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Juerg Nussberger - One of the best experts on this subject based on the ideXlab platform.

  • Volume expansion enhances plasma Endothelin-1.
    American Journal of Hypertension, 2003
    Co-Authors: Saad Abdel-sayed, Hans R. Brunner, Juerg Nussberger
    Abstract:

    We hypothesized that acute volume expansion by saline infusion triggers the release of Endothelin-1. Bolus intravenous saline infusion (8 mL/min) in six groups of conscious Wistar rats and spontaneously hypertensive rats did not change mean arterial pressure or heart rate (n = 8 to 12). At 1 min after infusion, the plasma Endothelin-1 level was significantly increased in Wistar rats and in spontaneously hypertensive rats by 42% and 61%, respectively (unpaired data). In 12 Wistar rats, the Endothelin-1 level increased from 0.68 ± 0.13 to 1.19 ± 0.17 fmol/mL (mean ± SEM, P < .0001, paired data). Thus, acute volume load by rapid saline infusion increases plasma Endothelin-1 levels. Vasoconstriction induced by Endothelin-1 may counteract enhanced circumferential stretch created by volume expansion.

  • Volume expansion enhances plasma Endothelin-1.
    American journal of hypertension, 2003
    Co-Authors: Saad Abdel-sayed, Hans R. Brunner, Juerg Nussberger
    Abstract:

    We hypothesized that acute volume expansion by saline infusion triggers the release of Endothelin-1. Bolus intravenous saline infusion (8 mL/min) in six groups of conscious Wistar rats and spontaneously hypertensive rats did not change mean arterial pressure or heart rate (n = 8 to 12). At 1 min after infusion, the plasma Endothelin-1 level was significantly increased in Wistar rats and in spontaneously hypertensive rats by 42% and 61%, respectively (unpaired data). In 12 Wistar rats, the Endothelin-1 level increased from 0.68 +/- 0.13 to 1.19 +/- 0.17 fmol/mL (mean +/- SEM, P

Saad Abdel-sayed - One of the best experts on this subject based on the ideXlab platform.

  • Volume expansion enhances plasma Endothelin-1.
    American Journal of Hypertension, 2003
    Co-Authors: Saad Abdel-sayed, Hans R. Brunner, Juerg Nussberger
    Abstract:

    We hypothesized that acute volume expansion by saline infusion triggers the release of Endothelin-1. Bolus intravenous saline infusion (8 mL/min) in six groups of conscious Wistar rats and spontaneously hypertensive rats did not change mean arterial pressure or heart rate (n = 8 to 12). At 1 min after infusion, the plasma Endothelin-1 level was significantly increased in Wistar rats and in spontaneously hypertensive rats by 42% and 61%, respectively (unpaired data). In 12 Wistar rats, the Endothelin-1 level increased from 0.68 ± 0.13 to 1.19 ± 0.17 fmol/mL (mean ± SEM, P < .0001, paired data). Thus, acute volume load by rapid saline infusion increases plasma Endothelin-1 levels. Vasoconstriction induced by Endothelin-1 may counteract enhanced circumferential stretch created by volume expansion.

  • Volume expansion enhances plasma Endothelin-1.
    American journal of hypertension, 2003
    Co-Authors: Saad Abdel-sayed, Hans R. Brunner, Juerg Nussberger
    Abstract:

    We hypothesized that acute volume expansion by saline infusion triggers the release of Endothelin-1. Bolus intravenous saline infusion (8 mL/min) in six groups of conscious Wistar rats and spontaneously hypertensive rats did not change mean arterial pressure or heart rate (n = 8 to 12). At 1 min after infusion, the plasma Endothelin-1 level was significantly increased in Wistar rats and in spontaneously hypertensive rats by 42% and 61%, respectively (unpaired data). In 12 Wistar rats, the Endothelin-1 level increased from 0.68 +/- 0.13 to 1.19 +/- 0.17 fmol/mL (mean +/- SEM, P

David J. Webb - One of the best experts on this subject based on the ideXlab platform.

