Mammalian bombesin-like peptides suppress sham drinking of salt by sodium-deficient rats.

Bombesin (BN) and its mammalian relatives, gastrin-releasing peptide (GRP) and neuromedin B (NMB), have been implicated in the control of food intake, and more recently systemic injections of BN have been shown to suppress need-free and sodium deficiency-induced salt (NaCl) intake. Postoral mechanisms that are activated by the ingestion of salt contribute to the termination of salt intake. The hypothesis that BN-like peptides potentiate postoral salt ingestion-contingent feedback and thereby accelerate the termination of salt intake was evaluated by measuring the effects of peripheral injections of BN (4, 6, 16 micrograms/kg), GRP (4, 8, 16 micrograms/kg), and NMB (4, 8, 16 micrograms/kg) on sham (gastric fistula open) and normal (gastric fistula closed) drinking of NaCl (0.5 M) by sodium-deficient male rats. Sodium deficiency was induced by injections of deoxy-corticosterone acetate and furosemide. Injections of 4 micrograms/kg BN produced a transient suppression in the sham drinking of salt and a more sustained reduction of salt intake when postoral factors were present in the normal drinking condition. In contrast, injections of 6 and 16 micrograms/kg BN produced the same pronounced suppression in salt intake in both the closed and open fistula test conditions. Only 16 micrograms/kg GRP was behaviorally effective, and this des: reliably suppressed both normal and sham drinking of salt. On an equimolar basis, BN was more potent than GRP. Injections of NMB had no effect on salt intake under any dose or fistula condition. The order of BN-like peptide potency in suppressing sham and normal drinking of salt by sodium-deficient rats (BN > GRP > NMB) is similar to the peptides' effects on feeding. When postoral feedback is minimized, the combination of BN or GRP and pregastric stimuli mimic the salt intake by rats in the fistula closed, normal drinking condition.