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CLINICAL STUDY: HEART FAILURE/CARDIAC TRANSPLANTATION

High-dose angiotensin-converting enzyme inhibition restores body fluid homeostasis in heart-transplant recipients

Randy W. Braith, PhD^*,*, Roger M. Mills, MD, FACC^*, Christopher S. Wilcox, MD, PhD, Gary L. Davis, MD^*, James A. Hill, MD, FACC^* and Charles E. Wood, PhD^*

^* Center for Exercise Science, College of Health and Human Performance, and the Departments of Medicine and Physiology, University of Florida, Gainesville, Florida, USA
Department of Medicine, Georgetown University, Washington, DC, USA

Manuscript received May 28, 2002; revised manuscript received October 4, 2002, accepted October 10, 2002.

^* Reprint requests and correspondence: Dr. Randy W. Braith, P.O. Box 118206, Center for Exercise Science, University of Florida, Gainesville, Florida 32611USA.
rbraith{at}hhp.ufl.edu

OBJECTIVES: We tested the hypothesis that salt and fluid retention in heart-transplant recipients (HTRs) is caused by a failure to reflexively suppress the renin-angiotensin-aldosterone system (RAAS).

BACKGROUND: It is known that extracellular fluid volume is expanded (12% to 15%) in HTRs who develop hypertension.

METHODS: Responses to volume expansion were measured in eight HTRs (ages 57 ± 6 years) and six liver-transplant recipients (LTRs) (ages 52 ± 2 years) both before and after treatment with captopril (225 mg/day). After three days of a standardized diet, 0.154 mol/l saline was infused at 8 ml/kg/h for 4 h. Blood pressure, hormones, and renal function were monitored for 48 h. After four months, the same subjects received captopril (225 mg/day), and the protocol was repeated.

RESULTS: Before captopril, saline infusion suppressed the RAAS in LTRs but not in HTRs, resulting in elimination of 86 ± 12% versus 50 ± 11% of the sodium load by 48-h postinfusion. Blood pressure increased only in the HTRs (+16 ± 5/9 ± 3 mm Hg) and remained elevated for 48 h (p 0.05). After captopril, sodium elimination was comparable in the liver (87 ± 13%) and heart groups (86 ± 12%) and blood pressure did not change in either group.

CONCLUSIONS: Heart transplant recipients have blunted diuretic and natriuretic responses to volume expansion that is mediated by their inability to suppress the RAAS. Pharmacologic suppression of the RAAS normalized defects in blood pressure and fluid homeostasis. These findings indicate that hypertension in HTRs is caused, in part, by a failure to reflexively suppress the RAAS when these patients become hypervolemic.

Abbreviations and Acronyms   ACE   angiotensin-converting enzyme   ACEi   angiotensin-converting enzyme inhibition   ALDO   aldosterone   ANG II   angiotensin II   ANP   atrial natriuretic peptide   AVP   arginine vasopressin   CRC   clinical research center   HTRs   heart-transplant recipients   LTRs   liver-transplant recipients   RAAS   renin-angiotensin-aldosterone system

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