Calcium levels in rat submandibular gland and saliva after sympathetic nerve stimulation in the presence of α, β1 and β2-adrenergic antagonists

Abstract

Calcium concentration was reduced by 51 per cent compared with unstimulated contralateral glands after 60-min of electrical stimulation to the sympathetic nerve. When the α-adrenergic antagonists, phentolamine or phenoxybenzamine, were given 20 min before stimulation, the decrease in glandular calcium concentration (45–47 per cent) was similar to that after nerve stimulation alone; with the selective β 2-adrenergic antagonist added to the phentolamine, the percentage decrease was similar to that found after phentolamine and sympathetic nerve stimulation only. When atenolol, a β 1-adrenergic antagonist, was given with phentolamine, there was no secretion after subsequent nerve stimulation, nor was calcium concentration different from that of unstimulated glands. When propranolol (3 mg/kg, body wt), or atenolol + butoxamine (3 mg/kg, body wt), was given prior to stimulation there was a decrease of 21–22 per cent in gland-calcium concentration. Calcium concentration of nerve-stimulated saliva was nearly 6m-equiv./1, and twice as high with phentolamine prior to stimulation; for butoxamine together with phentolamine the change was similar to that with phentolamine alone. When β-adrenergic antagonists were given prior to nerve stimulation, concentration of the saliva was either unchanged (propranolol) from that with nerve stimulation alone or somewhat decreased (atenolol + butoxamine). Thus sympathetic stimulation results in activation of α and β 1-adrenoceptors; calcium secretion is principally regulated by the β-adrenoceptors, and β 1-receptors have the principal role.