Activation of potassium transport induced by secretagogues in superfused submaxillary gland segments of rat and mouse.

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Abstract
In order to investigate the actions of acetylcholine (ACh), catcholamines and substance P on K transport in the submaxillary gland, measurements of net K flux to and from the gland tissue using flame photometry, Na efflux from the tissue using radioactive 22Na, and membrane potential and input resistance using micro-electrodes were carried out on isolated superfused segments of rat and mouse submaxillary glands. ACh (5.5 .times. 10-8 to 5.5 .times. 10-4 M), phenylephrine (5 .times. 10-7 to 5 .times. 10-4 M) or substance P (10-9 to 10-5 M) stimulation for 5 min induced a transient K release followed by a small K uptake after the cessation of stimulation. The K release was markedly enhanced by the simultaneous addition of ouabain (10-3 M). On the other hand, isoprenaline (2.5 .times. 10-9 to 2.5 .times. 10-5 M) induced a transient K uptake without any preceding K release. The K uptake was completely blocked by the addition of ouabain. Noradrenaline [norepinephrine] induced only K uptake at a low concentration (3 .times. 10-7 M), but induced transient K release followed by marked K uptake at higher concentrations (3 .times. 10-6 to 3 .times. 10-4 M). The K release induced by noradrenaline was suppressed by the addition of phentolamine (10-5 M), while the K uptake was suppressed by propranolol (5 .times. 10-6 M). The K release induced by ACh, phenylephrine, nordrenaline or substance P was severely reduced by Ca omission from the superfusing solution and restored by the readmission of Ca. The isoprenaline- or noradrenaline-induced K uptake was, however, little affected by Ca omission. Application of isoprenaline (2.5 .times. 10-6 M) induced an increase in 22Na efflux. The increase in 22Na efflux was completely abolished in the presence of ouabain. Local application to the tissue bath of isoprenaline (4.7 .times. 10-13 to 4.7 .times. 10-12 mol) or noradrenaline (5.7 .times. 10-12 to 5.7 .times. 10-11 mol) in the presence of phentolamine (10-5 M) induced membrane hyperpolarization without any appreciable change in input resistance. The hyperpolarization was abolished in the presence of ouabain (10-3 M) or propranolol (5 .times. 10-6 M) or in a K-free or low Na solution. Higher doses of both agonists, however, induced depolarization or biphasic responses (initial depolarization followed by hyperpolarization). The depolarizations were accompanied by a moderate reduction in input resistance. In the rat and mouse submaxillary gland acinar cells cholinergic, .alpha.-adrenergic or substance P stimulation causes K release (and perhaps Na uptake) resulting in activation of the Na-K pump, while .beta.-adrenergic receptor stimulation might directly activate the Na-K pump resulting in K uptake, or might cause Na uptake resulting in activation of the Na-K pump.