Conducted vasodilatation in human coronary arterioles

Conducted vasomotor responses in the coronary microcirculation match blood flow to metabolic requirements. Here we established whether conducted vasodilatation occurs in human coronary arterioles. Coronary arterioles were dissected from atrial appendage of patients (n=15). In isolated, pressurized arterioles (~ 100 μm) conducted dilatation was initiated by locally administering bradykinin (BK, 100 μM) ejected from a micropipette, positioned in close proximity to the vessel wall. Diameter changes were measured at local and upstream sites (500 and 1,000 μm from the stimulus) with videomicroscopy. Local administration of BK elicited vasodilatation (90±2%), which remained substantial at the upstream sites (500 μm, 53±7%; 1,000 μm, 46±9%). Administration of the gap junction uncoupler carbenoxolone (10 μM) did not affect local responses, but diminished conducted dilatation. The NO synthase inhibitor, L‐NAME had no affect on local responses (82±5%), but significantly reduced dilatation at upstream sites (500 μm, 17±3%; 1,000 μm, 24±6%). Both local and upstream dilatations to BK were diminished by Ca‐activated K‐channel blockers, TRAM34 and apamin and also with 30 mM K+. Thus, BK‐induced dilatation is propagated along the isolated human coronary arteriole. The conducted response is mediated by gap junctional hyperpolarisation spread, which is facilitated by NO. (NIH HL104126, BHF RE/08/004)