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1 Physiology, Indiana University Medical School, Indianapolis, IN, USA
* To whom correspondence should be addressed. E-mail: gbohlen{at}iupui.edu.
Sodium chloride hyperosmolarity increases intestinal blood flow during food absorption due in large part to increased nitric oxide production. We hypothesized that in vivo, sodium ions enter endothelial cells during NaCl hyperosmolarity as the first step to stimulate an increase in intestinal endothelial nitric oxide production. The perivascular NO concentration ([NO]) and blood flow were determined in the in vivo rat intestinal microvasculature at rest and hyperosmotic conditions, 330 mOsm and 380 mOsm, before and after the application of bumetanide (Na+/K+/2Cl- cotransporter inhibitor) or amiloride (Na+/H+ exchange channel inhibitor). Suppressing amiloride sensitive Na+/H+ exchange channels diminished hypertonicity linked increases in vascular [NO], while blockade of Na+/K+/2Cl- channels greatly suppressed increases in vascular [NO] and intestinal blood flow. In additional experiments we examined the effect of sodium ion entry into endothelial cells. We proposed that the Na+/Ca+ exchanger extrudes Na+ in exchange for Ca+2, thereby leading to the calcium-dependent activation of eNOS. We blocked the activity of the Na+/Ca+ exchanger during 360 mOsm NaCl hyperosmolarity with KB-R7943; complete blockade of increased vascular [NO] and intestinal blood flow to hyperosmolarity occurred. These results indicate that during NaCl hyperosmolarity, sodium ions enter endothelial cells predominantly through Na+/K+/2Cl- channels. The Na+/Ca+ exchanger then extrudes Na+ and increases endothelial Ca+2. The increase in endothelial Ca+2 causes an increase in eNOS activity, and the resultant increase in nitric oxide increases intestinal arteriolar diameter and blood flow during NaCl hyperosmolarity. This appears to be the major mechanism by which intestinal nutrient absorption is coupled to increased blood flow.
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