K channel inhibition-induced hyporemia in skeletal muscle: No evidence for pre-capillary sphincter action.

INTRODUCTION

Whether pre-capillary sphincters are present and regulate red blood cell (RBC) flux at the individual capillary level, especially in skeletal muscle, is controversial. Recently, blockade of K channels using the sulphonylurea glibenclamide (GLI) was demonstrated to reduce muscle blood flow and lower vascular conductance. The present investigation tested the hypothesis that, if pre-capillary sphincters were involved in GLI-induced blood flow reductions, a defined luminal narrowing would be evident in the proximate region of the capillaries.

METHODS

Videomicroscopy of the spinotrapezius capillary bed was performed under control (Krebs-Henseleit) and GLI (200 μM in Krebs-Henseleit) superfusion. Capillary RBC flux was measured within individual capillaries and their luminal diameter was measured using a calibrated digital ruler at the branch-point and subsequently downstream.

RESULTS

GLI reduced capillary RBC flux by 31% (p = 0.004). Despite the presence of a reduced RBC flux, no detectable reduction or, indeed, any change in capillary luminal diameter was present at any measurement site. The average diameter at the branching point was 4.9 ± 0.3 μm, and at 5, 10, 20 and 50 μm downstream, the average diameters were 4.8 ± 0.4, 4.8 ± 0.5, 5.0 ± 0.7, and 5.2 ± 0.4 μm, respectively and were unchanged by GLI (all P > 0.05).

CONCLUSIONS

Accordingly, the absence of any evidence for capillary luminal narrowing or constriction in these data support that the GLI-induced reductions in capillary RBC flux and muscle blood flow occur via upstream effects within the arteriolar bed. Decreases in skeletal muscle microcirculatory RBC flux with this K channel blocker were not regulated by any detectable capillary structural alterations.