Abstract

We hypothesized that the pathways utilized for conducted dilations along skeletal muscle microvasculature are dependent on the dilator used to initiate the conducted response. We initiated conducted responses by micropipette application of either 10−4M acetylcholine (ACh) or 10−5M pinacidil (PIN, a KATP channel opener) to the capillaries or the transverse arteriole (TA, located three branch orders proximal to the capillaries) in the anaesthetized hamster cremaster muscle model in situ. When the capillaries were stimulated we observed changes in diameter of the arteriole directly supplying the capillaries and when the TA was stimulated we observed the TA approx. 1000um upstream (US) and downstream (DS) from the site of dilator application. We reapplied ACh and PIN after a 30 min micropipette application of 40uM 18‐B‐glycyrrhetinic acid (BGA), a gap junction uncoupler, between sites of initiation and observation. Significant conducted dilations were produced in proximal arterioles when either ACh (3.6+/−0.9um) or PIN (3.1+/−0.5um) was applied to the capillaries. BGA significantly attenuated dilation to ACh (0.6+/−0.2um) but not dilations to PIN (3.4+/−0.8um). Significant conducted dilations were observed on the TA in response to both ACh (US: 9.6+/−2.0um, DS: 7.8+/−2.4um) and PIN (US: 5.2+/−1.4um, DS: 7.0+/−1.7um). BGA attenuated the conducted responses to ACh (US: 4.4+/−1.8um, DS: 2.6+/−1.6um), but not to PIN (US: 5.1+/−1.4um, DS: 10.9+/−4.4um). Therefore, conducted responses may use different transmission pathways that are dependent on the stimulus initiating the conducted response. NSERC and PREA.

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