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Role of rat vascular KATP channels in setting microvascular oxygen pressure at the onset of contractions (1106.15)
Author(s) -
Holdsworth Clark,
Ferguson Scott,
Wright Jennifer,
Fees Alexander,
Poole David,
Musch Timothy
Publication year - 2014
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.28.1_supplement.1106.15
Subject(s) - skeletal muscle , chemistry , glibenclamide , medicine , endocrinology , blockade , stimulation , blood pressure , hyperpolarization (physics) , anatomy , receptor , stereochemistry , nuclear magnetic resonance spectroscopy , diabetes mellitus
Effective blood‐muscle O 2 flux demands a sufficient microvascular O 2 driving pressure (PO 2 mv) which is set by the ratio of O 2 delivery‐O 2 utilization. Smooth muscle cell hyperpolarization contributes to exercise induced increases in skeletal muscle O 2 delivery mediated, in part, by ATP‐sensitive K + (K ATP ) channels. We hypothesized that K ATP channel blockade via glibenclamide (GLI) would speed the fall of PO 2 mv following the onset of skeletal muscle contractions. Spinotrapezius PO 2 mv (phosphorescence quenching) was measured in 12 adult male Sprague Dawley rats at rest and during 180 s of 1 Hz twitch contractions (~7 V) under control (CON) and GLI (5 mg/kg) conditions. GLI increased mean arterial pressure (ΔCON: 2 ± 1, ΔGLI: 17 ± 4 mmHg, p < 0.05) and decreased heart rate (ΔCON: 3 ± 2, ΔGLI: ‐9 ± 3 bpm, p < 0.05) but did not change baseline PO 2 mv (CON: 34.0 ± 2.2, GLI: 33.7 ± 1.6 mmHg, p > 0.05). Following the onset of contractions the time constant, mean response time and contracting steady‐state PO 2 mv were not different between conditions ( p > 0.05 for all). However, a clearly defined undershoot ( p < 0.05) of the contracting steady‐state PO 2 mv was evident with GLI (8.0 ± 2.6 %) but not during CON (1.6 ± 1.1 %). Our data indicate that blockade of K ATP channels does not impact PO 2 mv kinetics parameters during small muscle mass electrical stimulation, but can cause transient mismatch of O 2 delivery‐O 2 utilization prior to stabilizing at the contracting steady‐state PO 2 mv. This suggests that K ATP channels contribute substantially to skeletal muscle microvascular function during the crucial rest to contraction transition and therefore have the potential to mediate skeletal muscle performance decrements evident in disease states. Grant Funding Source : Supported by AHA Midwest Affiliate 0750090Z, NIH HL‐108328