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AJP - Renal Physiology, Vol 263, Issue 3 527-F533, Copyright © 1992 by American Physiological Society
ARTICLES |
J. Frokiaer, L. Knudsen, A. S. Nielsen, E. B. Pedersen and J. C. Djurhuus
Institute of Experimental Clinical Research, University of Aarhus, Denmark.
The effect of acute unilateral complete ureteral obstruction (UUO) on renal hemodynamics has been examined in a pig model. Pigs were operated on under general anesthesia, electromagnetic flow probes were inserted around renal arteries, and catheters were implanted in renal veins and aorta for blood sampling. The influence of 15 h of obstruction on the physiological variation in immunoreactive angiotensin II (ANG II) was measured together with detailed analysis of the renal handling of ANG II in anesthetized animals. Pelvic pressure rose significantly within 2 h to a maximum of 59.9 +/- 2.9 cmH2O (n = 10). The ipsilateral renal blood flow (RBF) was reduced by 30% from 319 +/- 35 to 241 +/- 42 ml/min (P = 0.001), whereas contralateral RBF did not change. A temporary significant increase in mean aortic blood pressure was seen during the first 2 h after UUO. Renal vascular resistance increased by 44% in the obstructed kidney from 37 +/- 3 to 55 +/- 9 mmHg.ml-1.min.g during the course of obstruction. Concomitantly, the plasma concentration of immunoreactive ANG II increased from all three sample sites by 8-15 times. This increase was highly significant compared with the sham-operated group. The results show that the pig kidney responds to UUO by a net secretion of ANG II from the ipsilateral kidney. Our observations on the ANG II renal secretion rate suggest that part of the immunoreactive ANG II in the renal venous effluent originated de novo from intrarenal generation.
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A. M. Jensen, E. H. Bae, R. A. Fenton, R. Norregaard, S. Nielsen, S. W. Kim, and J. Frokiaer Angiotensin II regulates V2 receptor and pAQP2 during ureteral obstruction Am J Physiol Renal Physiol, January 1, 2009; 296(1): F127 - F134. [Abstract] [Full Text] [PDF] |
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R. Norregaard, B. L. Jensen, S. O. Topcu, M. Diget, H. Schweer, M. A. Knepper, S. Nielsen, and J. Frokiaer COX-2 activity transiently contributes to increased water and NaCl excretion in the polyuric phase after release of ureteral obstruction Am J Physiol Renal Physiol, May 1, 2007; 292(5): F1322 - F1333. [Abstract] [Full Text] [PDF] |
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A. M. Jensen, C. Li, H. A. Praetorius, R. Norregaard, S. Frische, M. A. Knepper, S. Nielsen, and J. Frokiaer Angiotensin II mediates downregulation of aquaporin water channels and key renal sodium transporters in response to urinary tract obstruction Am J Physiol Renal Physiol, November 1, 2006; 291(5): F1021 - F1032. [Abstract] [Full Text] [PDF] |
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C. Li, W. Wang, T.-H. Kwon, L. Isikay, J. G. Wen, D. Marples, J. C. Djurhuus, A. Stockwell, M. A. Knepper, S. Nielsen, et al. Downregulation of AQP1, -2, and -3 after ureteral obstruction is associated with a long-term urine-concentrating defect Am J Physiol Renal Physiol, July 1, 2001; 281(1): F163 - F171. [Abstract] [Full Text] [PDF] |
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