Effect of dietary phosphorus, calcium, and phytase on performance of growing turkeys.

Female and male turkeys were fed 110, 73, 52, and 30% of the NRC (1994) nonphytate P (NPP) requirement without and with 500 phytase units (FTU)/kg during 4 to 14 or 16 wk of age, respectively. At 110% P (control; also 110% of NRC Ca), phytase was without effect. At 73% of NPP (100% Ca), without phytase, performance was similar to the control; with phytase, performance was equivalent, and in some stages, superior to the control. At 52% of NPP (90% Ca), performance was inferior without phytase and was variably similar or poorer than the control with phytase. At 30% NPP without phytase, poults gained poorly and showed a high incidence of leg disorder at 8 wk when they were removed from experiment; poults gained better with 80% NRC Ca compared with 110%. At 30% NPP with phytase, turkeys performed remarkably well, although suboptimally, at 80 or 110% NRC Ca. Phytase at 400, 300, and 200 FTU/kg with increasing age periods performed as well as 500 FTU/kg with 73% of NRC NPP (100% Ca) and 52% NRC NPP (90% Ca). These lower phytase levels were not as sufficient as 500 FTU/kg with 30% of NRC NPP; this inadequacy was more severe with higher dietary calcium. Phytase was effective in reducing dietary P requirements of growing turkeys when the NPP levels were below NRC (1994) requirements.

Secretory apical Cl- channels in A6 cells: possible control by cell Ca2+ and cAMP.

Distal kidney cells (A6) from Xenopus laevis were cultured to confluency on porous supports. Tissues were mounted in Ussing-type chambers to measure short-circuit current (Isc), transepithelial conductance and capacitance, and to analyse the fluctuation in Isc. In the absence of apical NaCl, but with normal basolateral NaCl Ringer's solution, extracellular addition of ATP, oxytocin, a membrane-permeant cAMP derivative, and forskolin produced a transient increase of the electrical parameters. Noise analysis revealed a spontaneous Lorentzian component. All responses depend strictly on the presence of basolateral Cl- and are caused by the activation of an apical (CFTR type) Cl- permeability. Repetitive treatment with ATP (or oxytocin) resulted in refractoriness. ATP and oxytocin acted antagonistically, whereas cAMP and ATP had additive effects. Incubation with the vesicular Ca2+ pump inhibitor thapsigargin or application of the Ca2+ channel blocker nifedipine elicited finite but variable Cl- channel activity. After treatment with nifedipine or thapsigargin, the response to oxytocin was severely impaired. We speculate that not only cAMP but also cell Ca2+ plays a crucial role in the activation of CFTR in A6. Ca2+ may be multifunctional but the rise in capacitance (apical area) observed with all stimulants strongly suggests its involvement in, and contribution to, exocytosis in the process of the CFTR-mediated transcellular Cl- movements.

Apical Cl- channels in A6 cells.

Short-circuit current (Isc), transepithelial conductance (Gt), electrical capacitance (CT) and the fluctuation in Isc were analyzed in polarized epithelial cells from the distal nephron of Xenopus laevis (A6 cell line). Tissues were incubated with Na+- and Cl--free solutions on the apical surface. Basolateral perfusate was NaCl-Ringer. Agents that increase cellular cAMP evoked increases in Gt, CT, Isc and generated a Lorentzian Isc-noise. The responses could be related to active, electrogenic secretion of Cl-. Arginine-vasotocin and oxytocin caused a typical peak-plateau response pattern. Stimulation with a membrane-permeant nonhydrolyzable cAMP analogue or forskolin showed stable increases in Gt with only moderate peaking of Isc. Phosphodiesterase inhibitors also stimulated Cl- secretion with peaking responses in Gt and Isc. All stimulants elicited a spontaneous Lorentzian noise, originating from the activated apical Cl- channel, with almost identical corner frequency (40-50 Hz). Repetitive challenge with the hormones led to a refractory behavior of all parameters. Activation of the cAMP route could overcome this refractoriness. All agents caused CT, a measure of apical membrane area, to increase in a manner roughly synchronous with Gt. These results suggest that activation of the cAMP-messenger route may, at least partly, involve exocytosis of a vesicular Cl- channel pool. Apical flufenamate depressed Cl- current and conductance and apparently generated blocker-noise. However, blocking kinetics extracted from noise experiments could not be reconciled with those obtained from current inhibition, suggesting the drug does not act as simple open-channel inhibitor.