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Role of angiotensin II under prolonged increased intraabdominal pressure (IAP) in pigs

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Abstract

Background: The aim of the study was to investigate the effect of the angiotensin II receptor antagonist losartan on renal hemodynamics and diuresis in pigs with increased intraabdominal pressure (IAP). Methods: The IAP was maintained at 30 mmHg for 3 h by intraperitoneal instillation of Ringer’s solution. Ten animals were treated with losartan; another 10 animals served as controls. Renal blood flow, hormones in renal vein blood, and diuresis were measured. Results: In control animals, the renal vascular resistance increased renal blood flow remained constant, the blood concentration of aldosterone increased and the diuresis decreased during increased IAP. Losartan prevented the increase in vascular resistance and improved renal blood flow under increased IAP. It also prevented the rise in aldosterone concentration and increased the urine output to baseline level. Conclusion: Our results suggest that the renal vasoconstriction associated with increased IAP is due to increased production of angiotensin II. The oliguria associated with increased IAP is probably due, at least partly, to increased reabsorbtion of sodium and water in the renal tubuli caused by increased tissue concentration of aldosterone.

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Authors and Affiliations

  1. Surgical Research Laboratory, Institute of Surgical Sciences, Haukeland University Hospital, N-5021 Bergen, Norway

    F. F. Gudmundsson, A. Viste, K. Grong & K. Svanes

  2. Institute of Clinical Chemistry, Endocrine Section, Haukeland University Hospital, N-5021 Bergen, Norway

    O. L. Myking

  3. Department of Pathology, The Gade Institute, Haukeland University Hospital, N-5021 Bergen, Norway

    L. Bostad

Authors
  1. F. F. Gudmundsson
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  2. A. Viste
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  3. O. L. Myking
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  4. L. Bostad
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  5. K. Grong
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  6. K. Svanes
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Correspondence to F. F. Gudmundsson.

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Gudmundsson, F., Viste, A., Myking, O. et al. Role of angiotensin II under prolonged increased intraabdominal pressure (IAP) in pigs . Surg Endosc 17, 1092–1097 (2003). https://doi.org/10.1007/s00464-002-9123-0

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  • DOI: https://doi.org/10.1007/s00464-002-9123-0

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