Dependence of intestinal arteriolar regulation on flow-mediated nitric oxide formation

Our hypothesis was that a large fraction of resting nitric oxide (NO) forma tion is driven by flow-mediated mechanisms in the intestinal microvasculatu re of the rat. NO-sensitive microelectrodes measured the in vivo perivascul ar NO concentration ([ NO]). Flow was increased by forcing the arterioles t o perfuse additional nearby arterioles; flow was decreased by lowering the mucosal metabolic rate by reducing sodium absorption. Resting periarteriola r [NO] of large arterioles (first order; 1A) and intermediate-sized arterio les (second order; 2A) was 337 +/- 20 and 318 +/- 21 nM. The resting [NO] w as higher than the dissociation constant for the NO-guanylate cyclase react ion of vascular smooth muscle; therefore, resting [NO] should be a potent d ilatory signal at rest. Over flow velocity and shear rate ranges of similar to 40-180% of control, periarteriolar [NO] changed 5-8% for each 10% chang e in flow velocity and shear rate. The relationship of [NO] to flow velocit y and shear rate demonstrated that 60-80% of resting [NO] depended on flow- mediated mechanisms. Therefore, moment-to-moment regulation of [NO] at rest is an ongoing process that is highly dependent on flow-dependent mechanism s.