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Abstract
Atrial natriuretic peptide (ANP), sodium nitroprusside and hydroxylamine increased cGMP accumulation in rat parotid acinar cells both in the presence and absence of forskolin but in a different manner. On the other hand, ANP decreased forskolin-stimulated cAMP accumulation, although sodium nitroprusside and hydroxylamine had no effect on cAMP accumulation. Amylase release stimulated by forskolin, dibutyryl-cAMP or isoproterenol was depressed by ANP, whereas sodium nitroprusside and hydroxylamine did not evoke the inhibition of forskolin-stimulated amylase release. These results suggest that the inhibition of cAMP accumulation and of amylase release by ANP were not mediated via cGMP produced by guanylate cyclase-A.
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