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1 Department of Physiology, New York Medical College, Valhalla, New York, USA
* To whom correspondence should be addressed. E-mail: gabor_kaley{at}nymc.edu.
Type 2 diabetes mellitus (T2-DM) markedly increases the incidence of ischemic heart disease (IHD), consequently mortality. However, the underlying mechanisms leading to IHD in T2-DM are not completely understood. We hypothesized that in T2-DM the regulation of coronary microvascular resistance by local mechanisms is altered. Thus, in coronary arterioles (diameter: ~ 80 µm~) isolated from male mice with T2-DM (C57BL/KsJ-db/db) and control littermates responses to changes in intraluminal pressure, flow and agonists with known mechanisms of action were studied. Increases in pressure (from 20-120 mmHg) resulted in similar myogenic responses of coronary arterioles of control and db/db mice, whereas dilations in response to cumulative concentrations of acetylcholine (ACh) and the NO donor NONOate were significantly decreased compared to those of control vessels. On the other hand, responses to adenosine were not different between vessels of control and db/db mice. Increases in flow (0-20 µL/min) resulted in dilations of control vessels (max: 38±4%) that were inhibited by the NO synthase inhibitor L-NAME. In contrast, arterioles of db/db mice exhibited greatly reduced dilations to flow (max: 4±6%) that were unaffected by L-NAME. In carotid arteries of db/db mice a superoxide dismutase (SOD)-sensitive, enhanced superoxide production was detected by dihydroethydine staining and lucigenin enhanced chemiluminescence. Correspondingly, intraluminal administration of SOD significantly augmented flow-, ACh- and NONOate-induced dilations of diabetic arterioles, responses that now could be inhibited by L-NAME. Collectively, these findings suggest that in T2-DM, due to an enhanced superoxide production, NO-mediation of agonist- and flow-induced dilation of coronary arterioles is reduced. This alteration in the regulation of coronary microvascular resistance may contribute to the development of ischemic heart disease in type 2 diabetes mellitus.
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