Pharmacological investigations of the mechanisms underlying the effects of peripheral 5-HT on flavour consumption and preference.

Systemic administration of serotonin (5-hydroxytryptamine, 5-HT) to non-deprived rats increased saline (0.9%) consumption (5-HT hyperdipsia), without altering saline preference in two-bottle test. When sodium saccharin (0.1%) was the test solution 5-HT suppressed both consumption and preference. 5-HT saline hyperdipsia was blocked by pretreatment with an angiotensin I converting enzyme inhibitor (MK421) and mimicked by isoprenaline-induced stimulation of renin production; saccharin consumption and preference were unaffected by either drug. However, methysergide (a 5-HT antagonist) attenuated the effects of 5-HT on saccharin consumption and preference, thus confirming that these effects are mediated via peripheral 5-HT receptors. It is suggested that the effects of 5-HT on saline consumption are mediated via stimulation of the renin-angiotensin system, but its effects on saccharin consumption and preference are mediated by a separate mechanism at some point subsequent to peripheral 5-HT receptors.