Stress-induced myocardial ischemia is a frequent manifestation of coronary heart disease and
sympathetic activation is an important precipitating and aggravating factor in such stress
induced ischemia. However the complex interplay between the sympathetic initiation of
myocardial ischemia ischemia-induced alterations in sympathetic neurotransmission as well as
changes in adrenoceptor density and post-receptor signal transduction that can occur during
ischemia remains incompletely understood. Not only the activation of myocardial fJ
adrenoceptors but also the activation of coronary IX-adrenoceptors can contribute to myocar
dial ischemia. However the role of fJ-adrenoceptor-mediated increases in contractility
relative to heart rate in the initiation of ischemia is not clear and the significance of
IX-adrenoceptor mediated changes in coronary vasomotor tone as well as the responsible
IX-adrenoceptor subtypes are highly controversial. Malignant arrhythmias may be triggered by
both IX- and fJ-adrenergic mechanisms. Current research in this field is focussed not only on
the underlying physiological and pathophysiological mechanisms but also on clinical treatment
strategies e. g. by fJ-blockade IX-blockade bradycardic agents and calcium antagonists.
Recent findings were presented and future research directions discussed during the 61
International Titisee Conference held at the Schwarzwald-Hotel Titisee March 29-31 1990
under the sponsorship of the Boehringer Ingelheim Foundation. Dr. Hasso Schroeder and Dr.
Hermann Frohlich deserve special thanks for their generous support and pleasant organization of
the meeting. The publication of the proceedings has been made possible by grants from Astra
Chemicals Bayer ICI Dr. Karl Thomae and Upjohn.
