Angiotensin II-induced hypertension in rats is only transiently accompanied by lower renal oxygenation.

ABSTRACT: Activation of the renin-angiotensin system may initiate chronic kidney disease. We hypothesised that renal hypoxia is a consequence of hemodynamic changes induced by angiotensin II and occurs prior to development of severe renal damage. Male Sprague-Dawley rats were infused continuously with angiotensin II (350?ng/kg/min) for 8 days. Mean arterial pressure (n?=?5), cortical (n?=?6) and medullary (n?=?7) oxygenation (pO2) were continuously recorded by telemetry and renal tissue injury was scored. Angiotensin II increased arterial pressure gradually to 150?±?18?mmHg. This was associated with transient reduction of oxygen levels in renal cortex (by 18?±?2%) and medulla (by 17?±?6%) at 10?±?2 and 6?±?1?hours, respectively after starting infusion. Thereafter oxygen levels normalised to pre-infusion levels and were maintained during the remainder of the infusion period. In rats receiving angiotensin II, adding losartan to drinking water (300?mg/L) only induced transient increase in renal oxygenation, despite normalisation of arterial pressure. In rats, renal hypoxia is only a transient phenomenon during initiation of angiotensin II-induced hypertension.

SUBMITTER: Emans TW 

PROVIDER: S-EPMC6218546 | biostudies-other | 2018 Nov

REPOSITORIES: biostudies-other