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

Abstract

In order to investigate the actions of acetylcholine (ACh), catecholamines 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 X 10(-8) to 5.5 X 10(-4) M), phenylephrine (5 X 10(-7) to 5 X 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 X 10(-9) to 2.5 X 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 induced only K uptake at a low concentration (3 X 10(-7) M), but induced transient K release followed by marked K uptake at higher concentrations (3 X 10(-6) to 3 X 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 X 10(-6) M). The K release induced by ACh, phenylephrine, noradrenaline or substance P was severely reduced by Ca omission from the superfusing solution and restored by the re-admission of Ca. The isoprenaline- or noradrenaline-induced K uptake was, however, little affected by Ca omission. Application of isoprenaline (2.5 X 10(-6) M) induced an increase in 22 Na efflux. The increase in 22Na efflux was completely abolished in the presence of ouabain. Local application to the tissue bath of isoprenaline (4.7 X 10(-13) to 4.7 X 10(-12) mole) or noradrenaline (5.7 X 10(-12) to 5.7 X 10(-11) mole) 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 X 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. It is concluded that 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.