We have evaluated the possibility that, in patients with left ventricular heart disease, the effects of aortic and mitral regurgitation on platelet alpha 2-adrenoceptors may depend on the origin and severity of the overload. Receptor density and binding affinities were estimated by their specific binding to [3H]-yohimbine. In blood donor controls (CON), the receptor density was 4.72 +/- 0.41 fmol/10(6) platelets (n = 31). In the volume overloaded patients (n = 35), the total density was elevated by 57% (p < 0.05) accompanied by a 69% (p < 0.05) increase in plasma epinephrine. Compared with CON, patients with pure aortic regurgitation (AVR, n = 12) showed a 91% (p < 0.0001), pure mitral regurgitation (MVR, n = 15) 43% (p < 0.05) and mixed mitral and aortic valve regurgitation (MOL, n = 8) 23% increase in receptor density. Furthermore, the elevation of the density in the aortic disease was significantly greater (p < 0.05) than in the mixed overload group. There was a weak positive correlation between the increase in receptor density and the ejection fractions (r = 0.27), suggesting that the former may be dependent on the severity of the volume overload. The results show that in left heart valvular disease, aortic regurgitation leads to a highly significant increase in alpha-adrenoceptor density, while the effects of mitral valve disease exhibit borderline significance. These findings probably point to the differences in the extent of influence of the origin and severity of the two forms of left ventricular volume overload (LVO), as well as the ensuing hemodynamic changes on the cardiac contractile apparatus.