1. Phosphatidylinositol turnover has been measured in intact, perfused rat hearts by measuring generation of inositol phosphates following [3H]‐inositol labelling. Stimulation of accumulations of inositol wonophosphate, inositol bisphosphate and inositol tris phosphate were observed during perfusion with either noradrenaline (3×10‐5 mol/l) or carbachol (10‐3 mol/l). 2. Stimulation by noradrenaline was antagonized by prazosin (10‐7 mol/l) but not by propranolol (10‐7 mol/l), indicating mediation via α‐adrenoceptors. Stimulation by carbachol was antagonized by atropine (10‐7 mol/l). 3. Transmural electrical stimulation of the hearts failed to increase inositol phosphate accumulation through α1‐adrenoceptors. A small stimulation mediated by muscarinic receptors was observed. Therefore α1‐adrenoceptors which stimulate phosphatidylinositol turnover probably do not have a synaptic localization in heart. 4. The development of methods for the study of phosphatidylinositol turnover in intact hearts will facilitate an investigation of relationships between this signal transduction pathway and cardiac function.
|Number of pages||5|
|Journal||Clinical and Experimental Pharmacology and Physiology|
|Publication status||Published - 1 Jan 1987|
- inositol tris phosphate
- muscarinic cholinergic receptor
- α ‐adrenoceptor