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 Hall, J. E. Articles by Guyton, A. C. Search for Related Content PubMed PubMed Citation Articles by Hall, J. E. Articles by Guyton, A. C.

Hypertension, Vol 2, 139-148, Copyright © 1980 by American Heart Association

ARTICLES

Control of arterial pressure and renal function during glucocorticoid excess in dogs

JE Hall, CL Morse, MJ Smith Jr, DB Young and AC Guyton

This study was designed to investigate the long-term effects of glucocorticoids on the control of mean arterial pressure (MAP) and renal function. Infusion of 10 mg/day of methylprednisolone (MP), a glucocorticoid with minimal mineralocorticoid activity, for 10 days in six intact conscious dogs maintained on a sodium intake of 78 mEq/day resulted in a decrease in MAP from 98 +/- 1 to 89 +/- 2 mm Hg, a decrease in sodium iothalamate space to 89 +/- 2% of control, and a marked increase in glomerular filtration rate (GFR), effective renal plasma flow (ERPF), and urinary sodium excretion. Chronic infusion of MP at doses of 2--800 mg/day in four dogs maintained on low (5 mEq/day) or high sodium intakes (160--223 mEq/day) also caused increases in GFR and ERPF, as well as natriuresis and decreased sodium iothalamate space, while causing either no change or a slight reduction in MAP. To determine whether glucocorticoids potentiate the chronic effects of angiotensin II (AII) on MAP and renal function, MP was infused in dogs undergoing AII infusion (5 ng/kg/min). During AII hypertension, chronic infusion of 5 or 10 mg/day of MP also resulted in a marked renal vasodilation, natriuresis, and reductions in sodium iothalamate space, while causing small reductions in MAP. Thus, we found no evidence that chronic glucocorticoid excess causes hypertension in dogs, or that glucocorticoids potentiate the blood pressure or renal effects of AII. Instead, glucocorticoids tended to reduce MAP, probably because of chronic renal vasodilation, increased excretion of sodium, and volume depletion.

This article has been cited by other articles:

				J A P Da Silva, J W G Jacobs, J R Kirwan, M Boers, K G Saag, L B S Ines, E J P de Koning, F Buttgereit, M Cutolo, H Capell, et al. Safety of low dose glucocorticoid treatment in rheumatoid arthritis: published evidence and prospective trial data Ann Rheum Dis, March 1, 2006; 65(3): 285 - 293. [Abstract] [Full Text] [PDF]

				R. de Matteo and C. N. May Inhibition of prostaglandin and nitric oxide synthesis prevents cortisol-induced renal vasodilatation in sheep Am J Physiol Regulatory Integrative Comp Physiol, April 1, 1999; 276(4): R1125 - R1131. [Abstract] [Full Text] [PDF]

				R. De Matteo and C. N. May Glucocorticoid-induced renal vasodilatation is mediated by a direct renal action involving nitric oxide Am J Physiol Regulatory Integrative Comp Physiol, December 1, 1997; 273(6): R1972 - R1979. [Abstract] [Full Text] [PDF]

				C. N. May and J. A. Bednarik Regional Hemodynamic and Endocrine Effects of Aldosterone and Cortisol in Conscious Sheep : Comparison With the Effects of Corticotropin Hypertension, August 1, 1995; 26(2): 294 - 300. [Abstract] [Full Text]