PT  - JOURNAL ARTICLE
AU  - G B Glavin
AU  - M A Carlisle
AU  - D D Smyth
TI  - Agmatine, an endogenous imidazoline receptor agonist, increases gastric secretion and worsens experimental gastric mucosal injury in rats.
DP  - 1995 Aug 01
TA  - Journal of Pharmacology and Experimental Therapeutics
PG  - 741--744
VI  - 274
IP  - 2
4099  - http://jpet.aspetjournals.org/content/274/2/741.short
4100  - http://jpet.aspetjournals.org/content/274/2/741.full
SO  - J Pharmacol Exp Ther1995 Aug 01; 274
AB  - The present experiments tested the actions of a putative endogenous imidazoline receptor agonist, agmatine, on gastric secretion and on experimental gastric mucosal injury in rats. Agmatine, given i.p. (0.5-20.0 mg/kg) or i.c.v. (0.5-2.5 micrograms), augmented basal gastric acid secretion in conscious rats to a maximum of 40% when given i.p. and 44% when given i.c.v. Agmatine also potentiated total secretory volume as well as gastric acid and pepsin output in pylorus-ligated rats. When administered before exposure to stress, agmatine significantly decreased gastric glandular mucus levels and exacerbated stress-induced gastric mucosal injury. These results are in contrast to our data showing that an exogenous agonist of I1-imidazoline receptors, moxonidine, is a potent antisecretory and gastroprotective agent. A precise physiological role for agmatine in blood pressure regulation and in gastrointestinal function awaits clarification. However, it is possible that agmatine functions as an "inverse agonist" at central imidazoline receptors, resulting in hypertension, augmented gastric secretion and exacerbated gastric mucosal injury.