  • Endothelin-1[1-31] is not elevated in men with chronic heart failure.
    Journal of Cardiovascular Pharmacology, 2004
    Co-Authors: Stephen J. Leslie, Neil R. Johnston, Fiona E. Strachan, Alan Bagnall, Gillian A. Gray, Martin A. Denvir, David E Newby, David J. Webb
    Abstract:

    Endothelin-1 [ 1 - 3 1 ] is a recently discovered member of the Endothelin family with vasoactive properties in several animal models and in man in vivo. It is generated from big Endothelin-1 by human mast cell chymase and may be a novel intermediary peptide in the production of Endothelin-1 { 1 - 2 1 } . Given that both big Endothelin-1 [ 1 - 3 8 ] and chymase activity are increased in chronic heart failure, the aim of this study was to determine whether plasma Endothelin-1 [ 1 - 3 1 ] concentrations are elevated in patients with chronic heart failure. Plasma Endothelin-1 [ 1 - 3 1 ] concentrations were measured by enzyme-linked immunosorbent assay in nine patients with chronic heart failure, and nine age- and sex-matched control subjects. Consistent with previous studies, plasma concentrations of big Endothelin-1 [ 1 - 3 8 ] were elevated in patients compared with controls (17.1 ′ 4.4 pg/mL vs 8.9 ′ 3.4 pg/mL, P = 0.002), although there were no differences in plasma Endothelin-1 [ 1 - 2 1 ] (3.3 ′ 0.4 pg/mL vs 3.4 ′ 0.7 pg/mL, P=0.7) or Endothelin-1 [ 1 - 3 1 ] (both 1.1 ′ 0.1 pg/mL, P=0.2) concentrations. We have demonstrated that patients with chronic heart failure have normal plasma Endothelin-1 [ 1 - 3 1 ] concentrations. This suggests that, in contrast to big Endothelin-1 [ 1 - 3 8 ] , plasma Endothelin-1 [ 1 - 3 1 ] is unlikely to be a useful prognostic marker in patients with chronic heart failure.

  • An investigation into the direct and indirect venoconstrictor effects of Endothelin‐1 and big Endothelin‐1 in man.
    British Journal of Clinical Pharmacology, 1995
    Co-Authors: William G Haynes, S Moffat, David J. Webb
    Abstract:

    1. Endothelin-1 is a potent endothelium-derived vasoconstrictor peptide that is generated through cleavage of its precursor big Endothelin-1 by 'Endothelin converting enzyme' (ECE) in resistance vessels, including those of the forearm vascular bed. In some animal tissues, but not in resistance vessels of healthy human subjects, Endothelin-1 appears to potentiate the actions of the sympathetic nervous system. We examined whether ECE activity is present in human hand veins and whether Endothelin-1 or big Endothelin-1 potentiate sympathetically mediated venoconstriction. 2. Six healthy subjects received dorsal hand vein infusion of local, non-systemic doses of Endothelin-1 (5 pmol min-1), big Endothelin-1 (50 pmol min-1) and, as a control, sodium chloride (0.9%; w/v) for 90 min. Vein diameter was measured using the Aellig displacement technique. Sympathetically mediated venoconstriction was elicited using the single deep breath reflex. 3. Endothelin-1 caused a progressive decrease in hand vein diameter, by 49% at 90 min (95% confidence intervals [CI]: -68 to -30%; P = 0.0001). Vein diameter did not change significantly after 90 min infusion of big Endothelin-1 (+3%; CI: -11 to +17%; P = 0.0007 vs Endothelin-1; P = 0.40 vs baseline) or sodium chloride (+2%; CI: -12 to +16%; P = 0.0002 vs Endothelin-1; P = 0.60 vs baseline). Venoconstriction to deep breath was not potentiated by Endothelin-1. 4. These results suggest that, in contrast to the situation in forearm resistance vessels, there is little or no local ECE activity in human hand veins and that Endothelin does not potentiate sympathetic responses in these cutaneous capacitance vessels.

