Losartan does not decrease renal oxygenation and norepinephrine effects in rats after resuscitated hemorrhage.

Area of Science:

• Nephrology
• Pharmacology
• Physiology

Background:

• Renin-angiotensin-system (RAS) blockers may increase acute kidney injury risk post-surgery and hemorrhage.
• Previous studies showed losartan did not cause renal hypoxia after hemorrhage without resuscitation.
• The effect of RAS blockers on kidney oxygenation during resuscitated hemorrhage remains unclear.

Purpose of the Study:

• To investigate losartan's impact on renal cortical and medullary oxygenation during resuscitated hemorrhage in rats.
• To assess the vasopressor effect of norepinephrine in rats treated with losartan during resuscitated hemorrhage.

Main Methods:

• Male Wistar rats received 7 days of losartan or control treatment.
• Hemorrhage (20% blood volume) followed by Ringer's acetate resuscitation.
• Measurements included mean arterial pressure, renal blood flow, and kidney tissue oxygenation.
• Norepinephrine's effect on blood pressure and renal blood flow was evaluated.

Main Results:

• Losartan reduced baseline mean arterial pressure but not renal blood flow.
• Renal oxygen consumption and tension were unaffected by losartan.
• Resuscitated hemorrhage lowered mean arterial pressure and renal blood flow.
• Losartan-treated rats exhibited a smaller increase in renal vascular resistance, mitigating cortical oxygen tension decrease.
• Medullary oxygen tension showed no significant difference between groups or post-hemorrhage.
• Norepinephrine's pressor and renal blood flow effects were similar in both groups.

Conclusions:

• Losartan does not compromise renal oxygenation following resuscitated hemorrhage due to blunted renal vascular resistance increase.
• Losartan treatment does not impede norepinephrine's efficacy as a vasopressor.
• Blood pressure management is feasible during losartan therapy even in hemorrhagic states.