Transfer of Nitric Oxide by Blood From Upstream to Downstream Resistance Vessels Causes Microvascular Dilation

Abstract

Oxygenated hemoglobin does not destroy nitric oxide (NO), but carries and releases NO in blood from upstream to downstream microvessels. Given that the circulation time from small arteries to capillaries is ~2‐4 seconds, NO in plasma or bound to proteins likely survives to downstream locations. To test this hypothesis, the vessel wall versus intravascular [NO] was measured in the in vivo sequential mesenteric and intestinal vessels of rats. NO microelectrodes demonstrated vessel wall [NO] was 25‐40% higher than blood [NO] in all vessels. Flow in mesenteric arteries was elevated by occlusion of collateral arteries to induce a flow mediated increase in arterial NO production. Both arterial wall and downstream arteriolar [NO] increased and the arterioles dilated as the blood [NO] was increased. To study receptor mediated NO generation, bradykinin was locally applied to upstream large arterioles and NO measured there and in downstream arterioles. At both sites, the [NO] and vessel diameters increased. When isoproterenol was applied to upstream vessels, they dilated but their [NO] and that of downstream arterioles did not increase and minor downstream dilation occurred. These observations indicate that NO can move in blood from upstream to downstream resistance vessels. This phenomenon may allow larger vessels to influence vascular tone in downstream vessels when local NO production is altered. (Support NIH HL‐20605)