Nitric oxide-dependent in vitro secretion of amylase from innervated or chronically denervated parotid glands of the rat in response to isoprenaline and vasoactive intestinal peptide.
The basal in vitro release of amylase was similar from rat parotid lobules of innervated and chronically denervated glands and was unaffected by the inhibitors used in this study. The secretion of amylase induced by isoprenaline or vasoactive intestinal peptide (VIP) was reduced by one-third to one-half from the lobules of the innervated glands and even more so from the lobules of the denervated glands by ODQ, an inhibitor of soluble guanyl cyclase which is activated by nitric oxide (NO) and catalyses the cGMP production. The use of N (omega)-propyl-L-arginine (N-PLA) revealed that the evoked secretion of amylase in the denervated glands depended on the activity of neuronal type NO synthase to synthesize NO. Since the denervated gland is virtually devoid of NO synthase-containing nerve fibres, the neuronal type NO synthase was most probably of a non-neuronal source. NO-dependent amylase secretion was agonist related, since amylase secretion evoked by bethanechol and neuropeptide Y was not reduced by ODQ or N-PLA. Hence, under physiological conditions, activation of beta-adrenoceptors (sympathetic activity) and VIP receptors (parasympathetic activity) is likely to cause secretion of parotid amylase partly through a NO/cGMP-dependent intracellular pathway involving the activity of neuronal type NO synthase, possibly of acinar origin.
Department of Pharmacology, Sahlgrenska Academy at Göteborg University, Medicinaregatan 15 D, Göteborg 413 90, Sweden.
Shariel
S
Sayardoust
J
J
Ekström
D000318:Adrenergic beta-Agonists / Q000494:pharmacology*; D000681:Amylases / Q000378:metabolism*; D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives* / Q000494:pharmacology; D017763:Autonomic Denervation; D018723:Bethanechol / Q000494:pharmacology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D005765:Gastrointestinal Agents / Q000494:pharmacology*; D006162:Guanylate Cyclase / Q000037:antagonists & inhibitors; D066298:In Vitro Techniques; D007545:Isoproterenol / Q000494:pharmacology*; D009478:Neuropeptide Y / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D010069:Oxadiazoles / Q000494:pharmacology; D010277:Parasympathomimetics / Q000494:pharmacology; D010306:Parotid Gland / Q000187:drug effects / Q000294:innervation / Q000378:metabolism*; D011810:Quinoxalines / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D014660:Vasoactive Intestinal Peptide / Q000494:pharmacology*
C095284:1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one; D000318:Adrenergic beta-Agonists; D004791:Enzyme Inhibitors; D005765:Gastrointestinal Agents; C109116:N(omega)-propargylarginine; D009478:Neuropeptide Y; D010069:Oxadiazoles; D010277:Parasympathomimetics; D011810:Quinoxalines; D018723:Bethanechol; D009569:Nitric Oxide; D014660:Vasoactive Intestinal Peptide; D001120:Arginine; D019001:Nitric Oxide Synthase; D000681:Amylases; D006162:Guanylate Cyclase; D007545:Isoproterenol