Premium
Activation of K IR channels and Na + /K + ‐ATPase is not obligatory to blunt sympathetic vasoconstriction in contracting human skeletal muscle (1170.6)
Author(s) -
Crecelius Anne,
Luckasen Gary,
Larson Dennis,
Dinenno Frank
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.1170.6
Subject(s) - vasoconstriction , chemistry , medicine , endocrinology , vascular smooth muscle , anesthesia , smooth muscle
Activation of inwardly‐rectifying potassium (K IR ) channels and Na + /K + ‐ATPase regulates muscle blood flow during mild exercise; whether these pathways are involved in the blunting of sympathetic α‐adrenergic vasoconstriction in active muscle is unknown. We tested the hypothesis that α 1 ‐adrenergic vasoconstriction (phenylephrine; PE) is augmented during exercise after inhibition of K IR channels and Na + /K + ‐ATPase. Young adults (n=11) were instrumented with a brachial artery catheter (drug infusions and blood pressure) and forearm blood flow (Doppler ultrasound) was measured and vascular conductance (FVC) calculated at rest, during minute 4 of steady‐state hyperemic conditions (moderate handgrip exercise or adenosine; ADO), and after 2 min of PE in these conditions: control (saline), combined inhibition of nitric oxide (NO; L‐NMMA) and prostaglandins (PGs; ketorolac) and combined inhibition of NO, PGs, K IR channels and Na + /K + ‐ATPase (L‐NMMA+ketorolac+BaCl 2 +ouabain). In control, exercise blunted PE‐mediated vasoconstriction (%ΔFVC) compared to ADO (‐21±3% vs ‐46±6%; P<0.05) and this was unchanged with L‐NMMA+ketorolac (‐24±3% vs ‐47±5%). The addition of BaCl 2 +ouabain had no effect on vasoconstriction during exercise (‐27±3%), indicating that activation of K IR channels and Na + /K + ‐ATPase is not obligatory to blunt sympathetic vasoconstriction in contracting human muscle. Support HL102720