Breakdown of blood pressure and body fluid homeostasis in heart transplant recipients

Objectives. This study was designed to investigate disturbances in arterial blood pressure and body fluid homeostasis in stable heart transplant recipients. Background. Hypertension and fluid retention frequently complicate heart transplantation. Methods. Blood pressure, renal and endocrine responses to acute volume expansion were compared in 10 heart transplant recipients (57 ± 9 years old [mean ± SD]) 20 ± 5 months after transplantation, 6 liver transplant recipients receiving similar doses of cyclosporine (cyclosporine control group) and 7 normal volunteers (normal control subjects). After 3 days of constant diet containing 87 mEq/24 h of sodium, 0.154 mol/liter saline was infused at 8 ml/kg per h for 4 h. Blood pressure and plasm vasopressin, angiotensin II, aldosterone, atrial natiuretic peptide and renin activity levels were determined before and at 30, 60, 120 and 240 min during the infusion. Urine was collected at 2 and 4 h. Blood pressure, fluid balance hormones and renal function were monitored for 48 h after the infusion. Results. Blood pressure did not change in the two control groups but increased in the heart transplant recipients (+ 15 ± 8/8± 5 mm Hg) and remained elevated for 48 h (p ≤ 0.05). Urine flow and urinary sodium excretion increased abruptly in the control groups sufficient to account for elimination of 86 ± 9% of the sodium load by 48 h; the increases were blunted (p ≤ 0.05) and delayed in the heart transplant recipients, resulting in elimination of only 51 ± 13% of the sodium load. Saline infusion suppressed vasopressin, renin activity, angiotensin II and aldosterone in the two control groups (p ≤ 0.05) but not in the heart transplant recipients. Heart transplant recipients had elevated atrial natriuretic peptide levels at baseline (p ≤ 0.05), but relative increases during the infusion were similar to those in both control groups. Conclusions. Blood pressure in heart transplant recipients is salt sensitive. These patients have blunted diuretic and natriuretic response to volume expansion that may be mediated by failure to reflexly suppress fluid regulatory hormones. These defects in blood pressure and fluid homeostasis were not seen in liver transplant recipients receiving cyclosporine and therefore cannot be attributed to cyclosporine alone. Abnormal cardiorenal neuroendocrine reflexes, secondary to cardiac denervation, may contribute to salt-sensitive hypertension and fluid retention in heart transplant recipients.