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Angiotensin II Inhibition of ATP‐Sensitive K + Currents in Rat Arterial Smooth Muscle Cells Through Protein Kinase C
Author(s) -
Kubo M.,
Quayle J. M.,
Standen N. B.
Publication year - 1997
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.1997.489bg.x
Subject(s) - calphostin c , protein kinase c , staurosporine , angiotensin ii , protein kinase a , calphostin , activator (genetics) , chemistry , medicine , endocrinology , patch clamp , mesenteric arteries , enzyme , biochemistry , biology , artery , receptor
1 The effects of the vasoconstrictor angiotensin II (Ang II) on whole‐cell ATP‐sensitive K + currents ( I k,atp ) of smooth muscle cells isolated enzymatically from rat mesenteric arteries were investigated using the patch clamp technique. 2 Ang II, at a physiological concentration (100 n m ), reduced I k,atp activated by 0.1 m m internal ATP and 10 μ m levcromakalim by 36.4 ± 2.3%. 3 The protein kinase C (PKC) activator 1‐oleoyl‐2‐acetyl‐sn‐glycerol (OAG, 1 μ m ) reduced I k,atp by 44.1 ± 2.7%. GDPβS (1 m m ), included in the pipette solution, abolished the inhibition by Ang II, while that by OAG was unaffected. 4 Pretreatment with the PKC inhibitors staurosporine (100 n m ) or calphostin C (500 n m ) prevented the Ang II‐induced inhibition of I k,atp . 5 Ang II inhibition was unaffected by cell dialysis with PKA inhibitor peptide (5 μ m ), and the PKA inhibitor Rp‐cAMPS (100 μ) did not reduce I k,atp . 6 Our results suggest that Ang II modulates K atp channels through activation of PKC but not through inhibition of PKA.