Abstract

Four week old Wistar-Kyoto (WKY) rats were divided into two groups. The experimental group (n=7) was receiving a high sodium diet (3.28% Na) and the control group (n=7) a normal sodium diet (0.22% Na). After 8 weeks, subjects were chronically implanted with the lateral cerebral ventricle (LCV) cannulas and with the femoral artery catheters. Three series of experiments were carried out on the experimental and control groups. In each series mean arterial pressure (MAP) and heart rate (HR) were recorded for 10 min before and 30 min after the LCV infusion. In series 1 artificial cerebrospinal fluid (aCSF) was administered (2 µl/15 s). In series 2 AVP was infused (20 ng/2 µl aCSF/15 s). In series 3 V1a receptor antagonist (V1 ANT), d(CH2)5[Tyr(Me)2,Ala-NH29]AVP, was applied (80 ng/µl aCSF/15 s). There was no difference in baseline MAP and HR between the experimental and control groups. LCV infusion of aCSF had no effect on MAP and HR. LCV infusion of AVP produced a significant increase of MAP, which was greater in the group on the high sodium diet than in the group on normal sodium diet. The experimental group showed a longer hypertensive effect of centrally applied AVP in comparison to the control. LCV administration of V1 ANT did not exert a significant effect on circulatory parameters. These results suggest that the prolonged high sodium diet does not induce hypertension in WKY rats, but it enhances the pressor function of the central vasopressinergic system.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.