  • venoconstriction to Endothelin 1 in humans role of calcium and potassium channels
    American Journal of Physiology-heart and Circulatory Physiology, 1993
    Co-Authors: William G Haynes, David J. Webb
    Abstract:

    : Recent studies in vitro have suggested that there may be an interaction between Endothelin-1 and ATP-sensitive K+ channels in vascular smooth muscle. Here we have investigated whether agents acting on membrane Ca2+ and K+ channels modulate Endothelin-1-induced venoconstriction in vivo in human subjects. In a series of studies, six healthy subjects received, on separate occasions, local infusions into dorsal hand veins of Endothelin-1 coinfused with 1) the ATP-sensitive K+ channel opener, cromakalim; 2) the dihydropyridine Ca2+ antagonist, nicardipine; 3) a control vasodilator, hydralazine; and 4) saline placebo. Endothelin-1 caused local venoconstriction with a maximum reduction in vein size of 66 +/- 4% at 60 min (P = 0.0001 vs. basal). Cromakalim prevented Endothelin-1-induced venoconstriction (9 +/- 10% maximum constriction; P = 0.68 vs. basal). By contrast, nicardipine, in a dose sufficient to block depolarization-induced constriction caused by K+ infusion, had only a partial effect on Endothelin-1-induced venoconstriction (35 +/- 8% maximum constriction; P = 0.001 vs. basal; P = 0.02 vs. Endothelin-1), whereas a 10-fold higher dose of nicardipine had no additional effect and hydralazine had no effect. In further studies, cromakalim, but not nicardipine, reversed Endothelin-1-induced venoconstriction. Cromakalim did not prevent constriction induced by norepinephrine. Although calcium entry through dihydropyridine-sensitive Ca2+ channels may account in part for the vasoconstrictor action of Endothelin-1 in humans, the abolition of Endothelin-1 responses by a K+ channel opener suggests additional mechanisms of action for Endothelin-1.

  • ENDOTHELIUM-DEPENDENT MODULATION OF RESPONSES TO Endothelin-1 IN HUMAN VEINS
    Clinical Science, 1993
    Co-Authors: William G Haynes, David J. Webb
    Abstract:

    1. We have investigated whether local vascular production of nitric oxide or prostacyclin regulates venoconstriction induced by the endothelium-derived peptide, Endothelin-1, in vivo in man. 2. Six healthy subjects received local dorsal hand vein infusion of Endothelin-1 for 60 min alone or, on two separate occasions, co-infused with the donator of nitric oxide, glyceryl trinitrate, or the vasodilator prostaglandin, prostacyclin. In further studies, Endothelin-l was co-infused with an inhibitor of nitric oxide production, N G -monomethyl-L-arginine, or after oral administration of the irreversible inhibitor of prostaglandin production, acetylsalicylic acid (aspirin). 3. At a low dose (5 pmol/min), Endothelin-1 alone caused slowly developing and long-lasting venoconstriction (maximal constriction: 66 ± 4%). Although glyceryl trinitrate partially prevented Endothelin-1-induced venoconstriction (maximum: 33 ± 5%), inhibition of nitric oxide production did not affect Endothelin-1-induced venoconstriction (maximum: 55 ± 4%). 4. Prostacyclin was more effective at blocking the venoconstriction in response to Endothelin-1 than glyceryl trinitrate (maximum: 12 ± 3%), and there was substantial potentiation of Endothelin-1-induced venoconstriction after pretreatment with aspirin (maximum: 90 ± 3%). 5. Despite the capacity of nitric oxide to attenuate responses to Endothelin-1, N G -monomethyl-L-arginine did not potentiate Endothelin-1-induced venoconstriction, suggesting little or no stimulated production of nitric oxide in human veins. However, the potentiation of responses to Endothelin-1 by aspirin indicates that endothelial production of prostacyclin attenuates responses to Endothelin-1 in human veins in vivo.

