertension in conscious rats.

Mortensen

Fink

1992

Hypertension

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The effect of salt intake on the hypertensive response to long-term infusion of endothelin-1 was investigated. Chronically instrumented male Sprague-Dawley rats (325-375 g) were used in a 15-day protocol that included 3 control days followed by 7 days of endothelin-1 infusion at 5.0 pmol • kg" 1 • min" 1 and 5 days of recovery. Rats were maintained on either a normal sodium chloride intake (2.0 meq Na + per day; normal sodium) or a high sodium chloride Intake (6.0 meq Na + per day; high sodium) throughout the protocol. Control rats received normal or high sodium intakes but not endothelin-1. In high-sodium rats, endothelin-1 produced a significant increase in mean arterial pressure and total peripheral resistance; a significant bradycardia was observed only on the first day after the start of the endothelin-1 infusion. Cardiac output, stroke volume, water balance, and urinary sodium and potassium excretion remained unchanged. Termination of endothelin-1 infusion resulted in rapid normalization of both arterial pressure and peripheral resistance. In contrast, normal sodium rats exhibited no alteration in mean arterial pressure, heart rate, total peripheral resistance, stroke volume, water balance, or urinary sodium and potassium excretion throughout the endothelin-1 infusion protocol. The hypertension produced by endothelin-1 infusion cannot be explained by alterations in salt or water balance since endothelin-1 infusion in high sodium animals produced significant increases in mean arterial pressure with no observable changes in water or electrolyte balance. These results indicate that endothelin-induced hypertension in conscious rats is a salt-dependent model of hypertension. Since the isolation of ET-1 by Yanagisawa et al 1 in 1988, this 21-amino acid peptide has been shown to have both relaxing and constricting effects on vascular smooth muscle via the release of relaxing factors such as prostacyclin, 2 atrial natriuretic factor, 3 and endotheliumderived relaxing factor 2 and via the mobilization of intracellular and extracellular calcium, 4 respectively. Substantial data also exist that describe ET-1 as a constrictor of nonvascular smooth muscle, 3 a secretagogue for the release of other hormones and circulating factors such as aldosterone 67 and adrenocorticotropic hormone, 8 a suppressant of the antidiuretic action of arginine vasopressin (AVP) in the kidney, 9 a modulator of adrenergic neuroeffector transmission, 10 a potent mitogen of vascular smooth muscle cells, 11 and a regulator of neuronal activity in specific brain regions. 12In agreement with these observations, autoradiographical studies using iodine-125-labeled ET-1 have revealed that this peptide has specific high affinity binding sites within the cardiovascular system (including cardiac tissue as well as the vascularure), 13 areas within and outside of the blood-brain barrier), 1314 and the spinal cord.15 These data and others suggest that ET-1 may be involved in numerous and diverse physiological processes. However, a role for ET-1 in blo...

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“…Urine samples were examined by RIA (Kitasato Biochemical Laboratories). R1A for ET-I was per formed essentially in the same manner as described by Ando [5] using a new polyclonal rabbit antibody specific for ET-I. The separation of bound from free ligands was performed by the double-antibody/polvethylene glycol method [5], Urinary NAG, (T-MG and Alb were determined by calorimetric analysis.…”

Section: Methodsmentioning

confidence: 99%

Value of Urinary Endothelin-1 in Patients with Primary Vesicoureteral Reflux

Komeyama

Takeda

Katayama

et al. 1993

Nephron

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By using a radioimmunoassay specific for endothelin-1 (ET-1), we measured urinary excretion of ET-1-like immunoreactivity (LI) in 63 spot urine samples of 48 patients with primary vesicoureteral reflux (VUR). And also, urinary excretion of N-acetyl-β-D-glucosaminidase (NAG), β₂-microglobulin (β₂-MG), microalbumin (Alb) and creatinine (Cr) were measured. There was no significant correlation in any of the pairs ET-1 and NAG, ET-1 and β₂-MG, and ET-1 and Alb. Comparing the grade of reflux according to the International Classification with urinary ET-1, urinary ET-l/Cr levels in patients with grade 2, 3 and 4 VUR were higher than normal, and the ratio of more than normal urinary ET-l/Cr increased in proportion to the grade of reflux, but it conversely decreased in grade 5. In conclusion, urinary ET-1 maybe an indicator of renal tubular injury in patients with primary VUR, and its meaning may be different from conventional urinary parameters.

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Endothelin-1-Like Immunoreactivity in Human Urine

Cited by 52 publications

References 8 publications

Plasma Immunoreactive Endothelin-1 Concentration in Human Fetal Blood: Its Relation to Asphyxia

Plasma Immunoreactive Endothelin-1 Concentration in Human Fetal Blood: Its Relation to Asphyxia

Salt-dependency of endothelin-induced, chronic hypertension in conscious rats.

Value of Urinary Endothelin-1 in Patients with Primary Vesicoureteral Reflux

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