Ionic milieu and control of K permeability in the parotid gland.
The roles of Mg, K, Na, and Cl ions in the biphasic K-permeability response (86Rb release) to receptor activation in the parotid gland were investigated. Both the transient and sustained phases of K release (86Rb release) were unaffected by alterations in Mg concentration. Elevating extracellular K enhanced 86Rb release presumably by decreasing the negativity of the membrane potential. Elevating extracellular K had no effect on the transient or sustained phases of 86Rb release due to carbachol and 1.0 mM Ca. Measurements of responses to carbachol with various substitutes for NaCl suggested that extracellular Cl and ionic strength are important for the K-permeability response. Experiments with LiCl suggested the operation of a Na-Ca exchange similar to that seen earlier in experiments with amylase release. When tetraethylammonium Cl was substituted for NaCl, the cation appeared to block K fluxes directly. Choline Cl, in partial substitution for NaCl, potentiated the sustained phase of response to substance P and, in complete substitution, produced both Ca-dependent and Ca-independent increases in 86Rb release. It was concluded that the 86Rb-release response in relatively (but not completely) insensitive to alteration in the ionic milieu. It was also concluded that Na regulates K permeability in part directly and in part by means of a Na-Ca exchange.
D000818:Animals; D002118:Calcium / Q000494:pharmacology; D002217:Carbachol / Q000494:pharmacology; D002463:Cell Membrane Permeability / Q000187:drug effects; D008274:Magnesium / Q000494:pharmacology; D008564:Membrane Potentials; D009994:Osmolar Concentration; D010306:Parotid Gland / Q000502:physiology*; D011188:Potassium / Q000494:pharmacology / Q000502:physiology*; D051381:Rats; D011950:Receptors, Cholinergic / Q000187:drug effects; D012964:Sodium / Q000494:pharmacology
D011950:Receptors, Cholinergic; D002217:Carbachol; D012964:Sodium; D008274:Magnesium; D011188:Potassium; D002118:Calcium