Different Mobilization of Calcium in Endothelin-1 -Induced Contractions in Human Arteries and Veins: Effects of Calcium Antagonists

Yang, Z.; Bauer, Erwin; Segesser, L. von; Stulz, P; Turina, M; Tf, Lüscher

doi:10.1097/00005344-199010000-00019

Cited by 75 publications

(31 citation statements)

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“…In the present study, pretreatment with the therapeutic concentrations of nifedipine (20-200 nM) only reduced the ET-1-induced contraction to 97.07-65.3% compared with the control. However, our results disagree with previous observations that Ca2+ antagonists do not prevent ET-1-induced contractions [49]. In our study, at high concentration (30 gIM), nifedipine significantly reduced the contraction to about 50% (P < 0.001, Figure 5).…”

Section: Discussioncontrasting

confidence: 99%

Interaction between endothelin and vasodilators in the human internal mammary artery.

He¹,

Yang²,

Mack³

et al. 1994

Brit J Clinical Pharma

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1. The internal mammary artery (IMA) is the primary choice as an arterial graft for coronary artery bypass surgery. Endothelin (ET) has been recently measured with an increased release after cardiopulmonary bypass for coronary artery bypass grafting. Threshold concentrations of ET‐1 have been found to amplify specifically contractions induced by noradrenaline and serotonin. This study was designed to investigate the effect of glyceryl trinitrate (GTN) and calcium antagonists on ET‐1 contraction in the human IMA. 2. Human IMA segments taken from 21 patients undergoing IMA‐coronary artery bypass grafting were mounted in an organ bath under the physiological pressure determined from their own length‐tension curves. Four ring segments were allocated into four groups. One served as a control and the others were treated with GTN (10, 100 nM, or 30 microM) for 5 min or nifedipine (20 or 200 nM, or 30 microM) for 25 min before concentration‐contraction curves to ET‐1 were established. In separate experiments, the concentration‐relaxation curves to GTN or nifedipine were established in the IMA rings precontracted with ET‐1 (10 nM). 3. Pretreatment of IMA with GTN for 5 min did not alter the ET‐1‐induced contraction. Pretreatment with 20 or 200 nM of nifedipine slightly but not significantly, altered the maximum contraction induced by ET‐1. Higher concentrations (30 microM) significantly reduced the maximum contraction force (P = 0.008). On the other hand, GTN caused 76.44 +/‐ 6.35% relaxation in ET‐1‐precontracted IMA. In contrast, the nifedipine‐induced relaxation was difficult to establish due to unsustained contraction to ET‐1.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussioncontrasting

confidence: 99%

Interaction between endothelin and vasodilators in the human internal mammary artery.

He¹,

Yang²,

Mack³

et al. 1994

Brit J Clinical Pharma

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“…Second, the precise mechanism of action of endothelin in vascular muscle is not clear but appears to involve a component sensitive to blockade of voltageoperated Ca2+ channels36,37 as well as a nonsensitive component.8'13'34'37 The nonblockable component is associated with an increase of intracellular free cytosolic calcium due to phospholipase C activation and generation of inositol trisphosphate (IP3)12,37-39 and possibly also to direct activation of protein kinase C. 40 The resulting membrane depolarization then appears to activate voltage-operated, calcium antagonist blockable L-type Ca2+ channels, leading to sustained contractions.37 '41 In addition, in certain vascular preparations such as the porcine coronary artery, endothelin may interact with the Ca2+ channel complex through a transducer macromolecule such as the membrane guanosine trisphosphate-binding proteins. 36 It has also been shown that the development of vascular tone depends more on calcium influx through slow Ca2+ channels in small than in large arteries.42 Even though the initiation of the cascade of events leading to sustained vasoconstriction may not be related to activation of voltageoperated Ca21 channels, it is therefore conceivable that the marked dependence of vascular tone on the activity of voltage-operated Ca2+ channels may account for the abolition of sustained endothelininduced vasoconstriction in resistance vessels.…”

Section: Discussionmentioning

confidence: 99%

Endothelin-1-induced vasoconstriction in humans. Reversal by calcium channel blockade but not by nitrovasodilators or endothelium-derived relaxing factor.

