Dependence of intestinal arteriolar regulation on flow-mediated nitric oxide formation |
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Authors: | Bohlen H G Nase G P |
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Institution: | Department of Physiology and Biophysics, Indiana University Medical School, Indianapolis, Indiana 46202, USA. gbohlen@iupui.edu |
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Abstract: | 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 approximately 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. |
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