In this study we investigated the influence of d(CH2)5-Tyr(Me)-[Arg8]
vasopressin (
AAVP) and [adamanteanacetyl1,0-ET-d-Tyr2,Val4,aminobutyryl6,Arg8,9]-[Arg8]
vasopressin (ATAVP), which are antagonists of
vasopressin V1 and
V2 receptors, and the effects of
losartan, a selective
angiotensin AT1 receptor antagonist, and
CGP42112A, a selective AT2 receptor antagonist, injected into the lateral septal area (LSA) on thirst and
hypertension induced by [Arg8]
vasopressin (AVP).
AAVP and ATAVP injected into the LSA reduced the drinking responses elicited by injecting AVP into the LSA. Both the AT1 and AT2
ligands administered into the LSA elicited a concentration-dependent decrease in the water intake induced by AVP injected into the LSA, but
losartan was more effective than
CGP42112A. The increase in MAP, due to injection of AVP into the LSA, was reduced by prior injection of
AAVP from 18 +/- 1 to 6 +/- 1 mm Hg.
Losartan injected into the LSA prior to AVP reduced the increase in MAP to 7 +/- 0.8 mm Hg. ATAVP and
CGP42112A produced no changes in the pressor effect of AVP. These results suggest that the dipsogenic effects induced by injecting AVP into the LSA were mediated primarily by AT1 receptors. However, doses of
losartan were more effective when combined with
CGP42112A than when given alone, suggesting that the thirst induced by AVP
injections into LSA may involve activation of multiple AVP and
angiotensin II receptor subtypes. The pressor response of AVP was reduced by
losartan and by
AAVP.
CGP42112A and ATAVP did not change the AVP pressor response. These results suggest that facilitator effects of AVP on water intake are mediated through the activation of
V1 receptors and that the inhibitory effect requires
V2 receptors. The involvement of AT1 and AT2 receptors can be postulated. Based on the present findings, we suggest that the AVP in the LSA may play a role in the control of water and arterial blood pressure balance.