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.
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