Contracting human skeletal muscle maintains the ability to blunt α1‐adrenergic vasoconstriction during KIRchannel and Na+/K+‐ATPase inhibition
Key result
Inhibition of KIR channels and Na+/K+-ATPase did not enhance α1-mediated vasoconstriction during exercise compared to control (Protocol 1: -27 ± 3%, P=0.2; Protocol 2: -21 ± 7%, P=0.9).
Why the study?
Does inhibition of KIR channels and Na+/K+-ATPase augment alpha-1 adrenergic vasoconstriction during exercise in young healthy humans?
Population
17 young healthy humans (Protocol 1 n=11, Protocol 2 n=6)
Comparison
Phenylephrine infusion during moderate rhythmic… vs Control (saline) and/or NO/PG inhibition alone
Design
Other
Authors
Discussion
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Member takes
Implication
Findings from healthy volunteers should not yet inform patient care; leaves open redundant pathways preserving functional sympatholysis.
Structured PICO
Does inhibition of KIR channels and Na+/K+-ATPase augment alpha-1 adrenergic vasoconstriction during exercise in young healthy humans?
P
Population
17 young healthy humans undergoing forearm blood flow measurements during rhythmic handgrip exercise and pharmacological infusions.
I
Intervention
Phenylephrine infusion during moderate (15% maximal voluntary contraction) rhythmic handgrip exercise or adenosine infusion, with combined inhibition of KIR channels and Na+/K+-ATPase (BaCl2 + ouabain) +/- NO/PG inhibition (l-NMMA + ketorolac), after local beta-blockade (propranolol)
C
Comparator
Control (saline) and/or NO/PG inhibition alone
O
Outcome
Phenylephrine-mediated vasoconstriction (%ΔFVC)surrogate
Main Result
p-value: p=0.2
Contracting human skeletal muscle maintains the ability to blunt alpha-1 adrenergic vasoconstriction even during combined KIR channel and Na+/K+-ATPase inhibition.
Cite This Study
Crecelius et al. (2015) studied Healthy (n=17). Inhibition of KIR channels and Na+/K+-ATPase (BaCl2 + ouabain) vs. Saline (control) was evaluated on PE-mediated vasoconstriction (%ΔFVC) during exercise (p=0.2). Inhibition of KIR channels and Na+/K+-ATPase did not enhance α1-mediated vasoconstriction during exercise compared to control (Protocol 1: -27 ± 3%, P=0.2; Protocol 2: -21 ± 7%, P=0.9).