Preclinical study reveals impaired sensory vasodilation in mesenteric arteries during IBD, indicating substance P interference with CGRP signaling disrupts vascular control.
Our study is the first to show that IBD causes profound impairment of sensory vasodilation and inhibition of sympathetic vasoconstriction in mesenteric arteries. This occurs alongside decreased SP-containing nerve density and increased expression of NK1 receptors for SP. In contrast, CGRP dilation, nerve density, and receptor expression are unchanged. Blocking NK1 receptors restores sensory vasodilation in MAs and increases CGRP-mediated vasodilation, indicating that SP interference with CGRP signaling may underlie impaired sensory vasodilation with IBD.
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Norton et al. (2021) studied this question.
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