Role of enkephalins in regulation of basal intestinal water and ion absorption in the rat
Fogel, R.; Kaplan, R.B.
American Journal of Physiology 246(4 Pt 1): G386-G392
1984
ISSN/ISBN: 0002-9513 PMID: 6326587 Document Number: 226324
Intraluminal administration of naloxone (10-4 M), a .mu.-opiate receptor antagonist, or diprenorphine (10-6 M), an opiate receptor antagonist with high affinity for both .delta.- and .mu.-receptors, decreased basal in vivo water and electrolyte absorption in the jejunum and ileum but not the colon of the rat. Diprenorphine (10-5 M) decreased basal colonic water transport. These changes were not due to a reduction in mucosal Na-K-ATPase activity. I.v. atropine prevented as well as abolished the changes in water transport due to naloxone. The diprenorphine-induced changes were not altered by atropine. Naloxone and diprenorphine acted by different receptors. Pretreatment with naloxone (10-4 M) prevented the increase in water transport due to morphine, a .mu.-agonist, whereas a higher concentration of naloxone (10-3 M) was required to inhibit the increase due to D-Ala-methionine-enkephalinamide, a .delta.-receptor agonist. In contrast, diprenorphine (10-6 M) abolished the absorption caused by morphine and D-Ala-methionine-enkephalinamide. Diprenorphine (3 .times. 10-7 M) partially prevented the morphine-induced increase in water absorption. Opiate receptor antagonists, therefore decrease basal intestinal and colonic water absorption in the rat, implicating endogenous opiates in the regulation of basal intestinal absorptive processes; the naloxone effect is mediated by cholinergic nerves, whereas diprenorphine acts by a different mechanism; the effect of naloxone (10-4 M) is due to an action at a .mu.-receptor as naloxone prevents the effect of the .mu.-agonist morphine but not the .delta.-agonist D-Ala-methionine-enkephalinamide; and diprenorphine prevents the effect of morphine as well as D-Ala-methionine-enkephalinamide, but the major effect of diprenorphine on basal absorption is mediated by the .delta.-receptor antagonism rather than an effect at the .mu.-receptor.