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Abstract
In man, circulating adrenaline has little or no direct effect on the control of blood pressure. A small proportion of adrenaline secreted by the adrenal medulla is accumulated in sympathetic nerve endings and may be re-released by sympathetic nerve stimulation. Recent pharmacological studies have suggested that adrenaline acts on a presynaptic β-receptor on sympathetic nerve endings to facilitate noradrenaline release, and it has been proposed that adrenaline re-released from these nerve endings is therefore a functionally important “co-transmitter”. Intermittently elevated secretion of adrenaline from the adrenal medulla could therefore lead indirectly to a sustained increase in neuronal release of noradrenaline and hence to hypertension.