ABSTRACT
Objective To investigate the effect of repeated and prolonged +Gz exposure on endocrine function of vessel in a rabbit model of atherosclerosis. Methods Twenty-four male New Zealand white rabbits were used to establish the model of atherosclerosis, and then randomly divided into control group and +Gz exposure group (12 each). Animals in control group underwent no +Gz exposure, while those in +Gz exposure group underwent +Gz exposure for 4, 8, and 12 weeks respectively (4 animals at each time point), and 4 animals from each group were sacrificed at each time point. The levels of angiotensin II (Ang II), endothelin (ET), heme oxygenase-1 (HO-1), carbon monoxide (CO) and cyclic guanosine-3', 5'-monophosphate (cGMP) were measured by radioimmunoassay and biochemical method, and the ultrastructure of aortic intima was examined by electron microscopy. Results Along with the prolongation of +Gz exposure, the contents of Ang II, ET, HO-1, CO and cGMP were increased in +Gz exposure group (P<0.05), but the increase stopped at the 12th week, and no obvious change in the above indices was observed in control group (P=0.05). The foam cells and collagen content under the aortic intima and in the shallow layer of aortic media were slightly increased in control group, but the foam cells and the interstitial collagen fibers were greatly increased after +Gz exposure for 8 and 12 weeks as compared with that in control group. Conclusion Repeated and prolonged +Gz exposure may induce the production of Ang II and ET, increase the secretion of HO-1, CO and cGMP, thus play a potential role in protecting the vessels from further injuries.
ABSTRACT
Objective To investigate the effect of repeated and prolonged +Gz exposure on endocrine function of vessel in a rabbit model of atherosclerosis. Methods Twenty-four male New Zealand white rabbits were used to establish the model of atherosclerosis, and then randomly divided into control group and +Gz exposure group (12 each). Animals in control group underwent no +Gz exposure, while those in +Gz exposure group underwent +Gz exposure for 4, 8, and 12 weeks respectively (4 animals at each time point), and 4 animals from each group were sacrificed at each time point. The levels of angiotensin II (Ang II), endothelin (ET), heme oxygenase-1 (HO-1), carbon monoxide (CO) and cyclic guanosine-3', 5'-monophosphate (cGMP) were measured by radioimmunoassay and biochemical method, and the ultrastructure of aortic intima was examined by electron microscopy. Results Along with the prolongation of +Gz exposure, the contents of Ang II, ET, HO-1, CO and cGMP were increased in +Gz exposure group (P<0.05), but the increase stopped at the 12th week, and no obvious change in the above indices was observed in control group (P=0.05). The foam cells and collagen content under the aortic intima and in the shallow layer of aortic media were slightly increased in control group, but the foam cells and the interstitial collagen fibers were greatly increased after +Gz exposure for 8 and 12 weeks as compared with that in control group. Conclusion Repeated and prolonged +Gz exposure may induce the production of Ang II and ET, increase the secretion of HO-1, CO and cGMP, thus play a potential role in protecting the vessels from further injuries.
ABSTRACT
To investigate whether brain AT1 receptor stimulation contributes as a hypertensive mechanism to deoxycorticosterone acetate (DOCA)-salt hypertension, losartan (1 mg/4l) or artificial cerebrospinal fluid (aCSF) was injected into the lateral cerebral ventricle in conscious control uninephrectomized Wistar rats or rats with DOCA-salt for 2 or 4 weeks, and mean arterial pressure (MAP) and heart rates (HR) were recorded. In rats with DOCA-salt treatment, resting MAP increased to 144 +/- 6 mmHg after 2 weeks and to 170 +/- 5 mmHg after 4 weeks versus 115- 120 mmHg in controls. In rats with 2 week DOCA-salt treatment, MAP started declining at 4 hr after intracerebroventricular (icv) injection of losartan, and significant decreases in MAP were found at 18 and 24 hr. In rats with 4 week DOCA-salt treatment, MAP was significantly decreased at 4, 18 and 24 hr. In both groups MAP decreased to that of control rats. In control rats, icv losartan had no effect on MAP and HR. Icv aCSF did not significantly change MAP and HR in either DOCA-salt hypertensive rats or control rats. Normalization of MAP after icv administration of the AT1 receptor antagonist suggests a significant role for brain AT1 receptor stimulation in the development and maintenance of hypertension in the DOCA-salt hypertensive rat model.