The amino acid exchange R145G in the inhibitory domain of the inhibitory subunit of the cardiac troponin complex (cTnI) causes Hypertrophic Cardiomyopathy. In previous studies we analysed the extent and rate of sarcomer shortening as well as its relaxation rate are in response to β1/2-, β1- and β2-adrenergic receptor (AR) stimulation in ventricle cells where contractions were induced by bipolar external stimuli (0.4 ms, 40 V). The localisation of adenovirus driven human cTnI-wt and cTnI-R145G in the sarcomeres is controlled with anti-human cTnI monoclonal antibodies which do not recognizing rat cTnI. In those studies we could show that neither GFP (green fluorescent protein) nor the human cTnI-wt have any influence on the contraction behaviour of adult rat ventricle cells compared with not infected cells. We were also able to show that the amino acid exchange R145G – compared with cTnI-wt – reduced shortening as well as rate of shortening and relaxation significantly in non-AR stimulated and in β1/2- and β2-AR stimulated ventricle cells. However, rates of shortening and relaxation were not reduced in ventricle cells stimulated via β1-AR (ISHR, Manchester, UK, 2006). In our recent studies we tested the influence of Forskolin on human cTnI-wt and cTnI-R145G infected ventricle cells to analyse on which level of the β-AR pathway the differences are localised. In Forskolin treated cells we could not detect any difference between both cell types. The observed effects might be evoked by factors far downstream of the β-adrenergic signalling pathway, e.g. by different calcium handling. The underlying mechanism is not known yet, but the results clearly underline that β1- and β2-adrenergic signalling act differently on regulation of contraction.