Drugs that, directly or indirectly produce activation of serotonin (5-
HT) receptors increase plasma concentrations of both prolactin and ren
in. The serotonergic regulation of prolactin and renin secretion share
several common characteristics. Serotonergic neurons originating in t
he dorsal raphe and terminating in the hypothalamus stimulate the secr
etion of both prolactin and renin. Destruction of cells in the hypotha
lamic paraventricular nucleus (PVN) inhibits both the prolactin and re
nin responses to 5-HT agonists and 5-HT-releasing drugs. Activation of
5-HT2 receptors increases the secretion of both prolactin and renin,
while activation of other 5-HT receptor subtypes has differential effe
cts on these hormones. However, there are also differences between the
serotonergic mechanisms that regulate the secretion of prolactin and
renin. Activation of 5-HT1A receptors increases the secretion of prola
ctin but not of renin. In addition, activation of peripheral 5-HT3 rec
eptors stimulates the secretion of renin, while activation of peripher
al 5-HT3 receptors increases plasma levels of prolactin but not renin.
In humans, the effect of 5-HT-releasing drugs and 5-HT agonists on pl
asma prolactin concentrations has been studied to a greater extent tha
n effects on most other hormones. In contrast, the renin response to 5
-HT agonists and 5-HT releasers has not been well characterized in hum
ans. Because of the important role of the renin-angiotensin system in
cardiovascular regulation, studies on the serotonergic regulation of r
enin release in humans could increase our understanding of cardiovascu
lar disorders associated with altered serotonergic function. Examples
include anxiety and consequences of cocaine abuse. In conclusion, comp
aring the serotonergic regulation of prolactin and renin secretion ind
icates similarities that might shed light on common brain mechanisms t
hat regulate neuroendocrine function.