Effect of VIP antagonist on VIP-, PGE2-, and acid-stimulated duodenal bicarbonate secretion.
Vasoactive intestinal peptide (VIP), prostaglandin E2 (PGE2), and luminal acidification are each potent stimulants of duodenal mucosal bicarbonate secretion. The present experiments were performed to determine whether the recently described VIP antagonist, [4Cl-D-Phe6,Leu17]VIP, suppresses VIP-stimulated duodenal mucosal bicarbonate secretion and to determine whether VIP serves as a mediator of bicarbonate secretion stimulated by acid or PGE2. In anesthetized rats, the effects of intravenous VIP, intraluminal PGE2, and intraluminal HCl on duodenal mucosal bicarbonate secretion both in the presence and absence of [4Cl-D-Phe6,Leu17]VIP were measured. The VIP antagonist inhibited duodenal bicarbonate secretion stimulated by both intravenous VIP and luminal acidification but not luminal PGE2. These findings suggest that VIP could be one mediator of acid-induced duodenal bicarbonate secretion and that the mechanism of PGE2-stimulated bicarbonate secretion is independent of VIP.
Algazi
M C
MC
Department of Medicine, UCSD, Medical Center.
Chen
H S
HS
Koss
M A
MA
Hogan
D L
DL
Steinbach
J
J
Pandol
S J
SJ
Isenberg
J I
JI
D000818:Animals; D001639:Bicarbonates / Q000378:metabolism*; D015232:Dinoprostone / Q000494:pharmacology*; D004386:Duodenum / Q000187:drug effects*; D006851:Hydrochloric Acid / Q000494:pharmacology*; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D014660:Vasoactive Intestinal Peptide / Q000037:antagonists & inhibitors* / Q000494:pharmacology
D001639:Bicarbonates; D014660:Vasoactive Intestinal Peptide; D015232:Dinoprostone; D006851:Hydrochloric Acid