THE EFFECTS OF HYPERINSULINEMIA ON MYOCARDIAL MASS - BLOOD-PRESSURE REGULATION AND CENTRAL HEMODYNAMICS IN RATS

Left ventricular hypertrophy is a condition with high mortality. An as sociation with insulin resistance and hyperinsulinaemia has recently b een suggested. The aim of this study was to examine the effects of iso lated hyperinsulinaemia on cardiac weight and haemodynamic regulation. Rats were exposed to hyperinsulinaemia for 7 weeks after adrenalectom y with corticosterone substitution and continuous infusion of proprano lol to control counter-regulatory mechanism (n = 15) (AIP group). Hypo glycaemia was prevented by glucose in the drinking water. Hyperinsulin aemic (AIP) rats were heavier and had increased relative masses of the myocardium (left ventricle 17% and right ventricle 20%), kidneys and adipose tissues in comparison with normoinsulinaemic adrenalectomized, corticosterone- and propranolol-treated controls (AP) (n = 10). Blood pressure in the insulin-exposed animals, measured weekly by the tail- cuff method in conscious rats, was not different from (AP) controls ov er 5 weeks, but increased in the sixth week. At the end of the seventh experimental week, blood pressure measured intra-arterially was also found to be elevated. Heart rate was not changed but total peripheral resistance was about twice that of controls (P < 0.001). Cardiac outpu t and stroke volume was 30-40% lower in the AIP rats (P < 0.05). It is concluded that exposure to elevated insulin levels with control of co unter-regulating mechanisms from beta-adrenergic mechanisms and adrena ls is not immediately followed by blood pressure elevation. It is, the refore, suggested that early onset of blood pressure elevation after i nsulin exposure might be caused by insulin counter-regulatory events, causing both insulin resistance and blood pressure elevation. The long term adaptations may involve a direct influence by insulin as a 'troph ic factor' on myocardial and on peripheral resistance vessels, followe d by increased blood pressure, decreased cardiac output and stroke vol ume.