Secretory responses of intact glomus cells in thin slices of rat carotid body to hypoxia and tetraethylammonium

Citation
R. Pardal et al., Secretory responses of intact glomus cells in thin slices of rat carotid body to hypoxia and tetraethylammonium, P NAS US, 97(5), 2000, pp. 2361-2366
Citations number
30
Categorie Soggetti
Multidisciplinary
Journal title
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
ISSN journal
00278424 → ACNP
Volume
97
Issue
5
Year of publication
2000
Pages
2361 - 2366
Database
ISI
SICI code
0027-8424(20000229)97:5<2361:SROIGC>2.0.ZU;2-E
Abstract
We have developed a thin-slice preparation of whole rat carotid body that a llows us to perform patch-clamp recording of membrane ionic currents and to monitor catecholamine secretion by amperometry in single glomus cells unde r direct visual control. In normoxic conditions (PO2 approximate to 140 mmH g; 1 mmHg = 133 Pa), most glomus cells did not have measurable secretory ac tivity, but exposure to hypoxia (PO2 approximate to 20 mmHg) elicited the a ppearance of a large number of spike-like exocytotic events. This neurosecr etory response to hypoxia was fully reversible and required extracellular C a2+ influx. The average charge of single quantal events was 46 +/- 25 fC (n = 218), which yields an estimate of approximate to 140,000 catecholamine m olecules per vesicle. Addition of tetraethylammonium (TEA; 2-5 mM) to the e xtracellular solution induced in most (>95%) cells tested (n = 32) a secret ory response similar to that elicited by low PO2. tells nonresponsive to hy poxia but activated by exposure to high external K+ were also stimulated by TEA, A secretory response similar to the responses to hypoxia and TEA was also observed after treatment of the cells with iberiotoxin to block select ively Ca2+- and voltage-activated maxi-K+ channels. Our data further show t hat membrane ion channels are critically involved in sensory transduction i n the carotid body. We also show that in intact glomus cells inhibition of voltage-dependent K+ channels can contribute to initiation of the secretory response to low PO2.