In vitro studies on active calcium absorption from ovine rumen.
From various in vivo and in vitro studies it has been shown that the rumen represents a significant site of Ca2+ absorption in sheep and goats. It was the aim of the present study to further characterize the underlying mechanisms. Unidirectional flux rates of Ca2+ across rumen wall epithelia of sheep were measured in vitro by applying the Ussing-chamber technique in the absence of electrochemical gradients. Under these conditions, significant Ca2+ net flux rates (Jnet) clearly indicate the presence of active mechanisms for Ca2+ transport. Short chain fatty acids (SCFAs) caused highest stimulation of Ca2+ Jnet (6.3 +/- 1.9 nmol.cm-2.h-1) when used as a mixture of acetate, proprionate and butyrate in physiological proportions (36, 15, 9 mmol.l-1, respectively). The effect of 30 mmol.l-1 butyrate (3.2 +/- 0.6 nmol.cm-2.h-1) was higher than respective amounts of propionate and acetate (0.6 +/- 0.8 nmol.cm-2.h-1 and 0.9 +/- 0.8 nmol.cm-2.h-1, respectively). Eliminating SCFAs resulted in Ca2+ Jnet of 0.4 +/- 1.1 nmol.cm-2.h-1. Addition of Ca channel blocker verapamil (mucosal 1 mmol.l-1) had no significant effect on SCFA-stimulated Jnet of Ca2+, whereas application of Na+/H- inhibitor amiloride (mucosal 1 mmol.l-1) further enhanced the Ca2+ Jnet by > 65%. The Ca(2+)-pump inhibitor vanadate had no significant effect on Jnet of Ca2+. Dietary Ca depletion enhanced calcitriol plasma concentrations but had no effect on active Ca2+ absorption across the rumen wall of sheep. In addition, no effect on active Ca2+ absorption could be observed during early lactation. In conclusion, there is clear evidence for the rumen as a main site for active Ca2+ absorption in sheep. Our results suggest the presence of a Ca2+/H+ exchange mechanism in the apical membrane of rumen epithelial cells which depends on SCFA absorption and which does not seem to be under the control of calcitriol. Basolateral Ca2+ extrusion occurs independently from Ca(2+)-pump activity and may be accomplished via Na+/Ca2+ exchange.
Schröder
B
B
Physiologisches Institut der Tierärztlichen Hochschule Hannover, Germany. bschroed@physiology.tiho-hannover.de
Vössing
S
S
Breves
G
G
D000042:Absorption / Q000187:drug effects / Q000502:physiology; D000584:Amiloride / Q000494:pharmacology; D000818:Animals; D001692:Biological Transport / Q000187:drug effects / Q000502:physiology; D002087:Butyrates / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002136:Calcium, Dietary / Q000493:pharmacokinetics*; D000252:Calcium-Transporting ATPases / Q000378:metabolism*; D004232:Diuretics / Q000494:pharmacology; D004594:Electrophysiology; D004847:Epithelial Cells / Q000378:metabolism; D005232:Fatty Acids, Volatile / Q000494:pharmacology; D005260:Female; D006706:Homeostasis / Q000187:drug effects; D066298:In Vitro Techniques; D007774:Lactation / Q000502:physiology; D008297:Male; D011388:Prolactin / Q000494:pharmacology; D012417:Rumen / Q000166:cytology / Q000201:enzymology*; D012756:Sheep; D012964:Sodium / Q000378:metabolism; D014638:Vanadates / Q000494:pharmacology; D014700:Verapamil / Q000494:pharmacology
D002087:Butyrates; D002121:Calcium Channel Blockers; D002136:Calcium, Dietary; D004232:Diuretics; D005232:Fatty Acids, Volatile; D014638:Vanadates; D000584:Amiloride; D011388:Prolactin; D012964:Sodium; D014700:Verapamil; D000252:Calcium-Transporting ATPases