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Biomedical subjects

T E Andreoli

Publications and source records attributed to T E Andreoli.

At least 91 records · Page 5Linked to original sources
PubMed1981

NaCl transport in mouse medullary thick ascending limbs. I. Functional nephron heterogeneity and ADH-stimulated NaCl cotransport.

We assessed the effects of antidiuretic hormone and cyclic adenosine monophosphate (cAMP) analogues on transepithelial voltage, Ve, and/or net chloride absorption in isolated mouse medullary (mTALH) and cortical (cTALH) thick ascending limbs of Henle; the passive NaCl permeability characteristics and electrical properties of the mTALH; and the effects of anion and cation substitutions and transport inhibitors on both basal and ADH-stimulated Ve and/or net chloride absorption in the mTALH. The data demonstrate that these two segments are functionally heterogeneous: ADH, at concentrations comparable to plasma levels seen in mammalian species during ordinary antidiuresis, and/or cAMP increase three- to fourfold the rate of NaCl absorption in the mTALH but not in the cTALH. The ion substitution and inhibitor data are consistent with the view that NaCl absorption in the mTALH depends on a secondary active transport process: NaCl entry across luminal membranes is a coupled process of indeterminate stoichiometry that is driven by the transmembrane electrochemical gradient for Na+, which is maintained by Na+-K+-ATPase. Finally, the data demonstrate that the mTALH is electrically leaky whether measured electrically, 11 omega . cm2, or isotopically, 50 omega . cm2, but essentially water impermeable; and that the mTALH is perm-selective for Na+ with respect to Cl-. The disparity between electrical resistances measured directly with respect to those calculated from tracer fluxes, together with the hybrid characteristics of mTALH junctional complexes (leaky to Na+ and Cl-; tight to water), may be reconciled by assuming that mTALH junctional complexes contain passive ion permeation pathways composed of narrow channels through which ions pass in single-file fashion.

Amiloride↗
PubMed1981

NaCl transport in mouse medullary thick ascending limbs. II. ADH enhancement of transcellular NaCl cotransport; origin of transepithelial voltage.

We measured the relations between tubular perfusion rate and the rate of net NaCl transport in medullary thick ascending limbs of Henle (mTALH) either in the presence or absence of ADH. These data, together with the known Na+, Cl-, and water permeability characteristics of the mTALH, were used to calculate tau NaCl (mol . s-1 . cm-2), the rate of conservative Cl- transport from lumen through cells to interspaces; and CNaCl, the effective NaCl concentration in lateral intercellular spaces. The experimental results indicate that in these tubules the rate of net Cl- absorption increases monotonically with perfusion rate, and that at a given perfusion rate ADH increases the rate of net salt absorption. The theoretical calculations show clearly that the ADH-mediated increase in salt absorption depends on an increase in the rate of conservative transcellular Cl- transport. However, the present analytical data do not permit a distinction between wholly electroneutral apical membrane NaCl entry with respect to a process in which apical membrane Na+/Cl- entry has a stoichiometry less than unity, and electrogenic Na+ transport accounts for the remaining component of net Na+ absorption. Identification of the stoichiometry of the Na+/Cl- apical membrane entry step will depend, among other factors, on identifying explicitly the diffusion resistance of paracellular fluid and the mode of passive ion transport across junctional complexes.

Animals↗
PubMed1981

NaCl transport in mouse medullary thick ascending limbs. III. Modulation of the ADH effect by peritubular osmolality.

We evaluated the effects of increasing bath osmolality on both the passive permeability properties and the ADH-dependent rates of net Cl- absorption in isolated mouse medullary thick ascending limbs of Henle (mTALH). Increases in both osmolality to 900 mosmol/kg H2O with 600 mM urea had no effect on either the electrical (PNa/PCl ratio, 1.7 and 1.9 with and without peritubular urea, respectively) or tracer (PNa, 0.21 and 0.22 micrometers . s-1 with and without peritubular urea, respectively) ionic permeability characteristics of the mTALH. However, this degree of urea bath hypertonicity reduced reversibly both JnetNaCl, the net rate of transepithelial NaCl absorption, and Ve, the spontaneous transepithelial voltage: JnetNaCl fell by 85% and Ve by 70%. Both of these latter effects could be accounted for quantitatively by an 85% reduction in tau NaCl, the rate of conservative transcellular NaCl transport. The inhibition of Ve by peritubular medium urea hypertonicity was not altered by supramaximal bath concentrations of ADH, supramaximal bath concentrations of cAMP analogues, or symmetrical addition of urea to perfusate and bath. Increases in peritubular medium mannitol concentrations also reduced Ve; the inhibition of Ve was not reversed by supramaximal bath concentrations of aDH. Cell volume remained unchanged with peritubular urea but was reduced by peritubular mannitol. These data indicate that in the mTALH increases in bath osmolality with nonelectrolytes inhibit tau NaCl noncompetitively with respect to ADH or cAMP and independently of cell volume. JnetCl was also reduced with increases in peritubular medium NaCl concentration and was associated with a reduction in cell volume.

