Involvement of K_ATP Channels in the Dilation of Cerebral Arteries During Chronic Inflammation in Rats

   Introduction. Chronic inflammation (CI) leads to encephalopathies, destabilization of cognitive abilities and psychoemotional state. The functioning of neurons depends on cerebral blood flow, which is regulated by changes in arterial diameter. Arterial reactivity is largely determined by the functioning of K_ATP channels, which can worsen in CI under the influence of
pro-inflammatory cytokines and free radicals.

   Aim. To study the contribution of K_ATP channels to the dilation of rat cerebral arteries during the development of chronic inflammation.

   Materials and Methods. In pial arteries of Wistar rats 3 months after cecal ligation and puncture (a model of CI), the following were performed: investigation of the dilatory response of arteries of different diameters to acetylcholine (ACh) and sodium nitroprusside (NP) before and after blockade of K_ATP channels with glibenclamide (GB); assessment of the contribution of K_ATP channels to the formation of vascular tone based on the number of arteries that constricted in response to the blocker GB and dilating in response to the activator pinacidil (PI).

   Results. In CI, the number of dilations in response to ACh decreased by 1.4–3.4 times in arteries with a diameter less than 40 µm and by 1.7–1.9 times in larger vessels compared to the control. Under the influence of NP, CI rats showed 1.6–1.7 times fewer dilations in large and 1.5 times fewer in small pial arteries compared to the control. In the control group, the number of dilations to ACh when co-applied with GB decreased by 2.2–3.4 times compared to the response to ACh alone, and for NP by 2.5–3 times. In the CI group, blockade of KATP channels did not significantly reduce the number of dilated arteries either in response to ACh or to NP. The contribution of KATP channels in large cerebral arteries to the formation of tone in large pial arteries during CI did not change compared to the control, while in small arteries it slightly decreased.

   Conclusion. In rats, the development of chronic inflammation led to a significant impairment of pial artery dilation. Unlike in controls, KATP channels of smooth muscle cells of animals with CI do not participate in the formation of the dilatory response of these vessels, although the contribution of K_ATP channels to maintaining vascular tone was preserved in large arteries and slightly reduced in small ones.

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