Active Potassium Secretion Research Articles

Demonstration of active potassium secretion in the late distal tubule.

Studies were performed in the rat, under steady-state conditions, to determine the mode of potassium transport in the late distal tubule. In these experiments the potential difference and potassium activity were measured simultaneously in steady-state fluid droplets in control rats, during acute infusion of KCl, and in potassium-deficient rats. The results demonstrate active potassium secretion in the late distal tubule of the control and KCl-infused animals, since the observed potassium activity of 11.14 +/- 1.39 in control animals and 25.26 +/- 2.96 meq/liter in potassium-loaded animals was significantly greater than the predicted values of 7.75 +/- 0.59 and 14.01 +/- 0.94 meq/liter in the same groups, respectively. In potassium-deficient animals, however, the observed potassium activity in luminal fluid of 4.03 +/- 0.55 meq/liter was not different from the predicted value of 4.26 +/- 0.32. In summary, this study demonstrates that potassium secretion in the late distal tubule of the rat occurs by an active process and fails to demonstrate active absorption in the same tubular segment.

Cyclic Adenosine Monophosphate Stimulates Active Potassium Secretion in the Rat Colon

To determine whether cyclic adenosine monophosphate influences active potassium transport in the rat colon, we studied the effect of dibutyryl cyclic adenosine monophosphate and theophylline on unidirectional transmural 42K fluxes across proximal colonic mucosa under short-circuited conditions. Active potassium secretion (-0.19 +/- 0.02 microEq/h X cm2) was present in animals maintained on a normal potassium diet. Both 0.5 mM dibutyryl cyclic adenosine monophosphate and 5 mM theophylline significantly increased net potassium secretion by 0.49 +/- 0.04 and 0.33 +/- 0.03 microEq/h X cm2, p less than 0.001, respectively; the stimulation of net potassium secretion was secondary to an increase in serosal-to-mucosal potassium transport without change in mucosal-to-serosal potassium movement. A similar increase in active potassium secretion (from -0.15 +/- 0.03 to -0.32 +/- 0.03 microEq/h X cm2, p less than 0.005) was produced by bethanechol, a cholinergic muscarinic agonist that alters sodium and chloride transport by a noncyclic adenosine monophosphate, calcium-dependent process. In animals maintained on a high potassium diet, active potassium secretion was significantly increased to -0.79 +/- 0.17 microEq/h X cm2 (p less than 0.001). In these potassium-loaded animals, theophylline produced a greater increase in active potassium secretion (0.91 +/- 0.10 vs. 0.33 +/- 0.03 microEq/h X cm2, p less than 0.001) than in animals fed a normal potassium diet. These studies demonstrate that cyclic adenosine monophosphate and noncyclic adenosine monophosphate mediated secretogogues stimulate active potassium secretion. We speculate that the mechanism by which cyclic adenosine monophosphate increases active potassium secretion is related to an increase in luminal potassium conductance.

Dietary modulation of active potassium secretion in the cortical collecting tubule of adrenalectomized rabbits.

