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1 Department of Medical Pharmacology and Physiology, University of Missouri, Columbia, MO, USA; Center for Diabetes and Cardiovascular Health, University of Missouri, Columbia, MO, USA; Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, IN, USA
2 Department of Medical Pharmacology and Physiology, University of Missouri, Columbia, MO, USA; Center for Diabetes and Cardiovascular Health, University of Missouri, Columbia, MO, USA
3 Department of Pediatrics, Wake Forest University Health Sciences, Winston-Salem, NC, USA; Department of Pharmacology, University of Vermont, Burlington, VT, USA
4 Department of Pharmacology, University of Vermont, Burlington, VT, USA
5 Department of Medical Pharmacology and Physiology, University of Missouri, Columbia, MO, USA; Department of Internal Medicine, University of Missouri, Columbia, MO, USA; Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, IN, USA
* To whom correspondence should be addressed. E-mail: msturek{at}iupui.edu.
Spontaneous transient outward K+ currents (STOCs) elicited by Ca2+ sparks and steady-state K+ currents modulate vascular reactivity, but effects of artery size, diabetic dyslipidemia, and exercise on these differentially regulated K+ currents are unclear. We studied the conduit arteries and microvessels of male Yucatan swine assigned to one of three groups for 20 weeks: control (C, n=7), diabetic dyslipidemic (DD, n=6), or treadmill-trained DD animals (DDX, n=7). Circumflex artery blood flow velocity obtained with intracoronary Doppler and lumen diameters obtained by intravascular ultrasound enabled calculation of absolute coronary blood flow (CBF). Ca2+ sparks were determined in pressurized microvessels and perforated patch clamp assessed K+ current in smooth muscle cells isolated from conduits and microvessels. Baseline CBF in DD was decreased vs. C. In pressurized microvessels Ca2+ spark activity was significantly lower in DD vs. C and DDX (P<0.05 vs. DDX). STOCs were pronounced in microvessel (~35 STOCs/min), in sharp contrast to conduit cells (~2 STOCs/min). STOCs were decreased 86% in DD vs. C and DDX in microvessels; in contrast, there was no difference in STOCs across groups in conduit cells. Steady-state K+ current in microvessels was decreased in DD and DDX vs. C; in contrast, steady-state K+ current in conduit cells was decreased in DDX vs. DD and C. We conclude that steady-state K+ current and STOCs are differentially regulated in conduit vs. microvessels in health and diabetic dyslipidemia. Exercise prevented diabetic dyslipidemia-induced decreases in baseline CBF, possibly via STOC regulated basal microvascular tone.
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