Maki Kuwahara - One of the best experts on this subject based on the ideXlab platform.

  • Pericardial mesothelial cells produce Endothelin-1 and possess functional Endothelin ETB receptors.
    European Journal of Pharmacology, 1998
    Co-Authors: Masayoshi Kuwahara, Maki Kuwahara
    Abstract:

    We investigated the Endothelin production and Endothelin receptor activity of pericardial mesothelial cells obtained from spontaneously hypertensive rats (SHR) and Wistar–Kyoto (WKY) rats. The pericardial mesothelial cells were maintained in vitro and the production of Endothelin-1 by these cells was evaluated by using a sensitive sandwich-type enzyme immunoassay for Endothelin-1 and big Endothelin-1. Endothelin receptor subtypes were pharmacologically analyzed by measuring the changes of intracellular Ca2+ concentration ([Ca2+]i) in pericardial mesothelial cells. Mesothelial cells from both strains produced more immunoreactive Endothelin-1 than big Endothelin-1. The production of immunoreactive Endothelin-1 progressively increased in a culture time-dependent manner. The amount of immunoreactive Endothelin-1 detected after 72 h in pericardial mesothelial cells of SHR was significantly (P

  • Production of Endothelin-1 and big-Endothelin-1 by pleural mesothelial cells.
    FEBS Letters, 1992
    Co-Authors: Masayoshi Kuwahara, Maki Kuwahara, Nobuhiro Suzuki
    Abstract:

    Immunoreactive Endothelin-1 (ET-1) and big-Endothelin-1 (big-ET-1) were detected in conditioned medium of cultured rat pleural mesothelial cells by using sensitive sandwich-type enzyme immunoassays. The amount of both ET-1 and big-ET-1 increased time-dependently. In both instances, maximal amount was detectable in conditioned medium obtained after 72 h in culture (ET-1: 117.1 ± 30.1 pg/106 cells; big-ET-1: 2.4 ± 2.1 pg/106 cells). Fetal calf serum markedly stimulated the production of both ET-1 and big-ET-1.

Hans R. Brunner - One of the best experts on this subject based on the ideXlab platform.

  • Volume expansion enhances plasma Endothelin-1.
    American Journal of Hypertension, 2003
    Co-Authors: Saad Abdel-sayed, Hans R. Brunner, Juerg Nussberger
    Abstract:

    We hypothesized that acute volume expansion by saline infusion triggers the release of Endothelin-1. Bolus intravenous saline infusion (8 mL/min) in six groups of conscious Wistar rats and spontaneously hypertensive rats did not change mean arterial pressure or heart rate (n = 8 to 12). At 1 min after infusion, the plasma Endothelin-1 level was significantly increased in Wistar rats and in spontaneously hypertensive rats by 42% and 61%, respectively (unpaired data). In 12 Wistar rats, the Endothelin-1 level increased from 0.68 ± 0.13 to 1.19 ± 0.17 fmol/mL (mean ± SEM, P < .0001, paired data). Thus, acute volume load by rapid saline infusion increases plasma Endothelin-1 levels. Vasoconstriction induced by Endothelin-1 may counteract enhanced circumferential stretch created by volume expansion.

  • Volume expansion enhances plasma Endothelin-1.
    American journal of hypertension, 2003
    Co-Authors: Saad Abdel-sayed, Hans R. Brunner, Juerg Nussberger
    Abstract:

    We hypothesized that acute volume expansion by saline infusion triggers the release of Endothelin-1. Bolus intravenous saline infusion (8 mL/min) in six groups of conscious Wistar rats and spontaneously hypertensive rats did not change mean arterial pressure or heart rate (n = 8 to 12). At 1 min after infusion, the plasma Endothelin-1 level was significantly increased in Wistar rats and in spontaneously hypertensive rats by 42% and 61%, respectively (unpaired data). In 12 Wistar rats, the Endothelin-1 level increased from 0.68 +/- 0.13 to 1.19 +/- 0.17 fmol/mL (mean +/- SEM, P