The Possible Role of Endothelin-1 in the Pathogenesis of Coronary Vasospasm

Kurihara, Hiroki; Yoshizumi, Masao; Sugiyama, Takao; Yamaoki, Kazuhide; Nagai, Ryozo; Takaku, Fumimaro; Satoh, Hiroyuki; Inui, Jun; Yanagisawa, Masashi; Masaki, Τοmoh; Yazaki, Yoshio

doi:10.1097/00005344-198900135-00033

Cited by 82 publications

(27 citation statements)

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“…Other studies demonstrated that calcium antagonists may effectively antagonize the ET-induced vasoconstriction in vitro and in vivo in dogs [35][36][37]. This effect is also observed in microvessels such as in intracerebral microarterioles [38].…”

Section: Discussionmentioning

confidence: 99%

“…GTN has been demonstrated to attenuate the vasoconstrictor effects of ET in the human fetal-placental circulation [50], coronary circulation [37], or rabbit aorta [51] although, in contrast, in human resistance vessels, blockade of voltage-operated Ca2+ channels but not cyclic GMP-dependent vasodilatation may be an effective tool to inhibit ET-induced vasoconstriction [30]. In addition, GTN has been shown to reverse completely the ET-induced phosphorylation of myosin light chain in coronary artery smooth muscle [52].…”

Section: Discussionmentioning

confidence: 99%

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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: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

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 Some have suggested that endothelin-1 (ET-1), one of the most potent vasoconstrictors described, 2 may act as an endogenous modulator of coronary vascular tone and may play a role in the setting of coronary vasospasm. [3][4][5] In addition, local release of vasoactive eicosanoids such as prostaglandin F 2␣ (PGF 2␣ ) in response to cardiac tissue injury causes significant coronary vasoconstriction that may dangerously interfere with adequate coronary blood flow. [5][6][7] Although previous studies have shown that both ET-1 and PGF 2␣ are potent coronary vasoconstrictors, the effects of ET-1 on smooth muscle contraction have often been evaluated separately from the effects of PGF 2␣ .…”

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confidence: 99%

“…[5][6][7] Although previous studies have shown that both ET-1 and PGF 2␣ are potent coronary vasoconstrictors, the effects of ET-1 on smooth muscle contraction have often been evaluated separately from the effects of PGF 2␣ . [3][4][5][6][7] Also, in most mechanistic studies, high unphysiological concentrations of ET-1 and PGF 2␣ have often been used to activate maximally the possible mechanisms of smooth muscle contraction. This is in sharp contrast to the in vivo conditions, where the coronary artery is usually exposed to more than one vasoconstrictor at the same time, and the increases in the concentration of vasoconstrictor agonists are usually within the physiological range.…”

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confidence: 99%

“…This is in sharp contrast to the in vivo conditions, where the coronary artery is usually exposed to more than one vasoconstrictor at the same time, and the increases in the concentration of vasoconstrictor agonists are usually within the physiological range. Although high concentrations of ET-1 alone or PGF 2␣ alone are predicted to and have been shown to cause significant coronary contraction, [3][4][5][6][7] it is not clear whether physiological concentrations of ET-1 enhance coronary vasoconstriction to small concentrations of PGF 2␣ . In addition, although high concentrations of ET-1 alone or PGF 2␣ alone are predicted to activate maximally one or more mechanisms of smooth muscle contraction, the cellular mechanisms involved in the possible ET-1 induced enhancement of coronary vasoconstriction to the vasoactive eicosanoid PGF 2␣ are unclear.…”

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Endothelin-1 Enhances Eicosanoids-Induced Coronary Smooth Muscle Contraction by Activating Specific Protein Kinase C Isoforms

