Simultaneous flux of potassium into and out of the dog intestine

Berger, Eugene Y.; Kanzaki, Grace; Homer, Mary A.; Steele, J. Murray

doi:10.1152/ajplegacy.1959.196.6.1270

Cited by 14 publications

(1 citation statement)

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“…However, the possibility that these high K values are influenced by the presence of bacteria, exfoliated epithelial cells and/or undigested vegetable matter cannot be excluded. The same criticism applies to the value of 60ram for canine feces reported by Berger, Kanzaki and Steele (1959). Phillips and Code (1966) reported that the "equilibrium concentration" of K in the luminal fluid perfusing canine large intestine is approximately 17mM and that this cannot be accounted for by the PD which had a mean value of 9.1mV (range 0.1-15.4mV); these authors concluded that active K secretion "may occur in the colon".…”

Section: Ion Transport By Mammalian Colonmentioning

confidence: 97%

Effect of aldosterone on ion transport by rabbit colonIn vitro

1978

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Segments of descending colon obtained from rabbits, that had been maintained on drinking water containing 25 mM NaCl and an artificial diet which contains 1% Na and is nominally K-free, respond to aldosterone in vitro (after a 30 to 60-min lag period) with a marked increase in the short-circuit current (Isc), an equivalent increase in the rate of active Na absorption (JNa net) and a decline in tissue resistance (Rt). Aldosterone also brings about a marked increase in the unidirection influx of Na into the cells across the mucosal membrane ("zero-time" rate of uptake) which does not differ significantly from the inrease m Isc. Treatment of control tissues with amphotericin B brings about sustained increases in Isc and JNa net to levels observed in aldosterone-treated tissues. However, addition of amphotericin B to the mucosal solution of aldosterone-treated tissues does not result in a sustained increase in Isc or JNa net and these values do not differ markedly from those observed in control tissues treated with amphotericin B. These findings, together with other evidence that Na entry in the presence of amphotericin B is sufficiently rapid to saturate the active Na extrusion mechanism at the baso-lateral membrane, are consistent with the notion that the aldosterone-induced protein increases the permeability of the mucosal membrane to Na but does not increase the "saturation level" of the active Na "pump" within the time-frame of these studies (3 hr). Finally, aldosterone has no effect on the bidirectional or net transepithelial movements of K under short-circuit conditions, suggesting that the enhanced secretion of K observed in vivo is the result of increased diffusion of K from plasma to lumen via paracellular pathways in response to an increased transepithelial electrical potential difference (lumen negative).

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Section: Ion Transport By Mammalian Colonmentioning

confidence: 97%