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Losartan increases renal blood flow during isoflurane anesthesia in sheep
Author(s) -
Ullman J.,
Eriksson S.,
Rundgren M.
Publication year - 2001
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1034/j.1399-6576.2001.450919.x
Subject(s) - medicine , losartan , renal blood flow , vasopressin , angiotensin ii , blood pressure , isoflurane , anesthesia , endocrinology , renin–angiotensin system
Background: Inhaled anesthetics cause a transient reversible depression of renal function by direct renal effects or indirectly by changes in neurohumoral systems or cardiovascular performance. When the sympathetic nervous activity is decreased during anesthesia, other vasoactive systems like vasopressin (AVP) and particularly the renin angiotensin system (RAS) are of importance for blood pressure maintenance. Little is known about how the renal circulation is affected by angiotensin receptor blockade during isoflurane anesthesia. Methods: The study was performed on isoflurane anesthetized sheep equipped with flow probes (placed around a femoral and a renal artery) and a pulmonary artery catheter. During stable conditions the sheep were given one or more of the following substances: isotonic saline (NaCl); losartan (LOS) 10 mg · kg −1 ; prazosin (PRAZ) 0.2 mg · kg −1 and a vasopressin V 1 ‐receptor antagonist (AVP‐a) 10 μg · kg −1 . Results: LOS and AVP‐a did not affect mean arterial pressure (MAP), whereas PRAZ lowered MAP significantly (from 98±12 to 65±7 mmHg). Renal blood flow (RBF) increased after LOS treatment (148±34 to 222±33 ml · min −1 ). The other substances were without effect on RBF. Femoral blood flow remained unchanged after all treatments. Conclusion: We conclude that the sympathoadrenal system is still the major determinant for blood pressure maintenance during isoflurane anesthesia in sheep. The apparently increased activity of the renin angiotensin system in this situation causes a reduction in renal blood flow, which is counteracted by angiotensin II AT 1 ‐receptor blockade.