Effects of ACE Inhibition and β-Blockade on Plasminogen Activator Inhibitor-1 and Transforming Growth Factor-β1 in Carotid Glomus and Autonomic Ganglia in Hypertensive Rats

Background Previous studies have demonstrated a high correlation between arterial hypertension and the development of lesions in the carotid glomus (CG) and autonomic ganglia (AG), characterized by extracellular matrix (ECM) expansion and reduction in the number of AG neurons. Because lowering blood pressure (BP) is the first step in controlling the deleterious effects of arterial hypertension, the objective was to evaluate possible differences between the β-blocker atenolol (AT) and the angiotensin-converting enzyme (ACE) inhibitor ramipril (RAM) regarding a protective role on CG and AG, as target organs in the spontaneously hypertensive rat (SHR). Methods Male 12-week-old SHR and Wistar-Kyoto rats (WKY) were divided into SHR; SHR-RAM, 1 mg/kg/d; SHR-AT, 100 mg/kg/d; and WKY rats. After 6 months, the animals were sacrificed and CG and AG were processed by hematoxylin and eosin (H&E) and Masson’s trichrome and immunohistochemistry (transforming growth factor-β1 and plasminogen activator inhibitor-1). Results At the end of the experiment, SHR-AT and SHR-RAM showed a similar control in BP compared with SHR. However, SHR-RAM presented a significant reduction in ECM expansion in CG, AG, and autonomic nerves. Moreover, the number of neurons in AG was preserved with AT and even more with RAM, when compared with SHR group. Transforming growth factor-β1 and plasminogen activator inhibitor-1 were increased in CG and AG in SHR and in SHR-AT, whereas SHR-RAM showed a similar expression to the WKY group. Conclusions According to these results, RAM but not AT provided a significant protective role against structural changes in CG as well as in AG caused by arterial hypertension in SHR. This effect seems to be independent of BP reduction.