Loss of [ 125I]-pindolol binding to β-adrenoceptors on rat nodose ganglion after chronic isoprenaline treatment

Abstract

The nodose ganglion contains the cell bodies of afferent nerves which convey predominantly sensory information from the viscera to the central nervous system (CNS). Autoradiographic studies show binding sites for β-adrenoceptor ligands are present on sections of the rat nodose ganglion and also on the corresponding inferior vagal ganglion in humans, indicating the presence of β-adrenoceptors in these ganglia. Since prolonged stimulation of β-adrenoceptors in rats with the nonselective β-adrenoceptor agonist isoprenaline (400 μg kg- −1 day- −1 s.c.) for 14 days results in desensitisation and/or down-regulation of receptors in peripheral tissues, such as heart, kidney and blood vessels, the effects of this treatment on the β-adrenoceptor population on the nodose ganglion have been examined. Using [ 125I]-pindolol as a radioligand, autoradiographic studies revealed that specific binding was reduced by 74% in ganglia from isoprenaline-pretreated rats compared to that in ganglia from vehicle-pretreated rats, demonstrating down-regulation of receptors by isoprenaline. [ 125I]-Pindolol binding was sensitive to inhibition by ICI 118,551 (selective β 2-adrenoceptor antagonist) but not to atenolol (selective β 1-adrenoceptor antagonist), indicating receptors are predominantly of the β 2-adrenoceptor subtype. No change n in binding was apparent over the vagus nerve. The nodose ganglion appears to be an additional site at which β 2-adrenoceptors may be down-regulated in vivo, possibly interfering with normal baro-, chemo- and sensory reflexes.