High salt intake elevates the prolonged blood pressure and renal sympathetic nerve activity response to intracerebroventricle angiotensin II infusion

University College London 2006 (2006) Proc Physiol Soc 3, C94

Oral Communications: High salt intake elevates the prolonged blood pressure and renal sympathetic nerve activity response to intracerebroventricle angiotensin II infusion

Belinda Lee Houghton1, Chunlong Huang1, Edward J Johns1

1. Physiology, BioSciences Institute, University College Cork, Cork, Ireland.

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Sodium intake, central angiotensin II (ANG II), and autonomic control of the cardiovascular system may be linked. AT1 receptor expression in the brain is upregulated by elevated sodium intake (Wang et al. 2003) and impacts on sympathetically mediated renal function (Huang & Johns, 1998). This may lead to a prolonged elevation in BP and renal sympathetic nerve activity (RSNA). We hypothesised that the prolonged BP and RSNA response to intracerebroventricle (ICV) ANGII infusion would be augmented in rats treated on a high salt (HS) diet versus a low salt (LS) diet. Four week old male Wistar rats were treated on a HS (3.0% NaCl, n=5) or LS (0.03% NaCl, n=5) diet for 6 weeks. Each animal was anaesthetised by 16.5mg/250ml chloralose/urethane I.P. injection. Cannulae were inserted into the right femoral artery (BP measurement) and vein (saline/anaesthetic infusion). A guide cannula was placed into the right lateral ICV for ANGII infusion (25ng/μl, 1 μl/min, 2 min). The left kidney was exposed and recording electrodes were sealed onto a renal nerve. BP and RSNA were averaged over a 5 min period during baseline measurements and 30 min post ICV infusion. Five minutes post ICV infusion, BP and RSNA were averaged over a 1 min period. RSNA was calculated as percentage of baseline values. Means ± S.E.M. were compared by ANOVA. Linear regression analysis compared %ΔRSNA versus %ΔBP at 30 min post ICV infusion. P<0.05 indicated significance. Baseline BP was similar between groups (HS: 89±3mmHg, LS: 84±3mmHg). Five minutes post ICV ANGII infusion, both groups showed a sharp increase in BP (HS ΔBP: 16±3 mmHg, LS ΔBP: 10±1 mmHg, P<0.05 for both groups) and reflex reduction in RSNA (HS RSNA: 88 ± 3%, LS RSNA: 78 ± 8%, P<0.05 for both groups). Thirty minutes post infusion, only the HS group showed an elevation in BP (HS ΔBP: 5.5±0.4mmHg, P<0.05, LS ΔBP: 4±2 mmHg) and RSNA (HS RSNA: 113 ± 2%, P<0.05, LS RSNA: 100 ± 3%) compared to baseline values. There was also positive linear relationship between % ΔRSNA versus % ΔBP in the HS group (r2=0.84, P<0.05), but not in the LS group (r2=0.009). Following ICV ANGII infusion, both groups exhibited an initial baroreflex response characterised by a sharp rise in BP and fall in RSNA. The HS group further showed a prolonged secondary response characterised by a concurrent elevation in BP and RSNA. These results suggest that chronic high dietary salt intake can elicit a uniquely biphasic response to ICV ANGII infusion.



Where applicable, experiments conform with Society ethical requirements.

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