Bozena Badzyńska1, Janusz Sadowski. 1. Laboratory of Renal and Body Fluid Physiology, M. Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland.
Abstract
AIMS: Treatment of arterial hypotension with norepinephrine (NE) is associated with renal vasoconstriction and may lead to ischemic kidney injury; the risk involved is still a matter of debate. METHODS: In anesthetized, acutely uninephrectomized rats, we examined changes in intrarenal hemodynamics induced by intravenous infusion of NE and angiotensin II (Ang II), at doses that increased arterial pressure by ∼25 mm Hg (20%). Renal blood flow (RBF) was determined using a Transonic probe, and superficial cortical, outer and inner medullary flows (CBF, OMBF, IMBF) as laser-Doppler fluxes. RESULTS: NE decreased regional intrarenal perfusion similarly, by 16, 15 and 16% for RBF, OMBF and IMBF, respectively (all changes significant). The respective decreases after Ang II were significantly greater and clearly differentiated: 45, 32 and 22%, respectively. The renal vascular resistance increased 47 ± 4% after NE and 131 ± 11% after Ang II, indicating that the latter drug induces much more pronounced renal vasoconstriction. CONCLUSION: An ∼15% decrease of renal perfusion may be taken as an indication of an impairment of renal circulation during antihypotensive NE therapy. While superiority of NE over Ang II is obvious, a further search for drugs even less harmful to renal perfusion and function is desirable.
AIMS: Treatment of arterial hypotension with norepinephrine (NE) is associated with renal vasoconstriction and may lead to ischemic kidney injury; the risk involved is still a matter of debate. METHODS: In anesthetized, acutely uninephrectomized rats, we examined changes in intrarenal hemodynamics induced by intravenous infusion of NE and angiotensin II (Ang II), at doses that increased arterial pressure by ∼25 mm Hg (20%). Renal blood flow (RBF) was determined using a Transonic probe, and superficial cortical, outer and inner medullary flows (CBF, OMBF, IMBF) as laser-Doppler fluxes. RESULTS: NE decreased regional intrarenal perfusion similarly, by 16, 15 and 16% for RBF, OMBF and IMBF, respectively (all changes significant). The respective decreases after Ang II were significantly greater and clearly differentiated: 45, 32 and 22%, respectively. The renal vascular resistance increased 47 ± 4% after NE and 131 ± 11% after Ang II, indicating that the latter drug induces much more pronounced renal vasoconstriction. CONCLUSION: An ∼15% decrease of renal perfusion may be taken as an indication of an impairment of renal circulation during antihypotensive NE therapy. While superiority of NE over Ang II is obvious, a further search for drugs even less harmful to renal perfusion and function is desirable.