Oct 1, 1989

Convergence of cAMP and phosphoinositide pathways during rat parotid secretion

The American Journal of Physiology
J S McKinneyR P Rubin

Abstract

Rat parotid acinar cells were employed to investigate the mechanism by which receptor agonists that activate the phosphoinositide pathway enhance the stimulatory effects of adenosine 3',5'-cyclic monophosphate (cAMP) on amylase secretion. Norepinephrine (NE), which activates both alpha- and beta-adrenoceptors, evoked a secretory response that was greater than the sum of the responses obtained when NE was employed as a beta-agonist (in the presence of prazosin) and as an alpha-agonist (in the presence of propranolol). The enhancement of amylase secretion induced by NE was accompanied by an augmented rise in Ca2+ influx, as determined by fura-2 analysis. NE-induced cAMP production was comparable to that evoked by NE as a beta-agonist, and the accumulation of [3H]inositol 1,4,5-trisphosphate (IP3) evoked by NE was comparable to that elicited by NE as an alpha-agonist. The beta-adrenoceptor agonist isoproterenol potentiated the rise in cytosolic Ca2+ elicited by the muscarinic agonist carbachol, while possessing no stimulatory effect of its own. Isoproterenol had no effect on carbachol-induced stimulation of [3H]IP3 or 1,3,4,5-[3H]inositol tetrakisphosphate accumulation. Ionomycin and dibutyryl cAMP in combination produced a simila...Continue Reading

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Mentioned in this Paper

Inositol Phosphates
Biochemical Pathway
Phosphatidylinositols
Adenosine
Calcium
August Rats
Phosphoinositide Pathway
Adrenergic beta-Agonists
Norepinephrine, (+, -)-Isomer
Process of Secretion

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