Addisonian patients can maintain potassium homeostasis despite the absence of mineralocorticoid. The present in vitro microperfusion studies examine what role the cortical collecting tubule might play in this process. All studies were performed on tubules harvested from adrenalectomized rabbits, which were maintained on 0.15 M NaCl drinking water and dexamethasone 50 mug/d. Perfusion and bath solutions were symmetrical Ringer's bicarbonate with [K] of 5 meq/liter. Initial studies on cortical collecting tubules from adrenalectomized animals ingesting a high potassium chow (9 meq K/kg body wt) demonstrated net potassium secretion against an electrochemical gradient (mean collected fluid [K] 16.5+/-2.6 meq/liter with an observed transepithelial voltage of -6.3+/-4.1 mV; predicted voltage for passive distribution of potassium being -28.2 mV). To examine whether this active potassium secretion could be modulated by dietary potassium, independent of mineralocorticoid, two diets identical in all respects except for potassium content were formulated. Potassium secretion was compared in cortical collecting tubules harvested from adrenalectomized animals on low (0.1 meq K) and high (10 meq K) potassium intake. Mean net potassium secretion by cortical collecting tubules was 2.02+/-0.54 peq mm(-1) min(-1) in the low potassium diet group and 5.34+/-.74 peq.mm(-1).min(-1) in the high potassium group. The mean transepithelial voltages of the collecting tubules did not differ between the two dietary groups. While net Na reabsorption was significantly greater in tubules from the high K group, this could not account for the differences in K secretion. These data demonstrate that: (a) the cortical collecting tubule can actively secrete potassium and that the magnitude of this potassium secretion correlates with potassium intake; (b) this active potassium secretory process in independent of mineralocorticoid. These findings support the hypothesis that the cortical collecting tubule may contribute to K homeostasis in Addison's disease.

The osmoregulatory role of the filter‐chamber in relation to phloem‐feeding in Eurymela distincta (Cicadelloidea, Homoptera)

ABSTRACT. The cicadelloid leaf‐hoppers, Eurymela distincta (Signoret) and Eurymela fenestrata (Le Pelletier & Serville), feed on the phloem sap of Eucalyptus spp. The osmotic pressure profile of haemolymph and gut fluids is consistent with a filtration mechanism based on passive osmosis. This is responsible for shunting water rapidly from foregut to hindgut in the relatively simple filter chamber. The osmotic gradient which drives the system is probably produced by active secretion of sodium and potassium into the Malpighian tubules and posterior midgut. Although the osmotic pressures in all parts of the system are higher, the mechanism is probably similar to that previously described for xylem‐feeding cicadas.The major haemolymph cations are sodium and magnesium and the concentrations of sodium and magnesium in the urine are higher than potassium. A variety of storage granules in the midgut contain calcium, phosphorus (as phosphate), ferric iron, zinc, magnesium, manganese and copper.

Mechanisms of transport of Na, Cl, and K in the human colon

Ionic transport across isolated, stripped, human colonic mucosa was studied in vitro using a modified short circuit current technique. Electrical potential difference and short circuit current were dependent on the presence of sodium ions in the mucosal bathing solution and were unaffected by addition of 10 mM glucose to the solution. Ouabain (10(-3) M) added to the serosal reservoir abolished both potential difference and short circuit current. Isotopic flux measurements across short-circuited colonic mucosa showed a net active sodium absorption which accounted for the observed short circuit current and was unaffected by 10 mM glucose. Chloride was also actively absorbed and this was unaffected by removal of sodium from the bathing solutions. Ouabain abolished net sodium absorption but had no effect on chloride absorption. There was a net active secretion of potassium which was abolished in sodium-free buffer. We conclude that sodium is actively absorbed via a rheogenic process which is not stimulated by glucose; chloride is actively absorbed via a nonelectrogenic process, not linked to sodium transport, and probably involving a Cl-HCO3- exchange; and postassium is actively secreted possibly via a Na+K+ exchange.

Effect of acid lumen pH on potassium transport in renal cortical collecting tubules.

In order to determine the effect of acid lumen pH on renal tubular potassium transport, cortical collecting tubules were dissected from rabbit kidneys and perfused in vitro. When the pH of the perfusate was lowered from 7.4 to 6.8, potassium secretion into the tubule lumen decreased by an average of 47%. The transepithelial voltage increased from a mean value of -32 mV (lumen negative) at pH 7.4 to -51 mV at PH 6.8. Net sodium absorption from the tubule lumen was essentially unchanged (5% mean decrease). Transepithelial voltage and potassium secretion returned to control values when the pH of the perfusate was raised to 7.4. Alterations in pH of the bath had no comparable effect on the transepithelial voltage, whether the bath pH was increased or decreased. We conclude that a decrease in the pH of the tubule fluid of itself inhibits active potassium secretion in this tubule segment, providing an additional explanation for the decrease in potassium excretion found in acidosis. The negative voltage (presumably caused by sodium absorption out of the lumen) is increased under these conditions, possibly because of reduction of a smaller counterbalancing positive voltage caused by potassium secretion into the lumen.

