Differential effects of sino-aortic denervations on cardiac noradrenaline stores, turnover and neuronal re-uptake in normotensive and renal hypertensive rabbits.

The effects of sino-aortic denervation (SAD) on cardiac noradrenaline stores, turnover and neuronal re-uptake were examined in normotensive rabbits and rabbits with two-kidney, two wrapped hypertension. Ten to 12 days after SAD, left ventricular (LV) noradrenaline stores were reduced in renal hypertensives to 43% of that of the sham-operated rabbits, although there was no overt evidence of heart failure. This did not occur after SAD of normotensive rabbits. The reduction in noradrenaline content was accompanied by a reduction in [3H]-noradrenaline turnover time (4.4 h) compared with renal hypertensive (7.4 h) and the normotensive subgroups (9.3 h). Noradrenaline turnover rates were elevated by 25% in hypertensive compared with normotensive rabbits. Left ventricular tyrosine hydroxylase, dopamine-beta-hydroxylase and type A monoamine oxidase activities were similar in normotensive and hypertensive rabbits and were unaffected by SAD. Following SAD of hypertensive rabbits cardiac neuronal uptake for alpha-methylnoradrenaline was reduced by 33% compared with either the hypertensive or the normotensive rabbits. Sino-aortic denervation did not affect neuronal uptake in normotensives. These results suggest that following SAD of hypertensive rabbits, cardiac noradrenaline stores are depleted by enhanced cardiac sympathetic activity (reduction in [3H]-noradrenaline turnover time) and a reduction in neuronal re-uptake. It appears that the hypertensive hypertrophied heart is less able to tolerate chronic sympathetic overactivity and/or liability in coronary oxygen supply brought about by SAD.