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AJP - Renal Physiology, Vol 265, Issue 3 391-F398, Copyright © 1993 by American Physiological Society
ARTICLES |
A. K. Bidani, K. A. Griffin, M. Picken and D. M. Lansky
Department of Medicine, Loyola University Medical Center, Maywood 60153.
The pathogenesis of glomerular injury in the remnant kidney (RK) model remains controversial. Increased glomerular transmission of systemic hypertension has been postulated to be an important pathogenic mechanism, but the precise relationship between systemic pressures and glomerular injury has not been defined because of the limitations of the tail-cuff method. Systolic blood pressure (BP) was continuously recorded radiotelemetrically at 10-min intervals for 6 wk in rats after approximately 5/6 renal ablation (n = 16) or sham ablation (n = 7). Overall mean systolic BP in RK rats was significantly higher than sham (138 +/- 3.3 vs. 117 +/- 1.3 mmHg, P < 0.01). Additionally, marked lability of systolic BP was observed in RK rats as compared with sham rats. Glomerular injury was essentially confined to RK rats, but the percentage of injured glomeruli ranged between 1 and 55%. Glomerular injury in individual animals was strongly correlated (r = 0.88) with the mean systolic BP during the last approximately 4 wk and with the frequency of systolic BP readings of > 140 mmHg. These data strongly suggest that transmission of systemic hypertension to the renal microvasculature plays a predominant role in the pathogenesis of glomerular injury in the RK model and also support the potential usefulness of the radiotelemetric technique to investigate hypertensive target organ injury.
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B. L. RISER, M. DENICHILO, P. CORTES, C. BAKER, J. M. GRONDIN, J. YEE, and R. G. NARINS Regulation of Connective Tissue Growth Factor Activity in Cultured Rat Mesangial Cells and Its Expression in Experimental Diabetic Glomerulosclerosis J. Am. Soc. Nephrol., January 1, 2000; 11(1): 25 - 38. [Abstract] [Full Text]
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E. St. Lezin, K. A. Griffin, M. Picken, M. C. Churchill, P. C. Churchill, T. W. Kurtz, W. Liu, N. Wang, V. Kren, V. Zidek, et al. Genetic Isolation of a Chromosome 1 Region Affecting Susceptibility to Hypertension-Induced Renal Damage in the Spontaneously Hypertensive Rat Hypertension, August 1, 1999; 34(2): 187 - 191. [Abstract] [Full Text] [PDF]
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C. E. Whitworth, M. M. Veniant, J. D. Firth, A. D. Cumming, and J. J. Mullins Endothelin in the Kidney in Malignant Phase Hypertension Hypertension, December 1, 1995; 26(6): 925 - 931. [Abstract] [Full Text]
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