Central blood pressure effects of substance P and angiotensin II: Role of the sympathetic nervous system and vasopressin

The role of the sympathetic nervous systme and of arginine vasopressine (AVP) in the mediation of the central cardiovascular effects of angitotensin II (ANG II) and substance P (SP) was investigated. ANG II and SP caused dose-dependent blood pressure increases when injected into the lateral brain ventricle (i.c.v.) of conscious rats; ANG II was tenfold more potent than SP. Peripheral blockade of α-adrenoceptors with prazosin or blockade of the vasopressor action of AVP by the AVP antagonist d(CH₂)₅ VDAVP both partially inhibited the pressor responses to central ANG II. Combined treatment with the two blockers produced almost complete inhibition of the central ANG II responses. Substance P injected i.c.v. produced increases in noradrenaline and adrenaline but not AVP in the plasma. Peripheral α-receptor blockade by prazosin reversed the central pressor effects of SP to depressor responses. The AVP antagonist did not alter the cardiovascular responses to SP. It is concluded that in onscious animals, stimulation of the sympathetic nervous system and release of AVP contribute to the central pressor action of ANG II to a similar extent and independently of each other. In contrast, the central pressor responses to SP appear to be exclusively mediated by the sympathetic nervous system without participation of AVP.