Abstract

We have studied several factors that may cause hypertension in renal transplant recipients. Cardiac output measurements suggest that hypertension is maintained by an increase in total peripheral resistance. Plasma noradrenaline concentration was significantly higher in both normotensive and hypertensive patients than in matched normal subjects. Plasma noradrenaline rose significantly in response to head-up tilt in normotensive, but not in hypertensive, patients. Resting plasma renin activity was significantly higher in both groups of patients than in normal subjects, but there was no relationship between plasma renin activity and blood pressure. Plasma renin activity did not change in response to head-up tilt or isoprenaline infusion in the patients. The rise in arterial pressure during noradrenaline infusion was significantly greater in hypertensive than in normotensive patients. Regression analysis showed a significant relationship between the combination of total exchangeable sodium and the rise in mean arterial pressure during noradrenaline infusion with resting mean arterial pressure.

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