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Biomedical subjects

A C Ericson

Publications and source records attributed to A C Ericson.

26 records · Page 2Linked to original sources
PubMed1982

Epithelial cell volume modulation and regulation.

Epithelial cell volume is a sensitive indicator of the balance between solute entry into the cell and solute exit. Solute accumulation in the cell leads to cell swelling because the water permeability of the cell membranes is high. Similarly, solute depletion leads to cell shrinkage. The rate of volume change under a variety of experimental conditions may be utilized to study the rate and direction of solute transport by an epithelial cell. The pathways of water movement across an epithelium may also be deduced from the changes in cellular volume. A technique for the measurement of the volume of living epithelial cells is described, and a number of experiments are discussed in which cell volume determination provided significant new information about the dynamic behavior of epithelia. The mechanism of volume regulation of epithelial cells exposed to anisotonic bathing solution is discussed and shown to involve the transient stimulation of normally dormant ion exchangers in the cell membrane.

Animals↗
PubMed1982

Heterogeneity in regulation of glomerular function.

The aim was to study differences in filtration driving forces and glomerular filtration rates between superficial and deep nephrons when urine flow rate was altered at the macula densa region. In young rats stop-flow pressures and single nephron glomerular filtration rates (SNGFR) were measured in the superficial proximal tubules and in the loops of Henle in the papilla. SNGFR was also measured with a modified Hanssen technique. The stop-flow pressures of superficial nephrons amounted to 30.9 +/- 0.8 mmHg (mean +/- SE) and those of juxtamedullary nephrons to 52.2 +/- 1.6 mmHg. In the stop-flow condition the net driving filtration forces were calculated to be about 19 mmHg and 50 mmHg for the superficial and deep glomeruli, respectively. In free flow conditions both net driving forces were calculated to be 19 mmHg. The micropuncture technique gave a SNGFR value for superficial nephrons of 29.6 +/- 2.9 and for deep nephrons of 84.1 +/- 8.5 nl x min-1 . g-1 kidney weight (KW). With a modified Hanssen technique the corresponding values were 25.8 +/- 3.3 and 27.7 +/- 2.9 nl . min-1 . g-1 KW. The tubuloglomerular feedback mechanism is considered to have a powerful regulatory influence on the glomerular filtration rate of deep nephrons.

Animals↗
PubMed1982

Efferent renal nerve activity during intracarotid and intracerebroventricular infusions of hypertonic sodium chloride solutions and isotonic volume expansion in the rat.

The change in renal nerve activity under conditions known to increase renal sodium excretion was studied. In adult Sprague Dawley rats, anaesthetized with Inactin, normotonic and hypertonic NaCl solutions were infused into 1) a vein, 2) a carotid artery and 3) the third ventricle. The left kidney was freed and placed in a plastic cup. A renal nerve was dissected free and placed on a stainless bipolar electrode. The nerve was cut distal to the electrode. The nerve signals were amplified and recorded on a tape recorder. Simultaneously integrated nerve signals and also atrial and venous pressures were recorded. Intracarotid infusion of a 1 M NaCl solution increased sodium output and temporarily decreased renal nerve activity by some 35%. Corresponding intravenous (i.v.) infusion gave an increase in renal nerve activity and also in sodium output. The latter increase was delayed compared with that caused by the intracarotid infusion. No variations in blood pressure were noted. In control experiments with a slow i.v. infusion of physiological saline, renal nerve activity increased throughout the experiment, while sodium excretion remained constant. During infusion of a 1 M NaCl solution into the third ventricle, renal nerve activity decreased in about half of the cases. This reduction was often accompanied by an increased arterial blood pressure and an increased sodium output. Arterial blood pressure increases were especially pronounced at the highest infusion rats, i.e. 800 ml-min-1. Isotonic volume expansion of 2% of the body weight resulted in a transient decrease in renal nerve activity by about 30%. Venous blood pressure rose and sodium output increased six-fold. The decrease in nerve activity was observed both when the vagal nerves were intact and when they were cut.

Animals↗
PubMed1982

Coupled NaCl entry into Necturus gallbladder epithelial cells.

