Article date: May 2003
By: Lucila Busch, Enri Borda in Volume 139, Issue 2, pages 399-407
The mechanism and receptor subtypes involved in carbachol‐stimulated amylase release and its changes after castration were studied in parotid slices from male rats.
Carbachol induced both amylase release and inositol phosphate (IP) accumulation in parotid slices from control and castrated rats, but castration induced a decrease of carbachol maximal effect. The effect of castration was reverted by testosterone replacement.
The selective M1 and M3 muscarinic receptor antagonists, pirenzepine and 4‐diphenylacetoxy‐N‐methylpiperidine methiodide, respectively, inhibited carbachol‐stimulated amylase release and IP accumulation in a dose‐dependent manner in parotid slices from control and castrated rats.
A diminution of binding sites of muscarinic receptor in parotid membrane from castrated rats was observed. Competition binding assays showed that both, M1 and M3 muscarinic receptor subtypes are expressed in membranes of parotid glands from control and castrated rats, M3 being the greater population.
These results suggest that amylase release induced by carbachol in parotid slices is mediated by phosphoinositide accumulation. This mechanism appears to be triggered by the activation of M1 and M3 muscarinic receptor subtypes. Castration induced a decrease of the maximal effect of carbachol evoked amylase release and IP accumulation followed by a diminution in the number of parotid gland muscarinic acetylcholine receptors.
The mechanism and receptor subtypes involved in carbachol‐stimulated amylase release and its changes after castration were studied in parotid slices from male rats.
Carbachol induced both amylase release and inositol phosphate (IP) accumulation in parotid slices from control and castrated rats, but castration induced a decrease of carbachol maximal effect. The effect of castration was reverted by testosterone replacement.
The selective M1 and M3 muscarinic receptor antagonists, pirenzepine and 4‐diphenylacetoxy‐N‐methylpiperidine methiodide, respectively, inhibited carbachol‐stimulated amylase release and IP accumulation in a dose‐dependent manner in parotid slices from control and castrated rats.
A diminution of binding sites of muscarinic receptor in parotid membrane from castrated rats was observed. Competition binding assays showed that both, M1 and M3 muscarinic receptor subtypes are expressed in membranes of parotid glands from control and castrated rats, M3 being the greater population.
These results suggest that amylase release induced by carbachol in parotid slices is mediated by phosphoinositide accumulation. This mechanism appears to be triggered by the activation of M1 and M3 muscarinic receptor subtypes. Castration induced a decrease of the maximal effect of carbachol evoked amylase release and IP accumulation followed by a diminution in the number of parotid gland muscarinic acetylcholine receptors.
British Journal of Pharmacology (2003) 139, 399–407. doi:10.1038/sj.bjp.0705260
DOI: 10.1038/sj.bjp.0705260
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