Endotheun causes prolonged potentiation of depolarizationinduced calcium influx, but desensitization of calcium release in coronary smooth muscle

D. L. Lee, M. Sturek

Research output: Contribution to journalArticle

Abstract

Endothelin (ET) increases Ca release and influx in vascular smooth muscle (VSM), resulting in slowly reversible contraction. We tested the hypothesis that myoplasmicfreeCa(Cam) regulation remains altered even after long recovery from short exposure to 10-8 M ET. Cam was determined in coronary smooth muscle cells using fura-2 microfluorometry (F340 / F380 ratio). The figure shows Cam responses to the first depolarization with 80 mM K (80K) and ET exposure, resulting largely from Ca influx and Ca release, respectively. Even after a brief, 2 min exposure to ET and long, 14 min recovery from ET the Cam response to the 2nd 80K was 38% greater than the 1st 80K (p<0.05, N=10). The Cam response to the 2nd ET exposure was abolished (NM). In cells not exposed to ET the Cam responses to both 80K depolarizations were similar (N=10). These data strongly indicate prolonged ET signaling in coronary smooth muscle. We further suggest that ET potentiation of the depolarization-induced Cam increase is the result of increased Ca influx and decreased buffering of Cam by the sarcoplasmic reticulum. (Support: NIH RCDA HL02872, HL41033, HL52490).

Original languageEnglish (US)
Pages (from-to)A67
JournalFASEB Journal
Volume10
Issue number3
StatePublished - Dec 1 1996

Fingerprint

endothelins
Endothelins
smooth muscle
Smooth Muscle
Muscle
Cams
Calcium
calcium
Depolarization
Cytophotometry
Recovery
sarcoplasmic reticulum
Fura-2
Sarcoplasmic Reticulum
Vascular Smooth Muscle
blood vessels
myocytes
Smooth Muscle Myocytes
Cells

ASJC Scopus subject areas

  • Biotechnology
  • Biochemistry
  • Molecular Biology
  • Genetics

Cite this

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title = "Endotheun causes prolonged potentiation of depolarizationinduced calcium influx, but desensitization of calcium release in coronary smooth muscle",
abstract = "Endothelin (ET) increases Ca release and influx in vascular smooth muscle (VSM), resulting in slowly reversible contraction. We tested the hypothesis that myoplasmicfreeCa(Cam) regulation remains altered even after long recovery from short exposure to 10-8 M ET. Cam was determined in coronary smooth muscle cells using fura-2 microfluorometry (F340 / F380 ratio). The figure shows Cam responses to the first depolarization with 80 mM K (80K) and ET exposure, resulting largely from Ca influx and Ca release, respectively. Even after a brief, 2 min exposure to ET and long, 14 min recovery from ET the Cam response to the 2nd 80K was 38{\%} greater than the 1st 80K (p<0.05, N=10). The Cam response to the 2nd ET exposure was abolished (NM). In cells not exposed to ET the Cam responses to both 80K depolarizations were similar (N=10). These data strongly indicate prolonged ET signaling in coronary smooth muscle. We further suggest that ET potentiation of the depolarization-induced Cam increase is the result of increased Ca influx and decreased buffering of Cam by the sarcoplasmic reticulum. (Support: NIH RCDA HL02872, HL41033, HL52490).",
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T1 - Endotheun causes prolonged potentiation of depolarizationinduced calcium influx, but desensitization of calcium release in coronary smooth muscle

AU - Lee, D. L.

AU - Sturek, M.

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N2 - Endothelin (ET) increases Ca release and influx in vascular smooth muscle (VSM), resulting in slowly reversible contraction. We tested the hypothesis that myoplasmicfreeCa(Cam) regulation remains altered even after long recovery from short exposure to 10-8 M ET. Cam was determined in coronary smooth muscle cells using fura-2 microfluorometry (F340 / F380 ratio). The figure shows Cam responses to the first depolarization with 80 mM K (80K) and ET exposure, resulting largely from Ca influx and Ca release, respectively. Even after a brief, 2 min exposure to ET and long, 14 min recovery from ET the Cam response to the 2nd 80K was 38% greater than the 1st 80K (p<0.05, N=10). The Cam response to the 2nd ET exposure was abolished (NM). In cells not exposed to ET the Cam responses to both 80K depolarizations were similar (N=10). These data strongly indicate prolonged ET signaling in coronary smooth muscle. We further suggest that ET potentiation of the depolarization-induced Cam increase is the result of increased Ca influx and decreased buffering of Cam by the sarcoplasmic reticulum. (Support: NIH RCDA HL02872, HL41033, HL52490).

AB - Endothelin (ET) increases Ca release and influx in vascular smooth muscle (VSM), resulting in slowly reversible contraction. We tested the hypothesis that myoplasmicfreeCa(Cam) regulation remains altered even after long recovery from short exposure to 10-8 M ET. Cam was determined in coronary smooth muscle cells using fura-2 microfluorometry (F340 / F380 ratio). The figure shows Cam responses to the first depolarization with 80 mM K (80K) and ET exposure, resulting largely from Ca influx and Ca release, respectively. Even after a brief, 2 min exposure to ET and long, 14 min recovery from ET the Cam response to the 2nd 80K was 38% greater than the 1st 80K (p<0.05, N=10). The Cam response to the 2nd ET exposure was abolished (NM). In cells not exposed to ET the Cam responses to both 80K depolarizations were similar (N=10). These data strongly indicate prolonged ET signaling in coronary smooth muscle. We further suggest that ET potentiation of the depolarization-induced Cam increase is the result of increased Ca influx and decreased buffering of Cam by the sarcoplasmic reticulum. (Support: NIH RCDA HL02872, HL41033, HL52490).

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