Phorbol esters block tetraethylammonium (TEA)-induced oscillatory contractions in arteries from stroke-prone spontaneously hypertensive (SHRSP) and normotensive rats

D. Johns, S. Watts, M. L. Tsai, R Clinton Webb

Research output: Contribution to journalArticle

Abstract

Tail artery segments from SHRSP, but not WKY rats exhibit oscillatory contractions in response to norepinephrine (NE). Previous studies have indicated that protein kinase C (PKC) agonists inhibit and PKC antagonists augment these agonist-induced oscillatory contractions. Because gap junctional conductance in several tissues is blocked by phorbol esters, it was hypothesized that oscillatory activity in SHRSP is dependent upon intercellular coupling. This study examines the effects of PKC agonists (TPA, mezerein) and an inactive phorbol ester on oscillatory contractions induced by TEA, an up-regulator of gap junctions. Helical strips of tail artery from WKY and SHRSP were mounted in a muscle bath for isometric recording. Oscillatory contractions were measured during a 10 min period of maximum oscillatory contractions in response to TEA (20 mM). TPA (10-6M) and mezerein (10-6 M) inhibited TEA-induced oscillatory contractions in tail arteries from both WKY and SHRSP. An inactive phorbol ester, TPA 4-0-methyl-ester did not alter oscillatory contractions. Because TEA is known to up-regulate gap junctions and induces oscillations in both WKY and SHRSP, these observations do not support the hypothesis of abnormal gap junctional activity in SHRSP.

Original languageEnglish (US)
JournalFASEB Journal
Volume11
Issue number3
StatePublished - Dec 1 1997
Externally publishedYes

Fingerprint

Tetraethylammonium
Phorbol Esters
Rats
Arteries
Stroke
Protein Kinase C
Tail
Gap Junctions
Inbred WKY Rats
Baths
Norepinephrine
Esters
Up-Regulation
Muscles
Muscle
Tissue
mezerein

ASJC Scopus subject areas

  • Biotechnology
  • Biochemistry
  • Molecular Biology
  • Genetics

Cite this

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title = "Phorbol esters block tetraethylammonium (TEA)-induced oscillatory contractions in arteries from stroke-prone spontaneously hypertensive (SHRSP) and normotensive rats",
abstract = "Tail artery segments from SHRSP, but not WKY rats exhibit oscillatory contractions in response to norepinephrine (NE). Previous studies have indicated that protein kinase C (PKC) agonists inhibit and PKC antagonists augment these agonist-induced oscillatory contractions. Because gap junctional conductance in several tissues is blocked by phorbol esters, it was hypothesized that oscillatory activity in SHRSP is dependent upon intercellular coupling. This study examines the effects of PKC agonists (TPA, mezerein) and an inactive phorbol ester on oscillatory contractions induced by TEA, an up-regulator of gap junctions. Helical strips of tail artery from WKY and SHRSP were mounted in a muscle bath for isometric recording. Oscillatory contractions were measured during a 10 min period of maximum oscillatory contractions in response to TEA (20 mM). TPA (10-6M) and mezerein (10-6 M) inhibited TEA-induced oscillatory contractions in tail arteries from both WKY and SHRSP. An inactive phorbol ester, TPA 4-0-methyl-ester did not alter oscillatory contractions. Because TEA is known to up-regulate gap junctions and induces oscillations in both WKY and SHRSP, these observations do not support the hypothesis of abnormal gap junctional activity in SHRSP.",
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T1 - Phorbol esters block tetraethylammonium (TEA)-induced oscillatory contractions in arteries from stroke-prone spontaneously hypertensive (SHRSP) and normotensive rats

AU - Johns, D.

AU - Watts, S.

AU - Tsai, M. L.

AU - Webb, R Clinton

PY - 1997/12/1

Y1 - 1997/12/1

N2 - Tail artery segments from SHRSP, but not WKY rats exhibit oscillatory contractions in response to norepinephrine (NE). Previous studies have indicated that protein kinase C (PKC) agonists inhibit and PKC antagonists augment these agonist-induced oscillatory contractions. Because gap junctional conductance in several tissues is blocked by phorbol esters, it was hypothesized that oscillatory activity in SHRSP is dependent upon intercellular coupling. This study examines the effects of PKC agonists (TPA, mezerein) and an inactive phorbol ester on oscillatory contractions induced by TEA, an up-regulator of gap junctions. Helical strips of tail artery from WKY and SHRSP were mounted in a muscle bath for isometric recording. Oscillatory contractions were measured during a 10 min period of maximum oscillatory contractions in response to TEA (20 mM). TPA (10-6M) and mezerein (10-6 M) inhibited TEA-induced oscillatory contractions in tail arteries from both WKY and SHRSP. An inactive phorbol ester, TPA 4-0-methyl-ester did not alter oscillatory contractions. Because TEA is known to up-regulate gap junctions and induces oscillations in both WKY and SHRSP, these observations do not support the hypothesis of abnormal gap junctional activity in SHRSP.

AB - Tail artery segments from SHRSP, but not WKY rats exhibit oscillatory contractions in response to norepinephrine (NE). Previous studies have indicated that protein kinase C (PKC) agonists inhibit and PKC antagonists augment these agonist-induced oscillatory contractions. Because gap junctional conductance in several tissues is blocked by phorbol esters, it was hypothesized that oscillatory activity in SHRSP is dependent upon intercellular coupling. This study examines the effects of PKC agonists (TPA, mezerein) and an inactive phorbol ester on oscillatory contractions induced by TEA, an up-regulator of gap junctions. Helical strips of tail artery from WKY and SHRSP were mounted in a muscle bath for isometric recording. Oscillatory contractions were measured during a 10 min period of maximum oscillatory contractions in response to TEA (20 mM). TPA (10-6M) and mezerein (10-6 M) inhibited TEA-induced oscillatory contractions in tail arteries from both WKY and SHRSP. An inactive phorbol ester, TPA 4-0-methyl-ester did not alter oscillatory contractions. Because TEA is known to up-regulate gap junctions and induces oscillations in both WKY and SHRSP, these observations do not support the hypothesis of abnormal gap junctional activity in SHRSP.

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