Article date: February 1995
By: Gary B. Glavin, Donald D. Smyth, in Volume 114, Issue 4, pages 751-754
Previous reports of the effects of α2‐adrenoceptor stimulation on gastric secretion are inconsistent because it was not clear whether the compounds were activating α2‐adrenoceptors and/or newly described imidazoline receptors. In the present experiments, the effects of moxonidine, an I1‐imidazoline receptor agonist and antihypertensive agent, on gastric secretion and on experimental gastric mucosal injury were examined.
Moxonidine (0.01, 0.1 and 1.0 mg kg−1, i.p.) potently inhibited basal (non‐stimulated) gastric acid secretion in conscious rats with an ED50 of 0.04 mg kg−1. Two hours following administration of the highest dose of moxonidine (1.0 mg kg−1), gastric acid output was completely suppressed. Moxonidine also significantly increased intragastric pH, at the two highest doses.
The α2‐adrenoceptor agonist, clonidine (0.01, 0.1 and 1.0 mg kg−1, i.p.) decreased basal acid secretion at the lowest dose (37%) and at the highest dose (46%), while the intermediate dose did not affect gastric acid output.
In an ethanol‐induced model of gastric mucosal injury, moxonidine decreased the length of lesions at the lowest and highest doses (0.01 and 1.0 mg kg−1) as well as the number of the lesions, at the highest dose (1.0 mg kg−1).
In pylorus‐ligated rats, moxonidine significantly decreased acid secretion (all doses), total secretory volume (1.0 mg kg−1) as well as pepsin output (1.0 mg kg−1).
In comparison to clonidine, moxonidine appears to be a more potent anti‐secretory and gastric‐protective compound. These data indicate a potential role for imidazoline receptor agonists in the management of gastroduodenal diseases associated with hypertension. The relative contribution of the central and peripheral effects of moxonidine to these gastrointestinal actions remains to be determined.
Previous reports of the effects of α2‐adrenoceptor stimulation on gastric secretion are inconsistent because it was not clear whether the compounds were activating α2‐adrenoceptors and/or newly described imidazoline receptors. In the present experiments, the effects of moxonidine, an I1‐imidazoline receptor agonist and antihypertensive agent, on gastric secretion and on experimental gastric mucosal injury were examined.
Moxonidine (0.01, 0.1 and 1.0 mg kg−1, i.p.) potently inhibited basal (non‐stimulated) gastric acid secretion in conscious rats with an ED50 of 0.04 mg kg−1. Two hours following administration of the highest dose of moxonidine (1.0 mg kg−1), gastric acid output was completely suppressed. Moxonidine also significantly increased intragastric pH, at the two highest doses.
The α2‐adrenoceptor agonist, clonidine (0.01, 0.1 and 1.0 mg kg−1, i.p.) decreased basal acid secretion at the lowest dose (37%) and at the highest dose (46%), while the intermediate dose did not affect gastric acid output.
In an ethanol‐induced model of gastric mucosal injury, moxonidine decreased the length of lesions at the lowest and highest doses (0.01 and 1.0 mg kg−1) as well as the number of the lesions, at the highest dose (1.0 mg kg−1).
In pylorus‐ligated rats, moxonidine significantly decreased acid secretion (all doses), total secretory volume (1.0 mg kg−1) as well as pepsin output (1.0 mg kg−1).
In comparison to clonidine, moxonidine appears to be a more potent anti‐secretory and gastric‐protective compound. These data indicate a potential role for imidazoline receptor agonists in the management of gastroduodenal diseases associated with hypertension. The relative contribution of the central and peripheral effects of moxonidine to these gastrointestinal actions remains to be determined.
DOI: 10.1111/j.1476-5381.1995.tb13268.x
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