Our hypothesis was that a large fraction of resting nitric oxide (NO) formation is driven by flowmediated mechanisms in the intestinal microvasculature of the rat. NO-sensitive microelectrodes measured the in vivo perivascular NO concentration ([NO]). Flow was increased by forcing the arterioles to perfuse additional nearby arterioles; flow was decreased by lowering the mucosal metabolic rate by reducing sodium absorption. Resting periarteriolar [NO] of large arterioles (first order; 1A) and intermediate-sized arterioles (second order; 2A) was 337 ± 20 and 318 ± 21 nM. The resting [NO] was higher than the dissociation constant for the NO-guanylate cyclase reaction of vascular smooth muscle; therefore, resting [NO] should be a potent dilatory signal at rest. Over flow velocity and shear rate ranges of ~40-180% of control, periarteriolar [NO] changed 5-8% for each 10% change in flow velocity and shear rate. The relationship of [NO] to flow velocity 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 mechanisms.
|Original language||English (US)|
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|Issue number||5 48-5|
|State||Published - Dec 12 2000|
ASJC Scopus subject areas
- Physiology (medical)