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The role of PKC‐B in the BKCa functionality of vascular smooth muscle of diabetic rats
Author(s) -
EspinosaTanguma Ricardo,
ÁlvarezMéndez Juan Antonio,
HernándezGarcía Ana Patricia,
AlgaraSuárez Paola
Publication year - 2016
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.30.1_supplement.1209.12
Subject(s) - vascular smooth muscle , contractility , protein kinase c , medicine , endocrinology , contraction (grammar) , bk channel , potassium channel , chemistry , diabetes mellitus , kinase , smooth muscle , biochemistry
Diabetes mellitus (DM) is a disease characterized by high blood glucose concentrations. Cardiovascular disorders associated with DM are the leading cause of high morbidity and mortality of this disease, where endothelial tissue as well as smooth muscle is damaged. For example, the contractility of the smooth muscle cells is increased partly due to a decrease in the activity of the calcium‐dependent high conductance potassium channels (BK Ca ), which along with other potassium conductance maintain membrane potential and vascular tone. Protein kinase C (PKC) is involved in signaling pathways that promote muscle contraction. Christiandimitropoulou (2002) reported that in the vascular smooth muscle of diabetic rats the outwardly currents flowing through the BK Ca channels are decreased. Likewise it was also reported that PKC can phosphorylate some residues of the carboxyl terminal of the alpha subunit of said channel. Data from our laboratories show that the inhibition of the classic isoforms of the PKC is associated with a decrease in the contraction of the mesenteric artery of diabetic rats, which suggests that the beta isoform may be involved in the vascular damage observed in DM. Objectives To study the role of the PKC‐B on BK Ca channels functionality and the aortic vascular contractility of diabetic rats induced by streptozotocine. Methods Tension and western blot experiments were performed on aortic rings. Results the NS11021, a BK Ca channel activator, significantly relaxes the rings of diabetic rats on a lesser scale than those of the control group, the PKC‐B LY333531 inhibitor does not modify the contractility induced by phenylephrine in normal rings but importantly relaxes those from diabetic rings. The effect of NS11021 is preserved even in the presence of LY333531. Western blot experiments suggest that smooth muscle from diabetic rats is less phosphorylated, indicating that BKCa activity is reduced compared with those from control rats. Conclusions vascular smooth muscle of diabetic rats show greater contractility and this may be due to a diminished activity of the BK Ca channels. Support or Funding Information Supported by C14‐FAI‐04‐33.33 to PAS, Conacyt 223350‐M to RET. Conacyt scholarship to JAM (295659)