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R M Culpepper

Publications and source records attributed to R M Culpepper.

24 records · Page 2Linked 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

Urinary acidification in a patient with glucose-6-phosphate dehydrogenase deficiency. A reevaluation of the role of the hexose monophosphate shunt in renal acid secretion.

The relationship between renal metabolism and urinary acidification is poorly understood. During the past decade evidence has accrued to suggest that the hexose monophosphate (HMP) shunt might serve in the process of urinary acidification by providing reducing equivalents for a redox-coupled membrane-bound proton pump that could transport protons into the tubular lumen. The major support for this hypothesis has come from the finding that HMP shunt activity increases with acute and chronic metabolic acidosis. In the present study, we examine the urinary acidification capacity of a young man with severe erythrocyte glucose-6-phosphate dehydrogenase (G-6-PD) deficiency and with unmeasurable G-6-PD activity in renal cortical tissue. We found that despite unmeasurable G-6-PD activity in renal tissue, the patient was capable of generating a maximally acid urine and increasing total acid secretion. Our findings suggest that the HMP shunt may not be necessary for the urinary acidification process.

Adolescent↗
PubMedDate not supplied

Glomerulopathies with fibrillary deposits.

Renal diseases involving glomerular deposits of fibrillary material are an important diagnostic challenge for the ultrastructural pathologist. Two primary disorders of this type, termed "fibrillary glomerulonephritis" (characterized by fibrils measuring approximately 20 nm in diameter) and "immunotactoid glomerulopathy" (characterized by larger, microtubular deposits), have been described. The possible relatedness of these two disorders and their potential association with other systemic illnesses are subjects of current debate. Other multisystemic diseases, including amyloidosis and various forms of cryoglobulinemia, can also present with fibrillary or microtubular deposits in the kidney. Five cases are presented in which fibrillar or microtubular structures were identified in renal biopsies by ultrastructural examination. The distinction between fibrillary glomerulonephritis, immunotactoid glomerulopathy, and other processes that have similar ultrastructural features are discussed.

Actin Cytoskeleton↗