VASOACTIVE INTESTINAL PEPTIDE CONTROL OF RENAL ADENYLATE CYCLASE: IN VITRO STUDIES OF CANINE RENAL MEMBRANES AND CULTURED CANINE RENAL EPITHELIAL (MDCK) CELLS

Vasoactive intestinal peptide (VIP) has been shown to stimulate adenylate cyclase activity in plasma membranes isolated from canine renal cortex, outer and inner medulla in vitro. Though related hormones such as glucagon also stimulate adenylate cyclase in these membrane preparations, it is likely t...

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Bibliographic Details
Published in:Experimental physiology 1989-05, Vol.74 (3), p.339-353
Main Authors: Griffiths, N. M., Simmons, N. L., Rugg, E. L.
Format: Article
Language:English
Subjects:
Adenylyl Cyclases - metabolism
Animals
Cell Line
Colforsin - pharmacology
Cyclic AMP - metabolism
Dogs
Epithelial Cells
Epithelium - drug effects
Epithelium - enzymology
Glucagon - pharmacology
Kidney - cytology
Kidney - drug effects
Kidney - enzymology
Vasoactive Intestinal Peptide - pharmacology
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Summary:Vasoactive intestinal peptide (VIP) has been shown to stimulate adenylate cyclase activity in plasma membranes isolated from canine renal cortex, outer and inner medulla in vitro. Though related hormones such as glucagon also stimulate adenylate cyclase in these membrane preparations, it is likely that VIP interacts with specific VIP receptors since the VIP receptor antagonist, (4Cl-D-Phe 6 , Leu 17 )-VIP, is capable of reducing the response to VIP, but not that to glucagon. Also binding of 125 I-VIP to cortical renal plasma membranes shows competition by unlabelled VIP, but not by glucagon. Strain 1 (and clone CL 8 l b cells derived from the established cultured dog kidney cell line, MDCK, have been shown also to respond selectively to VIP by an increase in adenylate cyclase activity and cyclic AMP accumulation in intact cells. A physiological correlate of VIP activation of adenylate cyclase has been sought by addition of VIP to reconstituted epithelial monolayers of strain 1 MDCK cells clamped in Ussing chambers. VIP addition to the basal-lateral cell aspects generates an inward short-circuit current that is sensitive to replacement of medium Cl - by NO 3 - , and to inhibition by the Cl - channel blocker, 3-nitro-2(3-phenylpropylamino)-benzoic acid, consistent with VIP stimulation of transepithelial Cl - secretion.
ISSN:0958-0670
0144-8757
1469-445X
DOI:10.1113/expphysiol.1989.sp003276