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Muscle contraction under capillaries in hamster muscle induces arteriolar dilatation via K_ATP channels and nitric oxide

Kenneth D. Cohen and Ingrid H. Sarelius

We tested the hypothesis that adenosine and nitric oxide can be sensed by capillaries and are implicated in the remote arteriolar dilatation initiated by muscle contraction. We also explored a role for K_ATP channel activity in this response. Small bundles of muscle fibres underlying a group of capillaries in cremaster muscles of anaesthetized hamsters were electrically stimulated to contract for 2 min at each of 2, 4 and 8 Hz. Diameter changes were measured in the inflow arteriole to the group of capillaries after muscle contraction in the presence or absence of 10^-6 M xanthine amine congener (XAC) to block A₁ and A₂ adenosine receptors, 10^-4 or 10^-3 M N-nitro-L-arginine (LNNA) to block nitric oxide production, or 10^-5 M glibenclamide to block K_ATP channel activity. Dilatations were unchanged with XAC (3.0 ± 0.5, 3.9 ± 0.7 and 6.1 ± 1.0 µm), but were significantly reduced with LNNA (to 1.8 ± 0.6, 3.5 ± 0.7 and 4.9 ± 0.7 µm) or glibenclamide (to 0.4 ± 0.3, 0.8 ± 0.7 and 1.9 ± 0.6 µm). Neither K_ATP channel activity nor nitric oxide was required for transmission or manifestation of the dilator response. Thus, muscle contraction can be sensed by capillaries and the signalling mechanism for the ensuing remote dilatation depends on K_ATP channel activity and on NO, but not adenosine. Local application of 10^-4 M adenosine, 10^-4 M sodium nitroprusside or 10^-5 M pinacidil directly to capillaries initiated remote arteriolar dilatations. Thus, capillaries can respond directly to known mediators of metabolic vasodilatation, but these signalling pathways are not invariably implicated in the response to muscle contraction.

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