Effect of endothelin-1 in man.

@article{Vierhapper1990EffectOE,
  title={Effect of endothelin-1 in man.},
  author={Heinrich Vierhapper and Oswald Wagner and Peter J. Nowotny and Werner Waldh{\"a}usl},
  journal={Circulation},
  year={1990},
  volume={81 4},
  pages={
          1415-8
        }
}
The effect of an intravenous infusion of human endothelin-1 on blood pressure and plasma concentrations of endothelin-1, potassium, sodium, renin, aldosterone, and atrial natriuretic factor was investigated in six healthy, sodium-loaded men. During the peptide's exogenous application (1.0, 2.5, and 5.0 ng/kg.min), its plasma concentrations rose from a basal value of 1.2 +/- 0.3 to 3.2 +/- 1.9, 9.9 +/- 7.6, and 56.5 +/- 50.3 pmol/l (p less than 0.01), respectively, and mean blood pressure rose… 
Effects of endothelin-1 on renal function in humans: implications for physiology and pathophysiology.
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According to this study, endothelin-1 participates in volume homeostasis in human, whereas pathophysiological concentrations can contribute to renal vasoconstriction and sodium retention, and calcium channel blockers may protect against these effects of endothelins-1.
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TLDR
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Effectiveness of enalapril versus nifedipine to antagonize blood pressure and the renal response to endothelin in humans.
TLDR
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Administration of Endothelin-1 in Humans
TLDR
The hemodynamic findings in this study are of major interest, though difficult to interpret, and the authors do not appear to have attempted to eliminate any observer bias in this unblinded study by use of a random-zero or semiautomated sphygmomanometer.
Endothelin-1-induced vasoconstriction in humans. Reversal by calcium channel blockade but not by nitrovasodilators or endothelium-derived relaxing factor.
TLDR
In human resistance vessels, blockade of voltage-operated Ca2+ channels but not cyclic GMP-dependent vasodilation may be an effective tool to inhibit ET-induced vasoconstriction and unmask the vasodilator effect of high ET dosages.
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TLDR
It is shown that systemic and renal vasoconstriction due to L-NAME are attenuated by BQ, which suggests that an interaction between endogenous nitric oxide production and endothelin-A receptor (ET-A) blocker BQ-123 activity participates in the maintenance of baseline systemic and kidney vascular tone in humans.
Cardiovascular and Endocrine Effects of Endothelin‐1 at Pathophysiological and Pharmacological Plasma Concentrations in Conscious Dogs
TLDR
The biphasic response of heart rate is consistent with baroreflex-mediated effects resulting from vasodilation at the pathophysiological level and vasoconstriction at the pharmacological level, and Hemodynamic data suggest an increase followed by a decrease in contractlllty at both levels, respectlvely.
Modulation of Endothelin Effects on Blood Pressure and Hematocrit by Atrial Natriuretic Peptide
TLDR
The increase in plasma immunoreactive ANP concentration resulting from endothelin infusion mediates the increase in hematocrit through an increase in vascular permeability to whole plasma, suggesting that ANP may modulate the vasoconstrictor actions of endothelins in vivo.
Effects of low-dose heparin infusion on arterial endothelin-1 release in humans.
TLDR
It is shown that it is possible to decrease ET-1 levels by use of low-dose heparin infusion in humans and this effect seems mediated by a simultaneous increase in nitric oxide levels and is completely reversed by a mild increase in insulin concentrations.
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TLDR
It is clear that this peptide is capable of causing profound cardiovascular, renal, and endocrine alterations in conscious dogs and the possible relevance of these observations to physiological processes and to pathological conditions such as hypertension remains to be established.
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TLDR
The results clearly indicate that the elimination ofET-1 from circulating blood and the ET-1-induced pressor response are not in parallel, and the relatively rapid disappearance of ET- 1 from the bloodstream is mostly due to the removal of the peptide by the parenchymal tissues, in the anesthetized rat.
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It is of clinical interest that natriuresis without diuresis can be induced by the simultaneous administration of hANP and dDAVP.
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Together, the results indicate a high density of ET-1 binding sites in the lung, liver, and kidney and that these organs may be important in removing circulating ET- 1, suggesting a role in cardiovascular regulation.
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TLDR
An assay to determine renin concentration (RC) has been developed which allows quantitation on a scale of Goldblatt units (G.U.) and provides a way of comparing results from various laboratories and avoids the interference of pseudorenin.
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TLDR
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