Atropine effects on Gastrin and Histamin! - USMLE Forums
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Old 12-18-2011
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GIT Atropine effects on Gastrin and Histamin!

Can any one vouch for this question from Kqbank:

If I apply Atropine to regulate gastric acid secretion is it true that doing so would decrease Gastrin, AcH, and Histamine?

I was under the impression that AcH decreased, Histamine and Gastrin unaffected.

The explanation states that the 3 above are multiplicative, or synergistic effect on acid secretion by parietal cells. So decreasing one decreases the others (but then why do we not state that Gastrin decreases not only with acidic pH in stomach, and with drug blocked of AcH or Histamine actions?).

Last edited by gear2d; 12-18-2011 at 06:41 PM. Reason: typo
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Old 12-18-2011
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Atropine blocks vagal stimulation, this is the M3 receptor where ACh normally acts on. It will not affect gastrin and histamine. In gastrin case it is stimulated by GRP on G cells.

Vagus --> GRP --> G cells --> Gastrin --> Gq

Vagus -->ACh --(ATROPINE BLOCK)-> M3 receptor --> Gq

Atropine is a muscarinic antagonist
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Old 01-02-2012
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Correct Answer

I could explain why Histamine and Ach will both decrease but not sure of Gastrin:
1 ) (+)Vagus-->(+)M3 recep/AcH-->on Parietal cells-->Hcl
2 ) (+)Vagus-->(+)M3 recep/AcH-->on ECL cells--> Histamine---Hcl
3 ) (+)Vagus-->(+)M1 rec/ (neurotransmitter ???)-->ECL cells--> Histamine---Hcl
4a) (+)VAgus-->(+)M3 recep/AcH-->on D cells in body-->somatostatins -->on ECL cells--> Histamine---Hcl
4b) (+)Vagus-->(+)M3recep/AcH-->on D cells in antrum-->somatostatins -- >Inhibition of G cells --> gastrin secretion

Thus, muscarinic antagonist (eg Atropine) blocks both the M1 and M3 receptors on the different cells and consequently decreased histamine,Ach and gastrin as seen in 1), 2), 3), 4a) and 4b) respectively.

check the schema:
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Old 03-06-2012
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Please look at the following link:

Unlike vagally mediated gastric acid secretion and pancreatic polypeptide release which can be blocked by atropine, vagal gastrin release is potentiated by atropine. This observation suggests the existence of a vagal-cholinergic pathway which normally (i.e., in the absence of atropine) inhibits gastrin release. (b) Because atropine (without sham feeding) increased basal gastrin levels, it is likely that the cholinergic pathway which inhibits gastrin release is active even when the vagus nerve is not stimulated by sham feeding.

However, in another link it was mentioned that atropine does not block the vagal effect on gastrin release.
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Gastrointestinal-Tract-, Pharmacology-, Physiology-

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