2001

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Abstract-Endothelin-1 (ET-1), a potent vasoconstrictor, has been implicated in the pathogenesis of coronary vasospasm by enhancing coronary vasoconstriction to vasoactive eicosanoids; however, the cellular mechanisms involved are unclear. We investigated whether physiological concentrations of ET-1 enhance coronary smooth muscle contraction to vasoactive eicosanoids by activating specific protein kinase C (PKC) isoforms. Cell contraction was measured in single smooth muscle cells isolated from porcine coronary arteries, intracellular free Ca 2ϩ ([Ca 2ϩ ] i ) was measured in fura-2-loaded cells, and the cytosolic and particulate fractions were examined for PKC activity and reactivity with isoform-specific anti-PKC antibodies using Western blots. In Hanks -7 mol/L) caused cell contraction (10%) and enhanced PGF 2␣ contraction (33%) with no additional increase in [Ca 2ϩ ] i (115Ϯ7 nmol/L). The ET-1-induced enhancement of PGF 2␣ contraction was inhibited by Gö6976 (10 -6 mol/L), an inhibitor of Ca 2ϩ -dependent PKC isoforms. Both ET-1 and PDBu caused an increase in PKC activity in the particulate fraction and a decrease in the cytosolic fraction and increased the particulate/cytosolic PKC activity ratio. Western blots revealed the Ca 2ϩ -dependent ␣-PKC and the Ca 2ϩ -independent ␦-, ⑀-, and -PKC isoforms. In resting tissues, ␣-and ⑀-PKC were mainly cytosolic, ␦-PKC was mainly in the particulate fraction, and -PKC was equally distributed in the cytosolic and particulate fraction. ET-1 (10 pmol/L) alone or PDBu (10 -7 mol/L) alone caused translocation of ⑀-PKC from the cytosolic to the particulate fraction, localized ␦-PKC more in the particulate fraction, but did not change the distribution of -PKC. PGF 2␣ (10 -7 mol/L) alone did not change PKC activity. In tissues pretreated with ET-1 or PDBu, PGF 2␣ caused additional increases in ␣-PKC activity. Thus, the enhancement of PGF 2␣ -induced coronary smooth muscle contraction by physiological concentrations of ET-1 involves activation and translocation of ␣-PKC in addition to ␦-and ⑀-PKC isoforms, and this may represent one possible cellular mechanism by which ET-1 could enhance coronary vasoconstriction to vasoactive eicosanoids in coronary vasospasm.

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Endothelin, an endothelial‐dependent vasoconstrictor in scleroderma. Enhanced production and profibrotic action

Kahaleh¹

1991

Arthritis & Rheumatism

225

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The vascular endothelium is an important functional unit in the regulation of the vascular and perivascular environment. Various chemical and physical stimuli mediate an endothelial-dependent vasoconstriction through the release of endothelial soluble factors, such as the recently recognized endothelium-derived vasoconstrictor peptide called endothelin. The presence of circulating endothelin and the effect of cold exposure on plasma endothelin levels were investigated in patients with scleroderma and in healthy control subjects. Radioimmunoassay demonstrated a mean f SD plasma level of 10.7 f 7.3 pg/ml in the patients (n = 19) and 3.7 f 2 in the control subjects (n = 16) (P < 0.005). These levels were also assessed in 5 control subjects and 5 scleroderma patients before and after 30 minutes of total body cooling (to 15OC). The endothelin level did not change significantly in either group; however, 2 scleroderma patients showed a significant increase after cooling. The effects of endothelin on fibroblast proliferation and collagen synthesis were evaluated in order to assess the impact of released endothelin on the interstitium. A significant mitogenic effect and a collagen synthesisenhancing effect, which were dose-dependent, were seen. The strong, characteristically prolonged, vasoconstrictor activity coupled with the profibrotic effect demonstrated here make it likely that disturbances in the From the Medical College of Ohio, Toledo.

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The Possible Role of Endothelin-1 in the Pathogenesis of Coronary Vasospasm

Cited by 82 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 Enhances Eicosanoids-Induced Coronary Smooth Muscle Contraction by Activating Specific Protein Kinase C Isoforms

Endothelin, an endothelial‐dependent vasoconstrictor in scleroderma. Enhanced production and profibrotic action

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