Differential changes in α- and β-adrenoceptor linked [⁴⁵Ca²⁺] uptake in platelets from patients with anorexia nervosa

[⁴⁵Ca²⁺] Uptake was studied in response to adrenaline, isoprenaline, noradrenaline, and (Bu)₂CAMP in platelets from patients with anorexia nervosa. In both controls and anorectics, adrenaline, isoprenaline, noradrenaline, and (Bu)₂CAMP stimulated [⁴⁵Ca₂₊] uptake. In receptor subtype characterisation studies on control platelets, adrenaline-stimulated [⁴⁵Ca²⁺] uptake was blocked by yohimbine (an α2-adrenceptor antagonist) and the specific β₂-adrenoceptor antagonist ICI 118,551, but not by atenolol (a β₁-antagonist). Isoprenaline action was blocked by ICI 118,551, but not by yohimbine. Noradrenaline-stimulated [⁴⁵Ca²⁺] uptake was blocked by yohimbine but not by ICI 118,551. In platelets from anorectic patients, there was a significant increase in noradrenaline-stimulated [⁴⁵Ca²⁺] uptake, a significant diminution in adrenaline and isoprenaline-stimulated [⁴⁵Ca²⁺] uptake, but no significant difference in (Bu)₂cAMP-stimulated [⁴⁵Ca²⁺] uptake, when compared with controls. Basal uptake was also significantly enhanced in anorectics and was found to be inhibited with verapamil but not adrenoceptor antagonist. These data firstly indicate that both α₂- and β₂-adrenoceptor activation elicits [⁴⁵Ca²⁺] uptake by platelets. It is proposed that this stimulated [⁴⁵Ca²⁺] uptake does not reflect changes in cytosolic Ca²⁺ but to localized changes of Ca²⁺ at the plasma membrane, possibly associated with receptor activation, per se. The respective increase and decrease of α-and β-adrenoceptor activity in platelets from anorectic patients is in accord with other reports of changes of adrenoceptor number and type in platelets and other cells from anorectic patients. There may also be an increase in calcium channel activity in platelets from anorectics.