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Functional changes in vascular reactivity to adenosine receptors activation in type I diabetic mice.
Author(s) -
Labazi Hicham,
Teng Bunyen,
Mustafa S. Jamal
Publication year - 2017
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.31.1_supplement.673.13
Subject(s) - medicine , endocrinology , streptozotocin , chemistry , phenylephrine , adenosine , agonist , adenosine receptor , contraction (grammar) , mesenteric arteries , cgs 21680 , receptor , diabetes mellitus , artery , blood pressure
Activation of adenosine receptors (ARs) have been implicated in a number of biological functions including cardiovascular and renal function. Diabetes is known to cause morphological and functional changes in the vasculature, resulting in abnormal responses to various stimuli such as adenosine. The aim for this study was to examine the effect of type I diabetes on the functional changes in conduit (aorta) and resistance arteries (mesenteric arteries, MA) to AR agonist's activation. Diabetes was induced in mice using streptozotocin (STZ, 10mg/Kg/day for 5 days; 12 weeks); concentration response curves (CRC) to acetylcholine, phenylephrine and selective agonists including A 1 AR (2‐Chloro‐N6‐cyclopentyladenosine, CCPA), A 3 AR (1‐[2‐chloro‐6‐ [[(3‐iodophenyl) methyl] amino]‐9H‐purin‐9‐yl]‐1‐deoxy‐N‐methyl‐β‐d‐ribofuranuronamide, Cl‐IBMECA), A 2A AR (4‐[2‐[[6‐Amino‐9‐( N ‐ethyl‐β‐D‐ribofuranuronamidosyl)‐9 H ‐purin‐2‐yl]amino]ethyl]benzenepropanoic acid hydrochloride, CGS‐21680) and A 2B AR (2‐[[6‐Amino‐3,5‐dicyano‐4‐[4‐(cyclopropylmethoxy)phenyl]‐2‐pyridinyl]thio]‐acetamide, BAY 60‐6583) were performed in isolated aortae and MA from STZ and vehicle groups. Diabetes did not affect AR agonists‐mediated relaxation/contraction CRCs in MA. However, aortae from diabetic mice exhibited a significant decrease (p<0.05) in A 1 R‐mediated vasoconstriction. In addition, the aorta from STZ mice exhibited an increase in phenylephrine‐mediated contraction (EC 50 6.88 ± 0.09 in STZ vs. 7.06 ± 0.09 in vehicle; p<0.05), while the relaxation to A 2A AR agonist (CGS‐21680) tended to decrease in aortae from the STZ‐treated group, it was not statistically significant. Our data suggest that STZ‐induced diabetes caused functional changes in conduit arteries (decreased A 1 R‐mediated contraction), and these changes may be a compensatory to counterbalance the increased vascular contractility observed in diabetes. Support or Funding Information Supported by HL027339