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This Article Full Text Full Text (PDF) All Versions of this Article: 288/3/H1233    most recent 00732.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (10) Citing Articles via Google Scholar Google Scholar Articles by Mokelke, E. A. Articles by Sturek, M. Search for Related Content PubMed PubMed Citation Articles by Mokelke, E. A. Articles by Sturek, M.

Diabetic dyslipidemia and exercise affect coronary tone and differential regulation of conduit and microvessel K⁺ current

Departments of ¹Medical Pharmacology and Physiology and ²Internal Medicine, School of Medicine, and ³Center for Diabetes and Cardiovascular Health, University of Missouri, Columbia, Missouri; ⁴Division of Neonatology, Department of Pediatrics, Wake Forest University Health Sciences, Winston-Salem, North Carolina; ⁵Department of Pharmacology, University of Vermont, Burlington, Vermont; and ⁶Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana

Submitted 21 July 2004 ; accepted in final form 27 October 2004

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 wk: 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 versus C. In pressurized microvessels, Ca²⁺ spark activity was significantly lower in DD versus 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 by 86% in DD versus 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 versus C; in contrast, steady-state K⁺ current in conduit cells was decreased in DDX versus DD and C. We conclude that steady-state K⁺ current and STOCs are differentially regulated in conduit versus microvessels in health and diabetic dyslipidemia. Exercise prevented diabetic dyslipidemia-induced decreases in baseline CBF, possibly via STOC-regulated basal microvascular tone.

Yucatan swine; Doppler flow; intravascular ultrasound; vasoreactivity; spontaneous transient outward K⁺ currents; coronary blood flow

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