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v. infusion of 20?ng/kg per min AngII produced similar increases in blood pressure in male and female rats (Table?1).[10, 11, 73] Moreover, studies in humans show no evidence for a hypotensive effect of low doses of i.v. AngII in women or a difference in the pressor effect of i.v. AngII in men and women.[14, 15, 74] As mentioned above, chronic s.c. administration of AngII increases vascular AT2 receptor expression[28] and the different pressor responses of male and female rodents to s.c. AngII administration may have been due a greater induction of vascular AT2 receptor expression in female than in male rodents as a consequence of the proinflammatory effects of AngII administered s.c.[4, 5] Chronic AngII infusion s.c. caused dose-related reductions in bodyweight gain or weight loss in rats at doses ��?200?ng/kg per min.[75-77] Weight loss of 21% occurred with 350?ng/kg per min, s.c., AngII over 7?days, [http://en.wikipedia.org/wiki/GPX4 GPX4] [http://www.selleckchem.com/products/ch5424802.html Alectinib supplier] which was mostly attributable to a reduction in food intake.[76] However, there was also skeletal muscle wasting due to enhanced protein degradation and skeletal muscle atrophy,[76, 78] reduction of liver triglyceride content[77] and a reduction in kidney weight.[62] In contrast with chronic s.c. AngII, chronic i.v. AngII administration did not cause weight loss in most studies. Rabbits maintained bodyweight during 6?weeks i.v. infusion of pressor doses of AngII, except for doses >?50?ng/kg per min, i.v., which caused natriuresis, diuresis and loss of bodyweight.[7] Rats also showed no effect of pressor doses of chronic i.v. AngII on bodyweight,[10, 79] except for doses ~100?ng/kg per min, i.v., which caused weight loss of approximately 4% over 9?days.[9] The much greater weight loss and anorexia produced by s.c. [http://www.selleckchem.com/products/azd9291.html Osimertinib datasheet] than i.v. AngII may reflect a systemic inflammatory response to the much higher doses of AngII administered s.c. Pressor doses of chronic AngII ��?200?ng/kg per min, s.c., cause aortic medial hypertrophy and perivascular infiltration by T cells and macrophages,[3, 80] vessel wall thickening, perivascular cellular infiltrates, myocyte injury and interstitial fibrosis in the heart[2, 81] and renal injury associated with proteinuria and marked vascular, glomerular and tubulointerstitial injury and interstitial fibrosis in mice and rats.[82-84] Very high doses of i.v. AngII (900�C1800?ng/kg per min for 72?h) cause acute renal failure, tubular necrosis and myocardial infarction in rabbits.[85] However, rats administered 10?ng/kg per min, i.v., AngII for 14?days, which produced a substantial 53?mmHg increase in blood pressure, showed much less impact on vascular, cardiac and renal pathology than rats administered similarly pressor doses of s.c. AngII.[86] The kidneys showed some mesangial thickening and arteriolar hyperplasia, but there was no significant increase in renal perivascular fibrosis or glomerular or tubulointerstitial injury, although 3?weeks of i.v.