et al. 1991

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The vascular effects of endothelin-1 (ET) in humans were investigated by brachial artery infusions of ET into 25 healthy volunteers. Forearm blood flow increased from a mean±SD value of 2.3± 1.5 to 2.5± 1.5 ml/min/100 ml forearm tissue (n=25, p<0.05) in response to low dose (0.5 ng/min/100 ml forearm tissue) ET infusion and decreased to 1.78±1.3 and 1.1±0.9 ml/min/100 ml forearm tissue (p<0.001) during higher dosages (25 and 50 ng/min/100 ml forearm tissue). Sodium nitroprusside (0.6 ,g/min/100 ml forearm tissue, n=6), acetylcholine (16 ,g/min/100 ml forearm tissue, n=7), nifedipine (6 pg/min/100 ml forearm tissue, n=6), and verapamil (80 ,ug/min/100 ml forearm tissue, n=6) were infused alone and in combination with ET ity in supernatants from cultured endothelial cells.4 Endothelin is a 21-amino-acid polypeptide that has been isolated from supernatants of cultured porcine endothelial cells.5 Endothelial cells produce and release endothelin-1 (formerly human or porcine endothelin),6 which has potent and long-lasting vasoconstrictor activity in vivo and in vitro.7-10 The peptide produces sustained increases of blood pressure in rats pretreated with atropine, propranolol, and bunazosin,5 but systemic vasodilation and a decrease of blood pressure have also been described after left atrial injection of endothelin-1 into cats.1'The precise cellular mechanism of action of endothelin-1 is not known, and differing results have been obtained with respect to the reversibility of endothelin-1-induced vasoconstriction. The contention that endothelin-1 may act as an endogenous Ca21 channel agonist5 has been disputed based on observations that endothelin-1-induced vasoconstriction is not

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“…146,147 This explains why ET-1-induced vasoconstriction is reversed by calcium channel blockers. [148][149][150][151] ET-1 rather acts in a paracrine than an endocrine mode of action, which is reflected by plasma levels of ET-1 in the picomolar range. 152,153 Infusion of an ET receptor antagonist into the brachial artery or systemically in healthy humans leads to vasodilation indicating a role of ET-1 in the maintenance of basal vascular tone.…”

Section: Endothelinmentioning

confidence: 99%

“…Additionally, ET-1 may also exert effects on the central and autonomic nervous system and alter baroreflex function. 148,149,[156][157][158][159][160][161][162][163][164][165] In the kidney, sodium reabsorption is modulated. 166 …”

Section: Endothelinmentioning

confidence: 99%

Working under pressure: the vascular endothelium in arterial hypertension

et al. 2000

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The vascular endothelium synthesizes and releases a spectrum of vasoactive substances like nitric oxide (NO) and endothelin (ET). In hypertension, the delicate balance of endothelium-derived factors is disturbed. ET acts as the natural counterpart to endothelium-derived NO, which exerts vasodilating, antithrombotic, and antiproliferative effects, and inhibits leukocyte-adhesion to the vascular wall. Besides its blood pressure rising effect also in man, ET induces vascular and myocardial hypertrophy, which are independent risk factors for cardiovascular morbidity and mortality. The derangement of endothelial function in hypertension is likely to be caused in part by genetic factors, but also due to elevated blood pressure itself. Due to its position between blood pressure and smooth muscle cells responsible for peripheral resistance, the endothelium is thought to be both target and mediator of arterial hypertension. Oxi-

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Different Mobilization of Calcium in Endothelin-1 -Induced Contractions in Human Arteries and Veins: Effects of Calcium Antagonists

Cited by 75 publications

References 0 publications

Interaction between endothelin and vasodilators in the human internal mammary artery.

Interaction between endothelin and vasodilators in the human internal mammary artery.

Endothelin-1-induced vasoconstriction in humans. Reversal by calcium channel blockade but not by nitrovasodilators or endothelium-derived relaxing factor.

Working under pressure: the vascular endothelium in arterial hypertension

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