ENHANCEMENT OF CENTRAL PRESSOR EFFECT OF AVP IN SHR AND WKY RATS BY INTRACRANIAL N-G-NITRO-L-ARGININE

The aim of the present study was to find out whether brain nitroxiderg ic system may be involved in modulation of central cardiovascular effe cts of arginine vasopressin (AVP) in normotensive (WKY) rats and wheth er its regulatory effects are altered in spontaneously hypertensive (S HR) rats. Two series of experiments were performed on conscious WKY an d SHR rats instrumented with the lateral cerebral ventricle (i.c.v.) c annula and with the femoral arterial catheters. In Series 1 (10 WKY, 7 SHR rats), i.c.v. application of 2.3 nmol (0.5 mu g) of N-G-nitro-L-a rginine (L-NNA), an inhibitor of NO synthesis, did not significantly a ffect baseline arterial blood pressure (MAP) and heart rate (HR). In W KY but not in SHR, i.c.v. administration of 5.8 nmol (1 mu g) of L-arg inine (L-ARG) elicited a small, significant decrease of MAP (P < 0.05) which could be reversed by i.c.v. pretreatment with L-NNA. In Series 2 (7 WKY, 8 SHR), administration of 10 pmol of AVP (10 ng) resulted in significant presser effect in both strains; MAP increase being signif icantly greater in SHR than in WKY rats (P < 0.05). I.c.v. pretreatmen t with L-NNA significantly intensified the presser response to central ly applied AVP both in WKY (P < 0.01) and in SHR (P < 0.01) rats; the maximum increase of blood pressure to combined administration of L-NNA and AVP being significantly greater in SHR than in WKY rats. The resu lts indicate existence of an interaction between the central vasopress inergic and nitroxidergic system in blood pressure regulation. It is s uggested that centrally released AVP increases availability of nitric oxide in the brain cardiovascular regions, whereas NO plays a compensa tory role by reducing central presser effect of AVP. Effectiveness of this compensatory mechanism is enhanced in the SHR rats.