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Am J Physiol Heart Circ Physiol 279: H2249-H2258, 2000;
0363-6135/00 $5.00
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Vol. 279, Issue 5, H2249-H2258, November 2000

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

H. Glenn Bohlen and Geoffrey P. Nase

Department of Physiology and Biophysics, Indiana University Medical School, Indianapolis, Indiana 46202

Our hypothesis was that a large fraction of resting nitric oxide (NO) formation is driven by flow-mediated 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.

microelectrode; intestine; arteriole


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