Changes of Hemodynamics and Renal Function due to Acute Cadmium Exposure in Rats

The systolic and diastolic pressures in anesthetized Sprague-Dawley male rats were greatly decreased after single-dose of Cd treatment without significant changes in heart rate. There was a fluid-shift into the third space and/or -loss through the kidney, since plasma Na+ concentration and hematocrit ratio were significantly increased by acute Cd exposure. The present study showed that the sustained hypotensive effect of single-dose Cd on the cardiovascular system might have resulted from the systemic hypovolemia. Furthermore, renal excretion of electrolytes, including Na+ and K+, and urine flow rate were increased by Cd intoxication. Interestingly, the ratio of Na+/K+ excretion was increased and reached the maximum level 3 hours after Cd injection and returned to the normal level after 7 hours. Nevertheless, there was no difference in the regression analysis of K+ excretion and urine flow rate in both groups. Therefore, the increase in the urine volume seemed to enhance the excretion of K+. This study strongly suggest that the hypotensive effect of Cd is mediated by systemic Na+ loss through the kidney and/or hypovolemia via fluid-shift.

Effects of cadmiumin vitro on contractile and relaxant responses of isolated rat aortas

<p><b>OBJECTIVE</b>Cadmium is known to affect the vascular tone of isolated blood vesselsin vitro and the arterial pressure of ratsin vivo. However, the mechanisms of cadmium actions on the vascular system have not been clarified. To elucidate the actions of cadmium on vascular tonus, effects of cadmium on vasocontractile and vasorelaxant responsesin vitro were investigated using aortic strips isolated from rats.</p><p><b>METHODS</b>Aortic strips isolated from male Wistar rats were incubated with CdCl(2) (10μM) for 24 hr, washed with fresh CdCl(2)-free medium, and then used for measurement of isometric tension and Western blot analysis of eNOS (endothelial nitric oxide synthase) and iNOS (inducible nitric oxide synthase).</p><p><b>RESULTS</b>In the aortas pretreated with cadmiumin vitro, the contractile response to phenylephrine was significantly higher than that in the control aortic strips pretreated with a vehicle. The sodium nitroprusside-induced relaxing response was significantly higher in the aortic strips pretreated with cadmium for 24 hr, compared with that in the control pretreated with a vehicle. The isoproterenol-induced relaxing response was also significantly higher in the cadmium-accumulated aortic strips.In vitro cadmium treatment slightly but not significantly increased the acetylcholine-induced relaxation of the aortic strips. Cadmium treatment induced expression of iNOS and significantly increased expression of eNOS in the aortic strips, while it did not affect expression of β-actin.</p><p><b>CONCLUSIONS</b>Cadmium treatmentin vitro augmented the α1 adrenoceptor-mediated contractile response, even though eNOS and iNOS were upregulated by cadmium treatment. NO-induced and β-adrenoceptor-mediated relaxing responses were also augmented by cadmium treatment. These results suggest that both vasocontractile and vasorelaxing responses are augmented in cadmium-accumulated aortas.</p>

Effects of Cadmium \it{in Vitro} on Contractile and Relaxant Responses of Isolated Rat Aortas

Objective: Cadmium is known to affect the vascular tone of isolated blood vessels in vitro and the arterial pressure of rats in vivo. However, the mechanisms of cadmium actions on the vascular system have not been clarified. To elucidate the actions of cadmium on vascular tonus, effects of cadmium on vasocontractile and vasorelaxant responses in vitro were investigated using aortic strips isolated from rats. Methods: Aortic strips isolated from male Wistar rats were incubated with CdCl2 (10 μM) for 24 hr, washed with fresh CdCl2-free medium, and then used for measurement of isometric tension and Western blot analysis of eNOS (endothelial nitric oxide synthase) and iNOS (inducible nitric oxide synthase). Results: In the aortas pretreated with cadmium in vitro, the contractile response to phenylephrine was significantly higher than that in the control aortic strips pretreated with a vehicle. The sodium nitroprusside-induced relaxing response was significantly higher in the aortic strips pretreated with cadmium for 24 hr, compared with that in the control pretreated with a vehicle. The isoproterenol-induced relaxing response was also significantly higher in the cadmium-accumulated aortic strips. In vitro cadmium treatment slightly but not significantly increased the acetylcholine-induced relaxation of the aortic strips. Cadmium treatment induced expression of iNOS and significantly increased expression of eNOS in the aortic strips, while it did not affect expression of β-actin. Conclusions: Cadmium treatment in vitro augmented the α1 adrenoceptor-mediated contractile response, even though eNOS and iNOS were upregulated by cadmium treatment. NO-induced and β-adrenoceptor-mediated relaxing responses were also augmented by cadmium treatment. These results suggest that both vasocontractile and vasorelaxing responses are augmented in cadmium-accumulated aortas.