Atrial Natriuretic Factor-Induced Amylase Output in the Rat Parotid Gland Appears to be Mediated by the Inositol Phosphate Pathway

Gi-1/Gi-2-dependent signaling by single-transmembrane natriuretic peptide clearance receptor

“…125 I-ANP binding was partially inhibited by the selective NPR-C ligand cANP-(4-23) and VIP, and this reflected the component of 125 I-ANP binding to NPR-C. 125 I-VIP binding was partially inhibited by ANP and cANP- (4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23), and this reflected the component of 125 I-VIP binding to NPR-C. The pattern of binding to tenia coli muscle cells was similar to that observed in gastric muscle cells (23).…”

“…We examined the ability of NPR-C to activate other effector enzymes in eNOS-deficient tenia coli smooth muscle cells; these cells expressed NPR-C and NPR-B but not NPR-A. Atrial natriuretic peptide (ANP), the selective NPR-C ligand cANP- (4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23), and vasoactive intestinal peptide (VIP) inhibited 125 I-ANP and 125 I-VIP binding to muscle membranes in a pattern indicating high-affinity binding to NPR-C. Interaction of VIP with NPR-C was confirmed by its ability to inhibit 125 I-ANP binding to membranes of NPR-C-transfected COS-1 cells. In tenia muscle cells, all ligands selectively activated G i-1 and G i-2 ; VIP also activated G s via VIP 2 receptors.…”

“…In tenia muscle cells, all ligands selectively activated G i-1 and G i-2 ; VIP also activated G s via VIP 2 receptors. All ligands stimulated phosphoinositide hydrolysis, which was inhibited by ANP- (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11), PTx, and antibodies to phospholipase C-␤3 (PLC-␤3) and G␤. cANP-(4-23) contracted tenia muscle cells; contraction was blocked by U-73122 and PTx and by antibodies to PLC-␤3 and G␤ in intact and permeabilized muscle cells, respectively.…”

“…A synthetic peptide consisting of the 37-amino acid intracellular sequence of NPR-C inhibited adenylyl cyclase activity in cardiac muscle membranes (4). cANP- (4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23) and/or ANP also stimulated phosphoinositide (PI) hydrolysis in aortic smooth muscle membranes (10) and isolated parotid acinar cells (6), suggesting G proteindependent activation of other effector enzymes [e.g., phospholipase C-␤ (PLC-␤)]. Our recent studies (23,30) showed that both ANP and cANP-(4-23) activate nitric oxide synthase (NOS) and stimulate nitric oxide (NO) formation in gastric smooth muscle cells that express endothelial NOS (eNOS).…”

Natriuretic peptides and their receptors

“…The participation of ANF in the regulation of gastrointestinal physiology is supported by the finding that ANF gene expression varies according to feeding and fasting conditions (17). Studies from our laboratory reported that centrally or peripherally applied ANF and CNP exert biological actions mainly through NPR-C activation in the liver, pancreas and salivary glands and NPRA/NPRB in the central nervous system (6,7,(47)(48)(49)(50)(51)(52)(53)61). Other gastrointestinal effects reported for ANF include regulation of intestinal motility and secretion as well as gastric acid secretion (9,29).…”