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AJP - Renal Physiology, Vol 262, Issue 6 927-F931, Copyright © 1992 by American Physiological Society
ARTICLES |
C. O. Watlington, L. B. Kramer, E. G. Schuetz, J. Zilai, W. M. Grogan, P. Guzelian, F. Gizek and A. C. Schoolwerth
Division of Endocrinology and Metabolism, Medical College of Virginia, Virginia Commonwealth University, Richmond 23298-0145.
Evidence for increased glucocorticoid 6 beta-hydroxylation (enhanced family 3A cytochrome P-450 activity) is found in certain reversible forms of human hypertension. This association was investigated in the spontaneously hypertensive rat (SHR). The proportion of injected [3H]corticosterone excreted in urine as 6 beta-[3H]OH-corticosterone was four- to fivefold higher in SHR than in control Wistar-Kyoto rats, before and after development of overt hypertension. Both hypertension and 6 beta-hydroxylation were inhibited by troleandomycin (a selective inhibitor of family 3A cytochromes P-450), consistent with a role for increased steroid 6 beta-hydroxylation in the genesis of hypertension in the SHR.
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