Beta-2 adrenergic effects on the sympathetic nervous system

The origin of the studies, described in this thesis, dates back to 1979. In that year my colleague, R.P. Verhoeven, studied the responsiveness of hyperthyroid patients to beta adrenoceptor activation [1]. In his experiments he made the serendipitous observation that the plasma levels of the sympathetic transmitter, noradrenaline, increased during infusion of the beta adrenoceptor agonist isoprenaline. At the time most of us felt that this could be explained by reflex increase in sympathetic nervous activity, due to the vasodilatation caused by isoprenaline, my promotor, Prof. Schalekamp, took a different view. He suggested that the increase in noradrenaline during infusion of isoprenaline could be mediated by presynaptic beta adrenoceptors, which would serve to facilitate the release of noradrenaline [2,3,4]. He gave the impetus to the studies that followed.