Changes in rat mast cell responses in sodium-free media. Lack of demonstrable sodium channel activity.
Exposure of rat mast cells to isotonic sucrose (employed as a sodium free medium) increased several-fold the sensitivity to calcium, which itself became a stimulus for exocytosis. Concentrations of the cation as low as 25 microM permitted maximal histamine release. Preincubation of cells in sucrose to allow sodium efflux before adding the ionophore A23187 led to a slower release of histamine. We postulate that sodium efflux can generate a membrane potential that causes the increased sensitivity to calcium and the delay in response after preincubation. The response to A23187 is somewhat unspecific since the ionophore can release histamine from internal calcium reservoirs. Saxitoxin or veratridine did not affect cell responses, so that sodium activity is not mediated through defined sodium channels.
Vieytes
M R
MR
Departmentos de Farmacología y Fisiología, Fac. de Veterinaria, Universidad de Santiago de Compostela, Lugo, Spain.
Alfonso
A
A
Bujan
M J
MJ
Louzao
M C
MC
Cavado
A
A
de la Cruz
L F
LF
Botana
L M
LM
D000818:Animals; D000001:Calcimycin / Q000494:pharmacology; D002118:Calcium / Q000494:pharmacology; D006636:Histamine Release / Q000187:drug effects*; D008407:Mast Cells / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D012530:Saxitoxin / Q000494:pharmacology; D012964:Sodium / Q000502:physiology*; D015222:Sodium Channels / Q000187:drug effects / Q000502:physiology*; D013395:Sucrose / Q000494:pharmacology; D014701:Veratridine / Q000494:pharmacology
D015222:Sodium Channels; D012530:Saxitoxin; D000001:Calcimycin; D013395:Sucrose; D014701:Veratridine; D012964:Sodium; D002118:Calcium