Inhibition of pressure natriuresis in mice lacking the AT2 receptor

metabolism, that may contribute to the intrarenal differences Inhibition of pressure natriuresis in mice lacking the AT2 receptor. observed between AT2 receptor knockout and wild-type mice. Background. Angiotensin II type 2 (AT2) receptor knockout mice have higher blood pressures than wild-type mice; however, the hypertension is imperfectly defined. We tested the hypothesis that renal mechanisms could be contributory. Angiotensin (Ang) II effects are mediated by at least Methods. We conducted pressure-natriuresis-diuresis exper- two receptor isoforms (AT 1 and AT2). The AT1 receptor iments, measured renal cortical and medullary blood flow by mediates vasoconstriction, aldosterone secretion, the laser Doppler methods, and explored cytochrome P450-dependent arachidonic acid metabolism by means of reverse tran- regulation of glomerular and renal tubular function, and scription-polymerase chain reaction. cardiovascular hypertrophy. AT2 receptor function and Results. Blood pressure was 15 mm Hg higher in AT2 recep- its involvement in hypertension remain incompletely untor knockout mice than in controls, and pressure diuresis and derstood. The AT 2 receptor is widely expressed during natriuresis curves were shifted rightward. At similar renal perfetal development. In adult tissues, AT2 receptor expres