Salivary gland K+ transport: in vivo studies with K+-specific microelectrodes.

Poulsen, J.C. Navarro; Bledsoe, Stephen W.

doi:10.1152/ajpendo.1978.234.1.e79

Cited by 17 publications

(13 citation statements)

References 10 publications

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“…The time course of the net K movement induced by ACh, a-adrenergic agonists and substance P in the present experiments resembles that induced by prolonged parasympathetic stimulation in the perfused cat and dog submaxillary glands in 8itU (Poulsen & Bledsoe, 1978), since the K release induced by agonists was transient and fell to the pre-stimulation level during stimulation ( Fig. 2A, B and D).…”

Section: Discussionsupporting

confidence: 71%

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

Katoh¹,

Nakasato²,

Nishiyama³

et al. 1983

The Journal of Physiology

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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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Section: Discussionsupporting

confidence: 71%

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

Katoh¹,

Nakasato²,

Nishiyama³

et al. 1983

The Journal of Physiology

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“…If this were the case in the present study, then the initial potential change of the parotid cells could be explained by increased K + efflux, with EAC h equal to E~. However, it is unlikely that K § accumulated in our tissue segments to the same extent as reported by Poulsen and Bledsoe (1977) in vivo since Petersen, Gray and Hall (1977) have shown that in the superfused parotid, the rapid flow of bathing fluid prevented any marked rise in [K +] in the bath effluent. As our recordings were obtained from superficial cells it is likely that K § released from the cells was rapidly removed.…”

Section: Discussionsupporting

confidence: 59%

“…Previous reports have described increased sodium and potassium permeability in submandibular gland acinar cells stimulated with acetylcholine (Petersen, 1970(Petersen, , 1972Nishiyama & Petersen, 1974a;Poulsen, 1974). Recently Poulsen and Bledsoe (1977) have demonstrated that the concentration of K § in the interstitial fluid of cat and dog submandibular glands could rise to as high as 18 ms during the period of parasympathetic nerve stimulation. If this were the case in the present study, then the initial potential change of the parotid cells could be explained by increased K + efflux, with EAC h equal to E~.…”

Section: Discussionmentioning

confidence: 92%

Membrane potential and resistance changes induced in salivary gland acinar cells by microiontophoretic application of acetylcholine and adrenergic agonists

Roberts

Petersen

1978

J. Membrain Biol.

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The effects of microiontophoretic applications of catecholamines and acetylcholine on parotid acinar cell membrane potential and resistance were investigated using intracellular microelectrode recording in superfused segments of mouse parotid or rat submandibular glands. Short pulses of acetylcholine and alpha-adrenergic agonists had similar effects, consisting of a marked decrease in membrane resistance accompanied by an initial depolization or hyperpolarization depending on the level of the resting membrane potential. This initial response was followed by a slow hyperpolarization occurring at a time when the resistance was increasing towards the prestimulation level. The equilibrium potential for the initial potential change caused by excitation of the cholinergic receptors was investigated directly by setting the membrane potential at different levels by injecting direct current and stimulating the same cell repeatedly with equal doses of acetylcholine. The equilibrium potential was found to be about -55 mV. The delayed hyperpolarization could not be reversed by passing hyperpolarizing current, but actually increased in size with higher membrane potentials. The minimum latency of the effect of acetylcholine or alpha-adrenergic agonists was 200-500 msec. Excitation of beta-adrenoceptors caused, after a long latency of several seconds, a small depolarization. Epinephrine induced a combined alpha- and beta-adrenergic response, with the alpha-component predominating. Blocking the alpha-adrenoceptors with phentolamine revealed the beta-adrenergic depolarization, while blocking the beta-adrenoceptors with propranolol caused the components of the alpha-adrenergic response to become more pronounced. All three receptors (alpha- and beta-adrenoceptors and cholinergic receptors) were present in individual acini.

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“…Cook and colleagues (5, 6) hypothesized that fluid secretion can be driven by K channels in the apical membrane of acinar cells. In fact, there is direct evidence for an apical maxi-K-like current in the acinar cells of frog skin (41) and for apical Ca 2ϩ -activated K ϩ currents in rat lacrimal acinar cells (44 (30,50). Because the K ϩ and Na ϩ concentrations of both the acinar secretions and the venous plasma outflow from salivary gland (which reflects the interstitial ion concentration) are plasma-like, this suggests that K ϩ and Na ϩ likely enter the primary saliva across the "leaky" tight junctions of the acinus.…”

Section: Discussionmentioning

confidence: 99%

Apical maxi-K (K_Ca1.1) channels mediate K⁺ secretion by the mouse submandibular exocrine gland

Nakamoto¹,

Romanenko²,

Takahashi³

et al. 2008

American Journal of Physiology-Cell Physiology

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The exocrine salivary glands of mammals secrete K+ by an unknown pathway that has been associated with HCO3− efflux. However, the present studies found that K+ secretion in the mouse submandibular gland did not require HCO3−, demonstrating that neither K+/HCO3− cotransport nor K+/H+ exchange mechanisms were involved. Because HCO3− did not appear to participate in this process, we tested whether a K channel is required. Indeed, K+ secretion was inhibited >75% in mice with a null mutation in the maxi-K, Ca2+-activated K channel (KCa1.1) but was unchanged in mice lacking the intermediate-conductance IKCa1 channel (KCa3.1). Moreover, paxilline, a specific maxi-K channel blocker, dramatically reduced the K+ concentration in submandibular saliva. The K+ concentration of saliva is well known to be flow rate dependent, the K+ concentration increasing as the flow decreases. The flow rate dependence of K+ secretion was nearly eliminated in K Ca 1.1 null mice, suggesting an important role for KCa1.1 channels in this process as well. Importantly, a maxi-K-like current had not been previously detected in duct cells, the theoretical site of K+ secretion, but we found that KCa1.1 channels localized to the apical membranes of both striated and excretory duct cells, but not granular duct cells, using immunohistochemistry. Consistent with this latter observation, maxi-K currents were not detected in granular duct cells. Taken together, these results demonstrate that the secretion of K+ requires and is likely mediated by KCa1.1 potassium channels localized to the apical membranes of striated and excretory duct cells in the mouse submandibular exocrine gland.

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Salivary gland K+ transport: in vivo studies with K+-specific microelectrodes.

Cited by 17 publications

References 10 publications

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

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

Membrane potential and resistance changes induced in salivary gland acinar cells by microiontophoretic application of acetylcholine and adrenergic agonists

Apical maxi-K (K_Ca1.1) channels mediate K⁺ secretion by the mouse submandibular exocrine gland

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Salivary gland K+ transport: in vivo studies with K+-specific microelectrodes.

Cited by 17 publications

References 10 publications

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

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

Membrane potential and resistance changes induced in salivary gland acinar cells by microiontophoretic application of acetylcholine and adrenergic agonists

Apical maxi-K (KCa1.1) channels mediate K+ secretion by the mouse submandibular exocrine gland

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Apical maxi-K (K_Ca1.1) channels mediate K⁺ secretion by the mouse submandibular exocrine gland