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 language||English (US)|
|State||Published - Dec 1 1997|
ASJC Scopus subject areas
- Molecular Biology