This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Sciotti, V. Articles by Gallant, S. Search for Related Content PubMed PubMed Citation Articles by Sciotti, V. Articles by Gallant, S.

Hypertension, Vol 10, 176-180, Copyright © 1987 by American Heart Association

ARTICLES

Resistance to mineralocorticoid-induced hypertensive vascular disease

V Sciotti and S Gallant

To support our contention that the Wistar-Furth rat is resistant to mineralocorticoid hypertension, we assessed the effects of deoxycorticosterone (DOC) administration or renal artery stenosis on the development of hypertension in the Sprague-Dawley and Wistar-Furth rat strains. Weekly administration of mineralocorticoid in the form of DOC pivalate resulted in rapid, severe hypertensive cardiovascular disease in Sprague-Dawley rats. Within 5 weeks the mean conscious systolic blood pressures in steroid-treated and control rats were 186 +/- 4 and 118 +/- 5 mm Hg, respectively. In contrast, blood pressures of Wistar-Furth rats were only moderately elevated, even after 10 weeks of DOC pivalate administration (136 +/- 2 vs 116 +/- 2 mm Hg for controls). Furthermore, none of the steroid-treated Wistar-Furth animals exhibited cardiovascular lesions. In parallel studies, littermates of these rat strains were subjected to renal artery stenosis and blood pressures were determined weekly in conscious rats. Silver clip constriction of the left renal artery, in the presence of the contralateral kidney, resulted in a rapid, sustained elevation of blood pressure in both Sprague-Dawley and Wistar-Furth rat strains (177 +/- 4 and 176 +/- 5 mm Hg, respectively). Corticosteroid levels were also determined in DOC-treated Sprague-Dawley and Wistar-Furth rats. The regimen employed resulted in a 10-fold increase in DOC levels as compared with controls, and the levels achieved were comparable in both strains. Thus, the Wistar-Furth rat appears to be selectively resistant to mineralocorticoid hypertensive vascular disease and thus affords a model for studying mechanisms of steroid hypertension.

This article has been cited by other articles:

				H. Otani, F. Otsuka, K. Inagaki, M. Takeda, T. Miyoshi, J. Suzuki, T. Mukai, T. Ogura, and H. Makino Antagonistic effects of bone morphogenetic protein-4 and -7 on renal mesangial cell proliferation induced by aldosterone through MAPK activation Am J Physiol Renal Physiol, May 1, 2007; 292(5): F1513 - F1525. [Abstract] [Full Text] [PDF]

				J. A. Florian, A. Dorrance, R. C. Webb, and S. W. Watts Mineralocorticoids upregulate arterial contraction to epidermal growth factor Am J Physiol Regulatory Integrative Comp Physiol, September 1, 2001; 281(3): R878 - R886. [Abstract] [Full Text] [PDF]

				M. E. Ullian, C. J. Robinson, C. T. B. Evans, J. Z. Melnick, and W. R. Fitzgibbon Role of Citrate Synthase in Aldosterone-Mediated Sodium Reabsorption Hypertension, April 1, 2000; 35(4): 875 - 879. [Abstract] [Full Text] [PDF]

				W. R. FITZGIBBON, E. L. GREENE, J. S. GREWAL, F. N. HUTCHISON, S. E. SELF, S. Y. LATTEN, and M. E. ULLIAN Resistance to Remnant Nephropathy in the Wistar-Furth Rat J. Am. Soc. Nephrol., April 1, 1999; 10(4): 814 - 821. [Abstract] [Full Text]