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

• Published in: Scientific reports Vol. 8; no. 1; pp. 16342 - 9
• Main Authors: Emans, Tonja W, Patinha, Daniela, Joles, Jaap A, Koeners, Maarten P, Janssen, Ben J, Krediet, C T Paul
• Format: Journal Article
• Language: English
• Published: England Nature Publishing Group 05.11.2018; Nature Publishing Group UK
• Subjects: Angiotensin; Angiotensin II; Angiotensin II - pharmacology; Angiotensin II Type 1 Receptor Blockers - pharmacology; Animals; Arterial Pressure - drug effects; Blood pressure; Circadian Rhythm - drug effects; Dose-Response Relationship, Drug; Drinking water; Hypertension; Hypertension - chemically induced; Hypertension - metabolism; Hypertension - physiopathology; Hypoxia; Kidney - drug effects; Kidney - metabolism; Kinetics; Male; Oxygen; Oxygenation; Rats; Rats, Sprague-Dawley; Receptor, Angiotensin, Type 1 - metabolism; Renal cortex; Renin; Renin-Angiotensin System - drug effects; Rodents; Telemetry
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/s41598-018-34211-2

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 (pO ) 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.