Local RAS and inflammatory factors are involved in cardiovascular hypertrophy in spontaneously hypertensive rats.

The renin-angiotensin system (RAS) and inflammation may play a decisive role in hypertensive end organ damage (EOD) including left ventricular (LV) hypertrophy and vascular remodeling. It is not clear whether the local RAS and inflammatory factors are involved in hypertensive EOD, and which RAS or inflammatory factors (systematic or local) is more important in EOD. Hemodynamics, cardiovascular hypertrophy, angiotensin II (Ang II) concentration and inflammatory factors in spontaneously hypertensive rats (SHR) were measured. mRNA expression of tissue RAS and inflammatory factors in SHR was assayed by real-time PCR. The independent effects and relative importance of hemodynamic factors and mRNA expression of RAS and inflammatory factors in local tissue on cardiovascular hypertrophy were assessed by stepwise multivariate regression analysis. It was found that blood pressure (BP), blood pressure variability, circulating Ang II, inflammatory factors, cardiac and aortic gene expressions of all the components of RAS and some inflammatory factors were elevated, and baroreflex sensitivity (BRS) was decreased in SHR. Changes of mRNA expressions of RAS components and inflammatory factors was unidirectional in the heart and aorta in SHR. It is the tissue RAS, rather the circulating RAS and inflammatory factors, that contributed to hypertensive cardiovascular hypertrophy. Statistically, LV hypertrophy was mainly determined by diastolic blood pressure and the cardiac angiotensin-converting enzyme gene expression, and aortic hypertrophy was mainly correlated with baroreflex sensitivity.