Role of K+ATP Channels, Endothelin A Receptors, and Effect of Angiotensin II on Blood Flow in Oral Tissues

Abstract

K+ATP channels are involved in CGRP-mediated vasodilation and in the vasoconstriction induced by endothelin or angiotensin II. In this study, we examined the effects of a K+ATP channel antagonist and an ET(A) receptor antagonist on resting blood flow in the pulp and gingiva, and observed their role in the vasodilation induced by tooth stimulation. We also investigated whether receptors for angiotensin II exist in the pulp and gingiva. Blood flow was measured with laser-Doppler flowmetry. Under control conditions, the K+ATP channel antagonist and angiotensin II caused a significant drop in blood flow in both target tissues. Blocking of ET(A) receptor did not change basal blood flow. The vasodilation observed after tooth stimulation remained unchanged following blockade of K+ATP channels and ET(A) receptors. Analysis of the data shows that open K+ATP channels exist during resting conditions in the pulp and gingiva, but that CGRP seems to induce vasodilation mainly via mechanisms other than K+ATP channels. ET(A) and AT1 receptors are found in the pulp and gingiva, but ET(A) receptors are not involved in modulation of a basal vascular tone in these tissues or in the vasodilation observed after tooth stimulation. Open K+ATP channels exist during resting conditions in both the dental pulp and gingiva, but calcitonin gene-related peptide seems to induce vasodilation via mechanisms other than the K+ATP channels.