Stimulation of sympathetic nerves to the toad heart produced increases in both the rate and force of cardiac beat. Although these responses were abolished by treatment with bretylium (10-6 mol ·l-1) or 6-hydroxydopamine (100 mg·kg-1), and surgical sympathetic denervation, they were not abolished by treatment with propranolol (10-6 mol·l-1) and phentolamine (3×10-6 mol·l-1), either alone or in combination. The responses remaining after adrenoceptor blockade could not be ascribed to the effects of neurally released dopamine, ATP, adenosine, histamine or a variety of neuropeptides, although the participation of an as yet unidentified co-transmitter cannot be ruled out. Quantitative analysis of the interactions between propranolol and adrenaline on cardiac adrenoceptors, after blockade of α-receptors and amine uptake mechanisms, revealed that these interactions do not comply with the conditions for simple competitivity. Therefore, in addition to its action on β-receptors, adrenaline seems to be producing excitation of the toad heart by acting on adrenoceptors which cannot be classified as either α-or β-receptors. These results, together with the existence of close neuromuscular gaps (<50nm) in the toad heart, are consistent with the hypothesis that sympathetic excitation of the toad heart is mediated by both "extra-junctionl" β-adrenoceptors, and "junctional" adrenoceptors which are neither α-nor β-receptors.
|Number of pages||8|
|Journal||Naunyn-Schmiedeberg's Archives of Pharmacology|
|Publication status||Published - Nov 1981|
- Amphibian heart