Intestinal absorption of calcium in vivo is dependent on endogenous nitric oxide
Schleiffer, R.; Galluser, M.; Raul, F.
Journal of Pharmacology and Experimental Therapeutics 275(3): 1427-1432
1995
ISSN/ISBN: 0022-3565 PMID: 8531112 Document Number: 452656
This study examines the role of nitric oxide (NO) in the regulation of calcium absorption in the small intestine. Calcium absorption was quantified by measuring 45Ca++ transport from lumen to blood in an intestinal segment (duodenum and 20 cm of the proximal jejunum) perfused by both intraluminal and vascular routes in anesthetized rats. When administered i.v. as bolus injections, N-G-nitro-L-arginine methyl ester (L-NAME, 10 mg cntdot kg-1), an inhibitor of NO biosynthesis, decreased calcium absorption with a concomitant increase in blood pressure and a decrease in mesenteric blood flow. Conversely, the nitrovasodilators 3-morpholinosydnonimine (2 mg cntdot kg-1) and S-nitroso-N-acetylpenicillamine (10 mu-g cntdot kg-1), which generate NO spontaneously, both increased calcium absorption with no change in mesenteric blood flow. When infused i.v., L-NAME (3 mg cntdot hr-1 cntdot kg-1 for 40 min) induced a decrease in calcium absorption that was reversed by the NO donor sodium nitroprusside (1.5 mg cntdot hr-1 cntdot kg-1 when infused for the last 20 min of the 40-min L-NAME infusion). Sodium nitroprusside infusion (1.5 mg cntdot hr-1 cntdot kg-1) caused an increase in calcium absorption that was not reversed by L-NAME (3 and 30 mg cntdot hr-1 cntdot kg-1). The present findings suggest that NO is involved in basal calcium absorption in rat small intestine in vivo.