Clinical and Experimental Pharmacology zyxwvu & Physiology zyxw (1985) 12, 205-209 zyx ROLE OF CARDIAC AND VASCULAR AMPLIFIERS IN THE MAINTENANCE OF HYPERTENSION AND THE EFFECT OF REVERSAL OF CARDIOVASCULAR HYPERTROPHY P. I. Korner, G. L. Jennings, M. D. Esler and A. Broughton Baker Medical Research Institute, Melbourne, Victoria, Australia (Received 10 December 1984) SUMMARY 1. Changes in amplifying capacities of the hypertrophied heart and resistance vessels account for the characteristic evolution of haemodynamic patterns in the course of essential hypertension. 2. Reversal of hypertrophy in established essential hypertension requires prolon- ged control of blood pressure. Redevelopment of hypertension on stopping drug therapy is slowest if there has been reversal of both vascular and cardiac hypertrophy. It may be possible to subsequently maintain normal blood pressure in a proportion of patients by non-pharmacological means following the initial period of drug therapy. 3. Preliminary findings suggest that in a majority of patients the sympathetic ner- vous system may be overactive, whilst a smaller subset may have dysfunction of volume regulation. Key words: cardiac and vascular hypertrophy, essential hypertension, haemodynamic patterns, long-term autoregulation theory, non-drug treatment, pathogenesis. THE LONG-TERM AUTOREGULATION THEORY There is wide agreement about the changes in haemodynamic patterns that occur in the course of essential hypertension. In mild (borderline) hypertension cardiac index (CI) is elevated and total peripheral resistance index (TPRI) is normal, whilst in established hypertension CI is normal and the entire elevation of blood pressure is accounted for by elevation in TPRI. Once there are com- plications, particularly cardiac dilatation, CI usually becomes subnormal and TPRI is even more raised (for references see Korner 1983). The long-term autoregulation theory of hypertension was one attempt to explain the evolu- tion of haemodynamic patterns from mild to established hypertension (Ledingham & Pelling 1967; Guyton et al. 1981). According to the theory, the high CI/normal TPRI pattern is caused by volume overload in patients with essential hypertension (Guyton et al. 1981). The resulting tissue perfusion, in excess of metabolic requirements, leads to a ‘compensatory’ vasoconstriction Correspondence: Professor P. I. Korner, Baker Medical Research Institute, Commercial Road, Prahran, Victoria 3181, Australia. zyxwvuts 205