Abstract 128: Angiotensin II Evoked Increases in Blood Pressure and Inflammatory Mediators in Adiponectin-Deficient Mice

Abstract

Chronic low grade inflammation is considered a predisposing factor for vascular dysfunction and subsequent elevation of blood pressures. Adipose tissue is a well-known source of mediators that are proinflammatory. Adiponectin (APN) is one of the few proteins secreted by the adipose tissue that is known to have anti-inflammatory properties. APN deficiency has been shown to result in significant increases in the plasma levels of inflammatory mediators when provided with an appropriate stimulus. Our research question is does a proinflammatory milieu accelerate or potentiate the development of hypertension? Male wild type C57Bl/6J and adiponectin deficient (adipo-/-) mice (24-28 wks, 28-30g) were implanted with radiotelemeters (TA11PA-C10, DSI) for chronic measurement of blood pressures. The mice were allowed to recover from surgery and baseline blood pressures recorded for 7-10 days. These mice were then implanted subcutaneously with osmotic pumps containing Angiotensin II (ANGII, 800ng/kg/min) and blood pressures were recorded for another 14 days. Baseline blood pressures in the adiponectin deficient mice (105±2 mmHg, n=3) were significantly lower than that of wild type C57BL/6J mice (116±6, n=3). After 14 days, ANGII infusion increased the blood pressures to similar levels in adiponectin deficient( 144±10 mmHg) and the wild type mice (138±7 mmHg). In a separate group of mice, the effects of chronic ANGII infusion on plasma TNFalpha levels were evaluated using ELISA. After 14 days of infusion, plasma TNFalpha levels were similar in adiponectin deficient (5.30±0.97 pg/ml,n=3) and wild type (4.94±0.84 pg/ml, n=6) mice. The data suggest that adiponectin deficient mice were more susceptible to the prohypertensive effects of ANGII and the increases in blood pressures were not associated with significant differences in circulating inflammatory mediators such as TNFalpha.