Abstract
Epidemiological studies have found that the risk for cardiovascular disease is increased in patients with epilepsy. The Renin Angiontensin System (RAS), an important player in vascular tone control, is also involved in many neurological disorders, including seizures and epilepsy. Although it has been reported that Angiotensin II (Ang II) release and Angiotensin receptors expression are altered in many cerebral areas in patients/animal models with neurological disorders, there are no data on the vascular function. We evaluated Ang I and Ang II-mediated vascular responses and to correlate their contractile responses to the pres- ence of endothelium and the protein levels of components of the RAS (AT1, AT2, Mas and ACE) in aorta isolated from genetically epileptic rats (WAR strain). The major finding was that the vascular contractile response induced by Ang I and Ang II is endothelium-dependent. Ang II induced contractions in aortas from Wistar rats either with intact endothelium (E+) (1.16 ± 0.04 g, n = 6) and endothelium-denuded (E-) (1.24 ± 0.04 g, n = 6). Maximum contractile response (ME) induced by Ang I was lower in Wistar E+ (0.45 ± 0.03 g, n = 6) compared with Wistar E- (1.13 ± 0.08 g, n = 6). Ang I and Ang II failed to induce contraction in WAR E+, whereas the ME induced by Ang I in WAR E- was lower (0.52 ± 0.04 g, n = 11) than in the Wistar. ME induced by Ang II in aortas from WAR was also lower (0.40 ± 0.03 g, n = 11) compared with Wistar. AT1 receptor expression in both E+ WAR and Wistar was lower than in both E- WAR and Wistar. AT2 and Mas receptor expression was higher in Wistar E- and E+ as compared to WAR E- and E+. ACE expression was higher in both E+ WAR and Wistar, but it was lower in both E- WAR and Wistar. Endothelium impairs the contractile response induced by Angiotensin in WAR, suggesting that endothelial relaxing factors play important role on the aorta contraction.
Highlights
Epidemiological studies have found that the risk for cardiovascular disease is increased in persons with epilepsy and it is related to premature death [1,2,3,4,5,6]
In order to study the vascular reactivity to the agonists of the renin-Angiotensin system (RAS), it was constructed concentration-effect curves for Angiotensin I (Ang I) and Angiotensin II (Ang II)
The influence of endothelium on the contractile responses induced by Ang I and Ang II in aortic rings isolated from Wistar audiogenic rats (WAR) and Wistar was examined by using intact-endothelium (E+, Figures 1(a) and 1(b)) and denuded (E, Figures 2(a) and (b)) arteries
Summary
Epidemiological studies have found that the risk for cardiovascular disease is increased in persons with epilepsy and it is related to premature death [1,2,3,4,5,6]. Argañaraz et al [8] have reported increased AT1 receptor expression in the cortex and in the hippocampus of patients with temporal lobe epilepsy, while AT2 receptor expression was elevated only in the hippocampus of these patients. According to these authors, changes in Angiotensin II (Ang II) release may occur via mechanisms that remain unknown. Ang II would have pro- or anti-epileptogenic function depending on its receptor activation Their findings suggest that the up-regulation of the AT1 receptor is related to increased tissue excitability in the hippocampus and cortical areas
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