Endogenous histamine contributes to drinking initiated without postprandial challenges to fluid homeostasis in rats.

A role for endogenous histamine and its receptor subtypes for mediating drinking elicited by eating was examined in adult male Sprague-Dawley rats in two experimental paradigms in which drinking was initiated without accompanying change in systemic fluid balance: (a) nondeprived rats eating a small (0.57 g) salted cracker; (b) nondeprived rats receiving IG infusion (through a chronic gastric catheter) of 2 ml 900 mOsm/kg NaCl. The ability of i.p., s.c., or ICV (through a surgically implanted chronic cannula in a lateral ventricle) injections of antagonists to H1, H2, or H3 receptors for histamine to inhibit drinking was examined. For rats ingesting a small cracker: systemic injection of H1 antagonists dexbrompheniramine (DXB) or pyrilamine (PYR) delayed the latency to initiate drinking. Systemic injection of H1 antagonists DXB, PYR, or terfenadine (TER; which fails to penetrate the blood-brain barrier) and ICV injection of DXB or PYR inhibited water intake. The H2 antagonist cimetidine (C) given i.p. or ICV failed to affect drinking. The H3 antagonist thioperamide (Th) given s.c. or ICV delayed the latency to drink and inhibited water intake. For rats receiving IG NaCl: systemic injection of H1 antagonists DXB or PYR or the H3 antagonist Th inhibited water intake, but the H2 antagonist C failed to inhibit drinking. Our findings extend the evidence for the involvement of endogenous histamine in drinking elicited by eating in rats by suggesting roles for peripheral and brain H1 and H3 receptors for drinking initiated by postprandial gastrointestinal osmotic consequences that are subthreshold for changes in systemic fluid balance.