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Role of BK Ca channels and PKC in mesenteric artery contractility of diabetic rats
Author(s) -
Suárez Paola Algara,
Pérez Cristóbal Joel González,
EspinosaTanguma Ricardo
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.917.2
Subject(s) - phenylephrine , protein kinase c , endocrinology , medicine , streptozotocin , nifedipine , contractility , contraction (grammar) , chemistry , mesenteric arteries , activator (genetics) , isometric exercise , diabetes mellitus , artery , calcium , kinase , blood pressure , receptor , biochemistry
The aim of this study was to analyze the effect of diabetes mellitus (DM), acting through protein kinase C (PKC), on vascular tone associated to BK Ca channel activity in rat mesenteric artery. Methods DM was induced in male Wistar rats by intravenous injection of streptozotocin (STZ, 60mg/kg) and mesenteric artery rings were isolated for isometric force studies. The effects of PKC inhibitor Bisindolymaleimide I (Bis 1) and BK Ca channel activator NS 1619 on phenylephrine induced contractions were evaluated and expressed as % force. Results NS1619 decreased maximal force in control but not in STZ rats (97.4 ± 16 % vehicle v.s. 81.6 ± 25% NS1619, p=0.011, n=7 for ctrl; 84 ± 13% v.s. 71.8 ± 36%, p=0.54, n = 6 for STZ). Bis1 decreased phenylephrine contraction in both control and STZ rats (61.8 ± 33%, p= 0.003, n =8 ctrl; 34 ± 12%, p=0.0001, n=6 for STZ); although inhibition was more prominent in STZ than in ctrl rats (p= 0.005). Relaxation due to nifedipine was higher for STZ (42±15% for ctrl v.s. 19.5 ±17 for STZ, p=0.031, n=6). Conclusions DM leads to elevated PKC and VOCC activity, probably through BK Ca channel inhibition which is not reversible by NS1619. Supported by: C12‐FAI‐03–60.60, UASLP