Augmentation of isoproterenol-stimulated tissue cyclic AMP level by cholinergic agonists in rat parotid gland.

Abstract

It was found that methacholine and carbamylcholine, in addition to their known inhibitory effect, augmented the effect of isoproterenol on tissue cyclic AMP accumulation. The effect of methacholine was dose dependent, and significant augmentation was obtained at 0.1 µM with the maximum being attained at about 0.5 µM, whereas more than 10 , LM were required to obtain the inhibitory effect.

Augmentation and inhibition of .BETA.-adrenergic agonists-stimulated tissue cyclic AMP accumulation by .ALPHA.-adrenergic agonists in rat parotid gland.

“…These results are consistent with our previous observations which showed that norepinephrinestimulated parotid cyclic AMP accumulation is decreased in the presence of phentolamine (YOSHIMuRA et al, 1985). The augmentation induced by phenylephrine was almost completely abolished by omission of calcium in the medium.…”

“…As reported in our previous paper (YOSHIMURA et al, 1985), the peak level of tissue cyclic AMP was usually attained at about 2 min after the addition of isoproterenol (the shortest time point examined). The tissue cyclic AMP level declined rapidly thereafter and reached a level only about 2-fold greater than the basal one (the level before the addition of isoproterenol).…”

“…An important issue is the mechanism of action of the increased calcium in the cell. Previously we have suggested (YOSHIMURA et al, 1985) that the increased calcium in the cell induced by cholinergic agonists and A23187 may act by modulating the process leading to the activation of adenylate cyclase and that cholinergic agonists augment norepinephrine-stimulated cyclic AMP accumulation in the presence, but not in the absence, of phentolamine. These results suggest that the augmentation induced by a-adrenergic agonist, like that by cholinergic agonists and A23187, may be mediated by the activation of adenylate cyclase.…”

“…In the previous paper (YOSHIMURA et al, 1985), however, we reported that muscarinic cholinergic agonists such as carbamylcholine and methacholine, in addition to their inhibitory effect on isoproterenol-stimulated tissue cyclic AMP accumulation, augment the effect of isoproterenol on tissue cyclic AMP accumulation in the rat parotid slices and suggested that the augmentation is mediated by an increase in influx of extracellular calcium into the cell. In the same paper we also showed that muscarinic cholinergic agonists do not augment the effect of norepinephrine on tissue cyclic AMP accumulation, but they significantly augment the effect of norepinephine on tissue cyclic AMP accumulation in the presence of phentolamine, an a-adrenergic antagonist.…”

Simulation of Regulated Exocytosis of Amylase from Salivary Parotid Acinar Cells by a Consecutive Reaction Model Comprising Two Sequential First-order Reactions

“…Protein exocytosis is induced mainly by intracellular cAMP while #uid secretion results from elevation of intracellular free calcium. Intracellular calcium also induces small amounts of amylase secretion (Putney, 1986;Yoshimura & Nezu, 1992). Yoshimura et al developed a perfusion system which shows the velocity of amylase release in 30 s increments (Yoshimura & Nezu, 1991;.…”