Evidence for Na+ independent active secretion of K+ and HCO - 3 by rat salivary duct epithelium.

In order to elucidate whether or not active secretion of potassium and bicarbonate by the rat submaxillary duct epithelium operates independently of sodium reabsorption, Na+ transport was blocked by amiloride, which is known to inhibit Na+ entry from lumen into cell. With 10(-4) M amiloride in HCO - 3 -Ringer at the luminal side, the transepithelial electrical potential difference approached zero, the Na+ conductance of the luminal cell membrane was drastically reduced, and the K+ conductance was significantly reduced. Net K+ secretion was reduced by 80%, whereas net HCO - 3 secretion was significantly increased. The remaining 20% of net K+ secretion proceeded at zero net Na+ transport and in the absence of significant chemical and electrical potential differences between lumen and interstitium of the duct. This active component of net K+ secretion was accompanied by an equal rate of active HCO - 3 secretion. These findings confirm the independence of this active secretion of K+ and HCO - 3 from Na+ transport. They indicate an electrically neutral secretion of K+ and HCO - 3, probably by the postulated luminal K+ -H+ -exchange mechanism. The 80% of net K+ secretion, which were abolished by amiloride together with Na+ reabsorption, seem to be functionally coupled with Na+ transport. The linkage of K+ -to- Na+ is probably mediated by a luminal carrier exchanging Na+ for K+ and H+.

The action of aldosterone on Na+ and K+ transport in the rat submaxillary main duct.

The main excretory duct of the submaxillary gland of normal and adrenalectomized rats was perfused with bicarbonate Ringer's solution and the following values were measured: the transepithelial electrical potential difference, the specific electrical resistance of the epithelium, and the transepithelial net fluxes for Na+ and K+. From the potential difference and the resistance, the short circuit current was calculated. Following adrenalectomy the short circuit current dropped to about one half, while the electrical resistance increased around twofold and the transepithelial potential difference remained constant. The reduction of short circuit current was accompanied by a 30% reduction of Na+ reabsorption whereas K+ secretion was only slightly diminished Acute substitution of aldosterone to adrenalectomized animals led to a restitution of the Na+ fluxes and showed a tendency to increase K+ secretion. Following the administration of Actinomycin D to normal animals, Na+ resorption declined as in adrenalectomized rats but K+ secretion remained essentially unchanged. From these observations it is concluded that the hypothetical aldosterone-induced proteins act only on Na-resorption and that they may act by both increasing the sodium permeability of the luminal cell membrane and stimulating active Na+ transport. The latter effect does not seem to consist of a non specific enhancement of the energy supply since it does not influence the active potassium secretion of the cell.

Renal transport sites for K, H and NH3. Effect of impermeant anions on their transport

The stop flow technique was used to locate the sites of the renal transport mechanisms for potassium, hydrogen and ammonium. Data were obtained which indicate that these cations are secreted in a very distal area of the nephron, presumably in the collecting ducts. Potassium reabsorption also occurs in a distal area immediately proximal to the secretory site. Infusions of thiosulfate, ferrocyanide and phosphate alter the stop flow concentration patterns so that secretion of the cations appears to take place throughout the distal tubule and to be coextensive with distal sodium reabsorption. No clear indication of potassium reabsorption is evident under these circumstances. It is suggested that these anions, because of the impermeability of the distal tubule to them and because of their negative charge, attract hydrogen and potassium into the tubular lumen as sodium is reabsorbed. In effect, an abnormal exchange mechanism is created at a site proximal to that where active secretion of hydrogen and potassium occurs.