Animals↗
PubMed1980

Interactions of temperature and ADH on transport processes in cortical collecting tubules.

We evaluated the temperature dependence of the permeability coefficients for ADH-independent and ADH-dependent zero volume flow diffusion of THO (PDw, micron/s), for ADH-dependent zero volume flow diffusion of the highly lipophilic solute n-[3H]butanol (PDb, micron/s), and for ADH-dependent lumen-to-bath osmosis (Pf, micron/s) in rabbit isolated cortical collecting tubules. The ADH-dependnet Pf and PDw data are consistent with the hypothesis that water crosses the apical plasma membranes of these tubules through narrow aqueous channels by single-file diffusion; and using the raw temperature-dependent data, we calculate that these channels contain congruent to six H2O molecules per channel, both in the presence and in the absence of ADH. Apparent activation energies (EA, kcal/mol), as an upper estimate of the true activation energies, were calculated for these transport processes. The EA for osmosis for 6-23 degrees C, 9.7 +/- 1.1 kcal/mol, was indistinguishable from that reported previously for 23-37 degrees C either in the presence of absence of ADH, and from the ADH-independent EA for THO diffusion, 10.11 +/- 0.68 kcal/mol, measured in the range 15-37 degrees C. We interpret these data to indicate that in the absence of ADH THO diffusion at zero volume flow is hindered primarily by the same sites, narrow channels in apical membranes. The apparent EA for ADH-dependent zero volume flow THO diffusion, 5.11 +/- 0.40 kcal/mol, measured over the temperature range 6-38 degrees C, is approximately half the apparent EA for osmosis in the presence or absence of ADH and ADH-independent THO diffusion. The former value, when corrected for diffusion constraints in series with apical plasma membranes, becomes indistinguishable from the latter values. These date are consistent with the possibility that two factors contribute to the ADH-mediated disparity between Pf and PDw in these tubules: cytosolic diffusion constraints that impede ADH-dependent THO diffusion but not osmotic volume flow, and narrow aqueous channels as the primary route for water flux through apical plasma membranes. Finally, the EA for n-butanol diffusion shows a break in the Arrhenius plot. Above 23 degrees C, the EA is 4.77 +/- 0.77 kcal/mol and n-butanol diffusion is impeded primarily by the cytosol. Below 23 degrees C, the EA rises to approximately 9 kcal/mol because the hydrophobic regions of apical plasma membranes contribute an increasing fraction of the total resistance to n-butanol diffusion.

Animals↗
PubMed1979

Ischemic heart disease in patients with uremia undergoing maintenance hemodialysis.

The 6-year cumulative incidence of ischemic heart disease (IHD) in 382 dialysis patients (mean age [SEM], 43 +/- 0.7 years) was studied. Of 101 patients with IHD, only 39 developed symptoms following dialysis (cumulative incidence, 20.8%). This group was older than those with IHD, and in 55%, IHD occurred in the first year of dialysis. Analysis by sex and race showed the rate of IHD in men and women to be similar, but the rate in whites was twice that in blacks. In men, the rate was not different from nondialysis men with similar coronary risk factors, whereas in dialysis women, the rate was twice that of nondialysis cohort. The development of IHD did not adversely affect long-term survival in patients without prior evidence of IHD. Death from myocardial infarction occurred in 3 of 320 patients ar risk. Atuopsy data in 33 patients revealed 70% stenosis of coronary arteries in 7, 4 of whom had antecedent disease. Our major conclusions are (a) the incidence of IHD during dialysis was not different from similarly matched nondialysis subjects; (b) the rate of IHD in dialysis women was greater than it was in nondialysis subjects; (c) coronary artery disease only affected long-term survival of patients with preexisting disease; (d) autopsy data did not suggest accelerated atherosclerosis.

Adult↗
PubMed1979

Effective luminal hypotonicity: the driving force for isotonic proximal tubular fluid absorption.

This Editorial Review summarizes certain considerations relevant to the mechanism(s) of isotonic fluid absorption by the mammalian proximal nephron. Recent evidence indicates that the paracellular pathway in this epithelium has a low diffusion resistance. Therefore it is possible that lateral intercellular spaces are in diffusion equilibrium with the peritubular medium. For such a circumstance, the driving forces for isotonic fluid absorption may reside in external solutions. But since the hydraulic conductance of mammalian proximal tubules is remarkably high, the effective osmotic pressure gradient between luminal and pertibular solutions required to drive isotonic fluid transport is relatively small. In the mammalian proximal nephron, effective luminal hypotonicity may provide the driving force for isotonic fluid transport. At least two mechanisms could account for the development of effective luminal hypotonicity. First, preferential absorption of bicarbonate results in a rise of luminal Cl- concentration. And because proximal tubules are more permeable to Cl- than to HCO3-, there develops a driving force for isotonic fluid transport. Second, trivial degrees of luminal hypotonicity may develop attendant on active Na+ absorption. We provide evidence that, of these two mechanisms, axial anion asymmetry is the dominant force for isotonic fluid transport.

