The Effects of Fructose Feeding on the Quantal Catecholamine Release from Adrenal Chromaffin Cells

  • Author / Creator
  • Abstract: Adrenal chromaffin cells release catecholamines in response to stress, via the exocytosis of large-dense core granules (LDCGs). Excessive stress responses, however, are harmful and can lead to the development of hypertension. The fructose-fed rats, an animal model with the symptom of hypertension, exhibit an elevated plasma catecholamine level. The object of my study was to test the hypothesis that fructose feeding may enhance the efficiency of quantal release of catecholamines from individual chromaffin cells. Carbon fiber amperometry was employed to detect quantal catecholamine release from chromaffin cells. When cells were stimulated by carbachol, a non-selective cholinergic agonist that robustly activates both muscarinic and nicotinic receptors, fructose feeding increased the amount of catecholamine released per cell as well as per individual events of exocytosis (i.e. the quantal size, Q). When cells were stimulated by dimethylphenylpiperazinium (DMPP), a selective nicotinic receptors agonist, fructose feeding caused an increase in cellular secretion which was associated with an increase in the number of events of exocytosis per cell and a smaller increase in Q. In contrast, both the carbachol and DMPP-evoked Ca2+ signals were reduced by fructose feeding. The following scenario may account for the above findings: fructose feeding recruited a population of granules with intermediate Q, resulting in an increase in the number of granules that underwent exocytosis when stimulated with nicotinic agonist. The co-activation of muscarinic and nicotinic receptors promoted some form of granule-granule fusion, resulting in the exocytosis of large Q granules which have more rapid release kinetics. My overall results suggest that fructose feeding enhances the secretion of catecholamine from rat chromaffin cells upon cholinergic stimulation. The augmentation of adrenal catecholamine release can contribute to the development of hypertension induced by high fructose consumption.

  • Subjects / Keywords
  • Graduation date
    Fall 2015
  • Type of Item
  • Degree
    Master of Science
  • DOI
  • License
    This thesis is made available by the University of Alberta Libraries with permission of the copyright owner solely for non-commercial purposes. This thesis, or any portion thereof, may not otherwise be copied or reproduced without the written consent of the copyright owner, except to the extent permitted by Canadian copyright law.
  • Language
  • Institution
    University of Alberta
  • Degree level
  • Department
  • Supervisor / co-supervisor and their department(s)
  • Examining committee members and their departments
    • Peter,Smith (Pharmacology)
    • Frances,Plane (Pharmacology)
    • Andy,Holt (Pharmacology)
    • Glen,Baker (Psychiatry)
    • Fred,Tse (Pharmacology)
    • Amy,Tse (Pharmacology)