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1 West Virginia University Medical Center, Morgantown, WV, USA
2 Section of Digestive Diseases, Department of Medicine, The Ohio State University, Columbus, OH, USA
* To whom correspondence should be addressed. E-mail: usundaram{at}hsc.wvu.edu.
Na-nutrient co-transport processes are not only important for the assimilation of essential nutrients, but also for the absorption of Na in the mammalian small intestine. The effect of constitutive nitric oxide (cNO) on Na-glucose (SGLT-1) and Na-amino acid co-transport (NAcT) in the mammalian small intestine is unknown. Inhibition of cNO synthase with L-NG-Nitroarginine methylester (L-NAME) resulted in the inhibition of Na-stimulated 3H-O-Methyl-D-glucose[3-OMG] uptake in villus cells. However, Na-stimulated alanine uptake was not affected in these cells. The L-NAME induced reduction in SGLT-1 in villus cells was not secondary to an alteration in basolateral membrane Na-K-ATPase activity which provides the favorable Na-gradient for this cotransport process. In fact, SGLT-1 was inhibited in villus cell brush border membrane (BBM) vesicles prepared from animals treated with L-NAME. Kinetic studies demonstrated that the mechanism of inhibition of SGLT-1 was secondary to a decrease in the affinity for glucose without a change in the maximal rate of uptake of glucose. Northern blot studies demonstrated no change in the mRNA levels of SGLT-1. Western blot studies demonstrated no significant change in the immuno-reactive protein levels of SGLT-1 in ileal villus cell BBM from L-NAME treated rabbits. These studies indicate that inhibition of cNO production inhibits SGLT-1, but not NAcT in the rabbit small intestine. Therefore, while cNO promotes Na-glucose co-transport it does not affect NAcT in the mammalian small intestine.
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