Arteriolar Occlusion Causes Independent Cellular Responses in Endothelium and Smooth Muscle

Objectives: To test the hypothesis that, arteriolar occlusion causes different cellular changes in endothelial and smooth muscle cells. Methods: Cheek pouch arterioles (resting diameter 41 ± 2 μ) of anesthetized hamsters were occluded briefly (<60 seconds) either upstream or downstream from an observation site. Changes in membrane potential and intracellular calcium concentration ([Ca²⁺]_i) of the endothelial or smooth muscle cells were determined by using fluorescence microscopy (ratiometric analysis). Results: The pressure in the occluded segment decreased by 17.4 ± 2.6 cm H₂O during upstream occlusion and increased by 16.8 ± 6 cm H₂O during downstream occlusion (n = 5). Upstream occlusion caused vasoconstriction of the occluded segment by 2.4 ± 0.4 μm, whereas downstream occlusion produced brief vasodilatation by 1.1 ± 0.2 μm. The endothelial cells hyperpolarized during upstream or downstream occlusion (ratio change: 2.26 ± 0.24% and 2.39 ± 0.42%, respectively; p < 0.01, n = 5). There were no changes in endothelial [Ca²⁺]_i. The smooth muscle cells depolarized (ratio change: -2.08 ± 0.14%, n = 5) with an increase in [Ca²⁺]_i (ratio change: 2.92 ± 0.16%, n = 6) during downstream occlusion. However, there was no detectable change in membrane potential or [Ca²⁺], of smooth muscle cells during upstream occlusion. All the changes rapidly recovered when occlusion was released. Responses of an in-situ isolated segment on a side branch revealed conducted dilatory signals caused by the occlusions. Conclusions: Our results show that the endothelial and smooth muscle cells respond independently to arteriolar occlusion. The endothelial and smooth muscle cells do not effectively communicate in [Ca²⁺]; or membrane potential during acute arteriolar occlusion. Hyperpolarizing signals in endothelium cause conducted dilation.