Regulation of capillary hemodynamics by K ATP channels in resting skeletal muscle.

Autor: Hirai DM; Department of Health and Kinesiology, Purdue University, West Lafayette, Indiana, USA.; Department of Kinesiology, Kansas State University, Manhattan, Kansas, USA., Tabuchi A; Department of Kinesiology, Kansas State University, Manhattan, Kansas, USA.; Department of Engineering Science, University of Electro-Communications, Tokyo, Japan., Craig JC; Department of Kinesiology, Kansas State University, Manhattan, Kansas, USA.; Department of Internal Medicine, University of Utah, Salt Lake City, Utah, USA.; Geriatric Research, Education and Clinical Center, Veterans Affairs Medical Center, Salt Lake City, Utah, USA., Colburn TD; Department of Kinesiology, Kansas State University, Manhattan, Kansas, USA., Musch TI; Department of Kinesiology, Kansas State University, Manhattan, Kansas, USA.; Department of Anatomy and Physiology, Kansas State University, Manhattan, Kansas, USA., Poole DC; Department of Kinesiology, Kansas State University, Manhattan, Kansas, USA.; Department of Anatomy and Physiology, Kansas State University, Manhattan, Kansas, USA.
Jazyk: angličtina
Zdroj: Physiological reports [Physiol Rep] 2021 Apr; Vol. 9 (8), pp. e14803.
DOI: 10.14814/phy2.14803
Abstrakt: ATP-sensitive K + channels (K ATP ) have been implicated in the regulation of resting vascular smooth muscle membrane potential and tone. However, whether K ATP channels modulate skeletal muscle microvascular hemodynamics at the capillary level (the primary site for blood-myocyte O 2 exchange) remains unknown. We tested the hypothesis that K ATP channel inhibition would reduce the proportion of capillaries supporting continuous red blood cell (RBC) flow and impair RBC hemodynamics and distribution in perfused capillaries within resting skeletal muscle. RBC flux (f RBC ), velocity (V RBC ), and capillary tube hematocrit (Hct cap ) were assessed via intravital microscopy of the rat spinotrapezius muscle (n = 6) under control (CON) and glibenclamide (GLI; K ATP channel antagonist; 10 µM) superfusion conditions. There were no differences in mean arterial pressure (CON:120 ± 5, GLI:124 ± 5 mmHg; p > 0.05) or heart rate (CON:322 ± 32, GLI:337 ± 33 beats/min; p > 0.05) between conditions. The %RBC-flowing capillaries were not altered between conditions (CON:87 ± 2, GLI:85 ± 1%; p > 0.05). In RBC-perfused capillaries, GLI reduced f RBC (CON:20.1 ± 1.8, GLI:14.6 ± 1.3 cells/s; p < 0.05) and V RBC (CON:240 ± 17, GLI:182 ± 17 µm/s; p < 0.05) but not Hct cap (CON:0.26 ± 0.01, GLI:0.26 ± 0.01; p > 0.05). The absence of GLI effects on the %RBC-flowing capillaries and Hct cap indicates preserved muscle O 2 diffusing capacity (DO 2 m). In contrast, GLI lowered both f RBC and V RBC thus impairing perfusive microvascular O 2 transport (Q̇m) and lengthening RBC capillary transit times, respectively. Given the interdependence between diffusive and perfusive O 2 conductances (i.e., %O 2 extraction∝DO 2 m/Q̇m), such GLI alterations are expected to elevate muscle %O 2 extraction to sustain a given metabolic rate. These results support that K ATP channels regulate capillary hemodynamics and, therefore, microvascular gas exchange in resting skeletal muscle.
(© 2021 The Authors. Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society.)
Databáze: MEDLINE
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