NaCl entry into Necturus maculosus gallbladder epithelial cells was studied by determination of the rate of fluid movement into the cell when the Na+-K+-ATPase was inhibited by 10(-4) M ouabain in the serosal bathing solution. The cell swelling was due to continuing entrance of NaCl into the cell across the apical membrane, which increased the solute content of the cell; the resultant rise in cell osmolality induced water flow and cell swelling. The rate of swelling was 4.3% of the cell volume per minute, equivalent to a volume flow across the apical membrane of 1.44 x 10(-6) cm/s, similar in magnitude to the normal rate of fluid absorption by the gallbladder. We determined the mechanism of NaCl entry by varying the ionic composition of the mucosal bath; when most of the mucosal Na+ or Cl- was replaced, cell volume did not increase during pump inhibition. The rate of NaCl entry was a saturable function of Na+ or Cl- in the mucosal bathing solution with K1/2 values of 26.6 mM for Na+ and 19.5 mM for Cl-. The mode of NaCl entry was probably not the parallel operation of Na+-H+ and Cl(-)-HCO-3 exchangers because of the lack of effect of bicarbonate removal or of the inhibitors amiloride and 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid. NaCl entry was reversibly inhibited by bumetanide in the mucosal bathing solution. Transepithelial NaCl and water absorption is the result of the coupled, carrier-mediated movement of NaCl into the cell across the apical membrane and the active extrusion of Na+ by the Na+-K+-ATPase in the basolateral membrane.

Animals↗
PubMed1982

Volume regulation by Necturus gallbladder: apical Na+-H+ and Cl(-)-HCO-3 exchange.

Necturus gallbladder epithelial cells exhibited volume regulatory swelling when exposed to a hypertonic mucosal bathing solution. The initial, osmotically induced shrinkage was followed by a rapid increase in cell volume back to the control value despite continuing hypertonicity of the mucosal perfusate. This volume regulatory increase occurred by osmotic water flow accompanying the transient cellular uptake of NaCl from the mucosal bathing solution. Volume regulatory increase required Na+ and Cl- in the mucosal bath; it was inhibited by amiloride or 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid but not by bumetanide or ouabain. The K1/2 for Na+ was 2.8 mM, the K1/2 for Cl- was 1.9 mM, and maximum velocity of fluid flow into the cell for both ions was greater than 10 x 10(-6) cm/s. Both volume regulatory increase and transepithelial fluid absorption involve NaCl flux across the apical membrane into the cells, but the nature of the NaCl fluxes differ in the two processes. During volume regulatory increase NaCl enters the cells by parallel Na+-H+ and Cl(-)-HCO-3 exchanges, whereas during transepithelial fluid absorption NaCl enters the cell by the coupled flux of NaCl.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1981

Flow resistance of the interlobular artery in the rat kidney.

The afferent and efferent arterioles are considered to be the most important resistance vessels within the renal vasculature, but there are indications that a pressure drop occurs along the interlobular artery. This pressure drop was investigated from two aspects: 1) In rat kidneys the "stop-flow pressure" in the efferent arterioles was measured with the micropuncture technique. At arterial pressures between 100 and 130 mmHg the stop-flow pressure did not exceed 85 mmHg, which means that the highest pressure at the end of the interlobular artery was 85 mmHg; 2) A mathematical model was constructed, assuming that the diameter of the interlobular artery decreased stepwise from 60 to 10 micrometers. The artery was divided into 20 segments, each segment containing one afferent arteriole. The flow in the afferent arterioles increased linearly from 100 nl . min-1 in the first segment to 130 nl . min-1 in the last segment. When the pressure in the first segment was 120 mmHg, it was calculated that the pressure in the last segment was 85 mmHg. These findings strengthen the theory that the interlobular artery may participate in the regulation of the intracortical blood flow in the rat kidney. We conclude that the afferent arteriole of the most superficial nephron is nearly maximally dilated and that the juxtamedullary nephron is able to either dilate or constrict its arteriole in normotensive and normohydrated rats.

Animals↗
PubMed1976

Renal renin output during continuous intracarotid infusions of iso- and hypertonic sodium chloride solutions in the rat.

On male Sprague Dawley rats isotonic NaCl during control and 1 M NaCl were infused either into the carotid artery or i.v. Glomerular filtration rate, sodium output and plasma renin activity were determined. Five of 19 animals reacted with no increase in sodium output for 1 M NaCl and are treated as a different group from the animals reacting with an increased sodium output. For the animals reacting with an increased sodium output a decrease in plasma renin activity was found together with an increase in glomerular filtration rate. In both groups the plasma sodium was constant. The animals not reacting with an increased sodium output had a higher initial plasma renin activity, which did not change during 1 M NaCl infusion. The responses were equal for both intracarotid and i.v. infusions but with a somewhat longer delay before the response occurred with i.v. infusions. These results might be explained by a central nervous effect and by a direct renal effect. Also during 1 M NaCl infusion a possible extracellular volume expansion, derived from water withdrawal from the cells into the extracellular space might occur.

Animals↗