Absorption↗
PubMed1979

Ischemic heart disease in the hemodialysis population.

We conclude that the incidence of IHD in men undergoing hemodialysis for end-stage renal disease was not greater than that seem in a nondialysis population of men with similar risk factors. In contrast, we found the rate of IHD in women with end-stage renal disease to be accelerated when compared to similar nondialysis subjects. Our data also suggest that during the 6 yrs of hemodialysis, ischemic heart disease did not represent a major mortality risk in patients who had not had symptoms of IHD prior to therapy although it dose pose a significant mortality risk in patients with evidence of established coronary artery disease prior to the onset of dialysis.

Adult↗
PubMed1979

External solution driving forces for isotonic fluid absorption in proximal tubules.

We have explored evidence that suggests that lateral intercellular spaces is the mammalian proximal nephron do not serve as a hypertonic "central compartment" driving volume absorption. A primary consideration is the very low transepithelial resistance of this tissue as demonstrated by several laboratories. By making the reasonable assumption that passive ion permeation occurs via a paracellular route, we have concluded that the diffusion resistance of the spaces in insufficient to allow the development of a significant compositional difference between the spaces and the peritubular medium. This conclusion led us to look for potential osmotic gradients existing between the luminal and peritubular solutions. From the perfusion rate dependence of osmotic volume flow in the absence of active transport in isolated convoluted and straight proximal tubules, we calculated that both segments have very high hydraulic conductances, on the order of 3,000-5,000 micron/sec. Consequently, slight differences in the effective osmolality of the external solutions are sufficient to explain net volume absorption both in vivo and in vitro. We have provided evidence for two such driving forces. First, the development of asymmetrical anion concentration differences along the length of the proximal nephron due to preferential reabsorption of HCO-3 provides a driving force if the reflection coefficient for HCO-3 exceeds that for Cl-. Second, slight luminal hypotonicity may develop as a consequence of active solute absorption. Although both mechanisms probably occur simultaneously in vivo, we consider the former to be quantitatively the most important.

Absorption↗
PubMed1978

Volume absorption in the pars recta. II. Hydraulic conductivity coefficient.

We evaluated the hydraulic conductivity (Pf, micron s-1) of superficial proximal straight tubules isolated from rabbit kidney. Tubules were perfused with hypotonic (270 mosmol/kg H2O) and bathed with isotonic (290 mosmol/kg H2O) NaCl buffers at 25 degrees C. Due to the tendency of transepithelial osmosis plus solute entry to produce osmotic equilibrium along the perfused length, we observed that the total net volume absorption ('JV, nl min-1) increased from 0.64 to 2.21 when the perfusion rate (VO, nl min-1) was increased from 11 to 45 in a group of tubules with an average length of 0.86 mm. From a 'JV of 2.21 nl min-1 at VO = 45 nl min-1 we computed a minimum Pf of 2,200 micron s-1. And extrapolation of the data to VO leads to infinity gave a Pf value of 5,200-7,600 micron s-1. The same perfusion rate dependence of 'JV in a group of tubules with an average length of 3.29 mm gave quantitatively similar results. A theoretical analysis of radial osmosis occurring simultaneously with axial osmotic equilibration showed that Pf values in the range of 3,000-4,000 micron s-1 accurately predicted the observed relations between VO, 'JV, and tubule length.

Absorption↗
PubMed1978

Volume absorption in the pars recta. III. Luminal hypotonicity as a driving force for isotonic volume absorption.

This paper examines the possibility that osmotic disequilibrium between luminal and bathing solutions may account for isotonic fluid absorption coupled to active Na+ absorption observed when superficial proximal straight tubules isolated from rabbit kidney are perfused and bathed with NaCl solutions in the absence of CO2, HCO3-, and luminal organic solutes. If luminal hypotonicity provides a driving force for isotonic fluid absorption under these conditions, the luminal fluid must be nearly isotonic; and steady-state luminal hypotonicity should develop sufficiently rapidly that the absolute rate of volume absorption ('JV, nl min-1) coupled to active Na+ transport is relatively independent of perfusion rate, so that the normalized rate of fluid absorption (JV, nl min-1 mm-1) is approximately constant. Our theoretical calculations indicate that these expectations are fulfilled. A 0.42-0.56 mM reduction in luminal NaCl concentration adequately accounts for the JV observed under such conditions, because of the high hydraulic conductivity of these tubules; and within the range of tubule lengths normally employed with isolated proximal straight tubules, JV is relatively indepedent of perfusion rate within the generally observed range of experimental error.

Absorption↗