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

https://doi.org/10.1016/0165-1838(96)00025-2Get rights and content

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 β2-adrenoceptor antagonist) but not to atenolol (selective β1-adrenoceptor antagonist), indicating receptors are predominantly of the β2-adrenoceptor subtype. No change n in binding was apparent over the vagus nerve. The nodose ganglion appears to be an additional site at which β2-adrenoceptors may be down-regulated in vivo, possibly interfering with normal baro-, chemo- and sensory reflexes.

References (30)

  • A.R. Kompa et al.

    Effect of chemical sympathectomy on (−)-isoprenaline-induced changes in cardiac β-adrenoceptor subytpes in the guinea-pig and rat

    J. Auton. Pharmacol.

    (1994)
  • M.T. Kowalski et al.

    Comparison of the effects of xamoterol and isoprenaline on rat cardiac β-adrenoceptors: studies of function and regulation

    Br. J. Pharmacol.

    (1990)
  • A.J. Lawrence et al.

    Visualisation of β-adrenoceptor binding sites on human inferior vagal ganglia and their axonal transport along the rat vagus nerve

    J. Hypertens.

    (1995)
  • M.J. Lohse et al.

    β-Arrestin: A protein that regulates β-adrenergic receptor function

    Science

    (1990)
  • S.W. Martin et al.

    Effects of chronic intravenous infusions of dopexamine and isoprenaline to rats on D1-, β1- and β2-receptor-mediated responses

    Br. J. Pharmacol.

    (1994)
  • Cited by (6)

    • 5-HT activates vagal afferent cell bodies in vivo: Role of 5-HT<inf>2</inf> and 5-HT<inf>3</inf> receptors

      2006, Neuroscience
      Citation Excerpt :

      We propose that the presence of these functional proteins allows circulating factors within the OA microcirculation to alter the activity of vagal afferents via direct actions on the cell bodies. Many functional proteins generated by vagal afferent also undergo axonal transport to the central terminals within the nuclei tractus solitarii (NTS) and to peripheral terminals in target tissues such as the heart and lungs (see Laduron, 1984a,b; Lewis et al., 1986, 1987, 1988; Allen et al., 1987; Gao et al., 1992; Krstew et al., 1998; Watkins et al., 1996; Fong et al., 2000). However, not all functional proteins undergo transport to the peripheral terminals.

    • Occipital artery injections of 5-HT may directly activate the cell bodies of vagal and glossopharyngeal afferent cell bodies in the rat

      2006, Neuroscience
      Citation Excerpt :

      This supports the contention that the differential expression of functional proteins allows for circulating factors to target a specific type of afferent. Many functional proteins generated by vagal afferent undergo axonal transport to the central terminals in the nuclei tractus solitarius (NTS) and to peripheral terminals in target tissues such as the heart (Laduron, 1984a,b; Lewis et al., 1986, 1987, 1988; Allen et al., 1987; Gao et al., 1992; Krstew et al., 1998; Watkins et al., 1996; Fong et al., 2000). As such, increased concentrations of circulating factors such as 5-HT, angiotensin II and arginine vasopressin, which occur in a variety of disease processes such as renin-dependent hypertension (see Morelowska-Spierzak et al., 1995), may have the ability to alter the synthesis and net transport of functional proteins to the central and peripheral afferent terminals.

    • Tachyphylaxis to 5-HT<inf>3</inf>-receptor-mediated activation of vagal afferents is prevented by co-activation of 5-HT<inf>2</inf> receptors

      2006, Brain Research
      Citation Excerpt :

      The use of phenylephrine has an important additional benefit in that this α1-adrenoceptor agonist will not directly activate vagal afferents. More specifically, although vagal afferents express β-adrenoceptors (Watkins et al., 1996), they do not appear to express α-adrenoceptors (see Meller et al., 1991, 1992). Resting hemodynamic values remained constant in each experiment.

    View full text