Mechanism of increased vessel wall nitric oxide concentrations during intestinal absorption

Abstract

Vasoactive compounds, including nitric oxide (NO) and hypertonic sodium, may diffuse from venous endothelial cells and blood to the arterial wall during intestinal absorption. This hypothesis was tested by measuring the perivascular NO concentration ([NO]) for paired small arteries and veins with NO-sensitive microelectrodes. Resting arterial and venous wall concentrations for nine vessel pairs (5 rats) were 353 ± 28 and 401 ± 48 (SE) nM. During mucosal absorption of 100 and 300 mg/dl glucose, the artery dilated 12 ± 1.5 and 17 ± 2%, [NO] increased to 540 ± 68 and 550 ± 49 nM, and venous wall [NO] increased to 557 ± 60 and 633 ± 70 nM. During venous occlusion to block diffusion of materials from venous blood to the artery wall, the arterial and venous [NO] decreased by 70–80%, and one-half of the arterial dilation subsided. Superfusion with 320 and 360 mosmol/l hypertonic sodium medium to simulate the sodium hyperosmolarity during mucosal absorption of glucose increased the arterial [NO] by 20–30 and 40–50%; 360 mosmol/l saline made hypertonic with mannitol did not significantly increase the [NO]. Although venous to arterial diffusion of NO occurred, the increased arterial [NO] during mucosal glucose absorption was primarily generated by the arterial wall in response to materials that diffused from venous blood, such as hypertonic sodium.