Transmitter-induced changes of the membrane voltage of HT29 cells.

The colonic carcinoma cell line HT29 was used to examine the influence of agonists increasing cytosolic cAMP and Ca2+ activity on the conductances and the cell membrane voltage (Vm). HT29 cells were grown on glass cover-slips. Cells were impaled by microelectrodes 4-10 days after seeding, when they had formed large plaques. In 181 impalements Vm was -51 +/- 1 mV. An increase in bath K+ concentration from 3.6 mmol/l to 18.6 mmol/l or 0.5 mmol/l Ba2+ depolarized the cells by 10 +/- 1 mV (n = 49) or by 9 +/- 2 mV (n = 3), respectively. A decrease of bath Cl- concentration from 145 to 30 mmol/l depolarized the cells by 11 +/- 1 mV (n = 24). Agents increasing intracellular cAMP such as isobutylmethylxanthine (0.1 mmol/l), forskolin (10 mumol/l) or isoprenaline (10 mumol/l) depolarized the cells by 6 +/- 1 (n = 13), 15 +/- 3 (n = 5) and 6 +/- 2 (n = 3) mV, respectively. In hypoosmolar solutions (225 mosmol/l) cells depolarized by 9 +/- 1 mV (n = 6). Purine and pyrimidine nucleotides depolarized the cells dose-dependently with the following potency sequence: UTP greater than ATP greater than ITP greater than GTP greater than TTP greater than CTP = 0. The depolarization by ATP was stronger than that by ADP and adenosine. The muscarinic agonist carbachol led to a sustained depolarization by 27 +/- 6 mV (n = 5) at 0.1 mmol/l, and to a transient depolarization by 12 +/- 4 mV (n = 5) at 10 mumol/l. Neurotensin depolarized with a half-maximal effect at around 5 nmol/l.(ABSTRACT TRUNCATED AT 250 WORDS)