The objectives of this study were to determine the effects of chronic angiotensin II (ANG II) infusions on ANG II content and angiotensinogen expression in the mouse kidney and the role of the angiotensin II type 1 receptor (AT 1R) in mediating these changes. C57BL/6J male mice were subjected to ANG II infusions at doses of 400 or 1,000 ng⅐kg Ϫ1 ⅐min Ϫ1 either alone or with an AT 1R blocker (olmesartan; 3 mg⅐kg Ϫ1 ⅐day Ϫ1) for 12 days. Systolic and mean arterial pressures were determined by tail-cuff plethysmography and radiotelemetry. On day 13, blood and kidneys were collected for ANG II determinations by radioimmunoanalysis and intrarenal angiotensinogen expression studies by quantitative RT-PCR, Western blotting, and immunohistochemistry. ANG II infusions at the low dose elicited progressive increases in systolic blood pressure (135 Ϯ 2.5 mmHg). In contrast, the high dose induced a rapid increase (152 Ϯ 2.5, P Ͻ 0.05 vs. controls, 109 Ϯ 2.8). Renal ANG II content was increased by ANG II infusions at the low dose (1,203 Ϯ 253 fmol/g) and the high dose (1,258 Ϯ 173) vs. controls (499 Ϯ 40, P Ͻ 0.05). Kidney angiotensinogen mRNA and protein were increased only by the low dose to 1.13 Ϯ 0.02 and 1.26 Ϯ 0.10, respectively, over controls (1.00, P Ͻ 0.05). These effects were not observed in mice infused at the high dose and those receiving olmesartan. The results indicate that chronic ANG II infusions augment mouse intrarenal ANG II content with AT 1R-dependent uptake occurring at both doses, but only the low dose of infusion, which elicited a slow progressive response, causes an AT 1R-dependent increase in intrarenal angiotensinogen expression. telemetry; mouse kidney; hypertension CHRONIC INFUSIONS OF ANGIOTENSIN II (ANG II) lead to elevations in intrarenal ANG II content associated with reductions in renal function and sodium excretion and hypertension (26,29,31,35). An increase in intrarenal ANG II content is also associated with enhanced oxidative stress and chronic proinflammatory and proliferative responses that result in progressive tissue injury (7,18). Indeed, every model of experimental ANG II-dependent hypertension is characterized by augmentation of intrarenal ANG II content to levels much greater than can be explained on the basis of equilibration with the systemic circulation (8,23,39).Augmentation of intrarenal ANG II occurs by several processes. ANG II is actively accumulated in the kidney via internalization mainly by the ANG II type 1 receptor (AT 1 R) (20,38,39). However, megalin, an abundant protein in proximal tubule cells, can also bind and internalize ANG II (6). In addition, the kidneys express all components of the reninangiotensin system (RAS) and can therefore generate angiotensin peptides from locally formed angiotensinogen (9,11,17,25). Increased ANG II exerts a positive effect on the expression of angiotensinogen mRNA and protein by proximal tubule cells in ANG II-infused rats that translates into an elevation of angiotensinogen excretion in the urine (13,14,27). The intrarenal activi...

Although a typical course of electroconvulsive therapy (ECT) consists of 6 to 12 treatments, remission of depression has rarely been reported after a single treatment. We present the case of a 25-year-old woman hospitalized for a major depressive episode and suicidality, in the context of bipolar 1 disorder, whose symptoms fully remitted with 1 ECT. We also review the literature on rapid response to ECT.