Abstract 403: Metabolic Characteristics of Spontaneously Hypertensive Rats Compared With Normotensive Controls
Objectives: To differentiate the metabolic responses of spontaneously hypertensive rats (SHR) compared to normotensive Wistar Kyoto (WKY) rats.
Methods: Blood pressure and pulse wave velocity (PWV) measurements were conducted on 25 week old SHR and WKY rats. At the time of termination, vital organs were harvested and weighed, and serum was collected for analysis of blood lipids, liver enzymes, and urea levels.
Results: SHR exhibited higher readings for mean arterial pressure (MAP) (p< 0.0001), peak velocity (PWV) (p=0.017), heart/body weight (BW) ratio (p<0.0001), and left ventricular wall/BW ratio (p<0.0001) compared to WKY. WKY displayed higher weight gain and blood lipid levels (serum triglycerides, total cholesterol, LDL-C, and HDL-C) compared to SHR (p<0.0001). Blood lipid levels were positively correlated with weight gain, and negatively correlated with MAP and left ventricular wall/body weight ratio. Weight gain and MAP were negatively correlated (r=-0.60, p<0.0001). Serum AST levels were higher among SHR compared to WKY (p=0.026), and serum AST was positively correlated with left ventricular wall/BW ratio (r=0.35, p=0.030). There was no correlation between AST levels and liver/BW ratio or MAP. Serum urea levels were higher among SHR compared to WKY (p=0.0032), and positively correlated with MAP (r=0.42, p=0.011) and heart/BW ratio (r=0.43, p=0.0096). There were no differences in kidney/BW ratios, however, the peri-renal adipose/BW ratio was lower in SHR compared to WKY (p=0.001), and negatively correlated with MAP (r=-0.41, p=0.018).
Conclusion: The positive relationship between serum AST and left ventricular wall/BW ratio, but not liver/BW ratio, suggests a possible response to changes in cardiac muscle, independent of blood pressure. Serum urea levels responded to MAP and heart/BW ratio. These metabolic responses of SHR compared to WKY invite further investigation of possible mechanisms underlying the link with cardiovascular dysfunction.
Author Disclosures: J. Clark: None. P. Zahradka: None. C. Taylor: None.
- © 2014 by American Heart Association, Inc.