Haemodynamic effects of lead(II) acetate, ethanol, and their combination in rats

The aim of the study was to analyse the haemodynamic background of the hypertension-inducing effect of lead and the role of alcohol effect in hypertension caused by lead. Daily lead acetate doses of 0 or 500 mg/kg were administered to Sprague-Dawley male rats. One half of each group received water containing 5% w/v sugar (without ethanol), while the other half of each group received water containing 5% w/v sugar and 10% v/v ethanol, respectively, to drink. At the end of the 12th week ECG and haemodynamic tests were performed with the method of McDevitt and Nies (1976). The tests were repeated after the administration of 5 microg noradrenaline (NA) by i.v. infusion for 3 min. Lead acetate administration increased the arterial blood pressure and total peripheral resistance (TPR), the organ fractions of the cardiac output and blood flow of the parietal bone, and the vascular resistance of the liver and kidneys, and decreased the cardiac output, the blood flow of the liver and kidneys, and the vascular resistance of the parietal bone. Ethanol administration decreased the blood flow of the intestines and increased the vascular resistance of the intestines. Following the simultaneous administration of lead acetate and ethanol, lead acetate reversed (inhibited) the decreasing effect of ethanol on gastrointestinal organ fraction and blood flow. Lead acetate pre-treatment decreased the blood-pressure-increasing effect of NA; it augmented the increasing effect on vascular resistance of the stomach and the reducing effect on parietal bone organ fraction and blood flow. Lead acetate causes hypertension in male rats, in which the decreased blood flow to the kidneys may play a role; ethanol, ingested in a low dose, does not cause hypertension, and though it can decrease the enhanced vascular tone caused by lead, it is not able to prevent "lead-hypertension"; the considerably increased blood flow in the bones (parietal bone) caused by the lead salt may contribute to the increase and maintenance of the blood lead level. The anticipated mechanism may explain the increased cardiovascular risk proportional to the increased lead concentration in the bones.