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K R Wong

Publications and source records attributed to K R Wong.

21 records · Page 2Linked to original sources

Proton nuclear magnetic resonance measurement of diffusional water permeability in suspended renal proximal tubules.

Diffusional water permeability was measured in renal proximal tubule cell membranes by pulsed nuclear magnetic resonance using proton spin-lattice relaxation times (T1). A suspension of viable proximal tubules was prepared from rabbit renal cortex by Dounce homogenization and differential sieving. T1 measured in a tubule suspension (22% of exchangeable water in the intracellular compartment) containing 20 mM extracellular MnCl2 was biexponential with time constants 1.8 +/- 0.1 ms and 8.3 +/- 0.2 ms (mean +/- SD, n = 8, 37 degrees C, 10 MHz). The slower time constant, representing diffusional exchange of water between intracellular and extracellular compartments, increased to 11.6 +/- 0.6 ms (n = 6) after incubation of tubules with 5 mM parachloromercuribenzene sulfonate (pCMBS) for 60 min at 4 degrees C and was temperature dependent with activation energy Ea = 2.9 +/- 0.4 kcal/mol. To relate T1 data to cell membrane diffusional water permeabilities (Pd), a three-compartment exchange model was developed that included intrinsic decay of proton magnetization in each compartment and apical and basolateral membrane water transport. The model predicted that the slow T1 was relatively insensitive to apical membrane Pd because of low luminal/cell volume ratio. Based on this analysis, basolateral Pd (corrected for basolateral membrane surface convolutions) is 2.0 X 10(-3) cm/s, much lower than corresponding values for basolateral Pf (10-30 X 10(-3) cm/s) measured in the intact tubule and in isolated basolateral membrane vesicles. The measured P,/Pd> 1, low Ea and inhibition of Pd by pCMBS provide strong evidence that water transport in the proximal tubule basolateral membrane is facilitated by a specialized aqueous pore or narrow channel.

Animals↗

Human platelet diffusional water permeability measured by nuclear magnetic resonance.

To examine whether water transport in human platelets is mediated by an aqueous pore or channel, the ratio of osmotic to diffusional water permeability coefficients (Pf/Pd) was measured. Pd was measured from protein spin-lattice relaxation times in a dense platelet suspension (approximately 20% intracellular exchangeable water) using 20 mM solution Mn as a paramagnetic quencher. The decay of magnetization was biexponential with time constants of 1.3 and 6.9 ms (10 MHz, 37 degrees C), corresponding to a Pd of (2.9 +/- 0.2) X 10(-3) cm/s (SE; n = 8). Pd did not depend on concentrations of Mn (6-20 mM) or of platelets (2-4 X 10(10) platelets/ml), but increased to 4.5 X 10(-3) cm/s with addition of gramicidin (6 micrograms/10(10) platelets). 54Mn uptake studies showed less than 1% of equilibrium uptake of Mn into platelets in 30 min at 37 degrees C. The activation energies (Ea) for Pd were 4.5 kcal/mol (less than 28 degrees C) and 16.3 kcal/mol (greater than 28 degrees C). Pf was measured by a stopped-flow light scattering technique as reported previously [M. M. Meyer and A. S. Verkman, Human platelet osmotic water and nonelectrolyte transport, Am. J. Physiol. 251 (Cell Physiol. 20): C549-C557, 1986], in which the time course of platelet volume was measured in response to a 100 mM inwardly directed sucrose gradient. At 37 degrees C, Pf was (2.7 +/- 0.2) X 10(-3) cm/s and independent of [Mn]. The measured platelet Pf/Pd of 0.93 +/- 0.1 suggests that unlike water transport in erythrocytes, platelet water transport is not associated with an aqueous channel.

Blood Platelets↗

Effect of atrial natriuretic factor on acid-base homeostasis.

Both micropuncture and clearance studies have shown that the anion excreted in the urine in response to the increased glomerular filtration rate and solute load induced by atrial natriuretic factor (ANF) depends on the pre-existing acid-base status. In normal animals, the kidney is relatively better at reabsorbing bicarbonate than chloride, as ANF increases luminal flow so that a chloruresis without bicarbonaturia ensues. In contrast, during chronic hypochloraemic metabolic alkalosis, alkalaemia renders the kidney unable to reabsorb the increment in filtered bicarbonate induced by ANF so that bicarbonaturia occurs with amelioration of the alkalosis. Since the relative magnitudes of chloride versus bicarbonate excretion rates in response to ANF are a function of the plasma anion concentrations, ANF tends to correct acid-base disorders.

Acid-Base Equilibrium↗