PubMed Health⌕ Search

Biomedical subjects

D W Good

Publications and source records attributed to D W Good.

At least 55 records · Page 3Linked to original sources
PubMed1988

Active absorption of NH4+ by rat medullary thick ascending limb: inhibition by potassium.

These experiments were designed to determine the relative contributions of active NH4+ transport and voltage-driven NH4+ diffusion to direct NH4+ absorption by the medullary thick ascending limb of the rat. Medullary thick ascending limbs were perfused in vitro with solutions containing 25 mM HCO3 and 4 mM total ammonia. Under steady-state conditions, the lumen-positive transepithelial voltage (VT) was not sufficient to account for the observed decrease in lumen NH4+ concentration, consistent with active absorption of NH4+. Flux calculations based on VT and measured NH4+ permeability (6 x 10(-5) cm/s) indicate that the majority (at least 65%) of total ammonia absorption is due to active transport of NH4+. The remainder of NH4+ absorption can be accounted for by voltage-driven diffusion. Increasing the potassium concentration from 4 to 24 mM in perfusate and bath markedly inhibited total ammonia absorption but did not affect VT, NH4+ permeability, or HCO3 absorption. These results are consistent with inhibition of the active component of NH4+ absorption by potassium. The active NH4+ absorption is likely mediated by cotransport of Na+, NH4+, and Cl- across the apical cell membrane. Inhibition of active NH4+ absorption by an increase in potassium concentration may be due, in part, to competition between NH4+ and K+ for a common binding site on the Na+ -K+ -2Cl- cotransport system.

Absorption↗
PubMed1988

Attitudes and habits of chiropractors concerning referral to other health care providers.

Referral attitudes and habits were examined in a survey of Minnesota chiropractors. A questionnaire was developed and mailed to 1160 chiropractic physicians that included items concerning referral methods and frequency, factors prompting referral, and providers to whom referrals were directed. Of 531 respondents in active practice, 97.2% reported making referrals during 1985. Most referrals were made to orthopedic surgeons and neurologists with 76.1% of respondents reporting that referrals were made to these specialists on four or more occasions. A majority of respondents (57%) reported that referrals often were made to established consultants [corrected]. Doctors frequently submitted requests to medical physicians for patient records (66.2%) and 71.1% [corrected] reported referring patients for CT scans. The most commonly reported factor leading to a decision to refer was the need for a second opinion, and patient insistence for referral was the least common. Doctor characteristics and demographic [corrected] factors such as age, practice setting (rural or urban location) and practice arrangement (solo or group) were generally unrelated to referral attitudes or habits. However, respondents under the age of 40 did report a slightly higher frequency of requests for patient records than doctors older than 40.

Adult↗
PubMed1987

Transepithelial ammonia concentration gradients in inner medulla of the rat.

Transport of NH3 from loops of Henle to medullary collecting ducts has been proposed to play an important role in renal ammonia excretion. To determine whether transepithelial ammonia concentration gradients capable of driving this transport are present in the inner medulla, micropuncture experiments were performed in control rats and in rats with chronic metabolic acidosis. In situ pH and total ammonia concentrations were measured to calculate NH3 concentrations ([NH3]) for base and tip collecting duct, loop of Henle, and vasa recta. In control and acidotic rats, [NH3] in the loop of Henle was significantly greater than [NH3] in the collecting ducts. [NH3] did not differ in loop of Henle and adjacent vasa recta in either group of rats, indicating that NH3 concentration gradients between loop and collecting duct represent NH3 gradients that are present between medullary interstitium and collecting duct. During acidosis, an increase in collecting duct ammonia secretion was associated with an increase in the NH3 concentration difference between loop of Henle and collecting duct but occurred in the absence of a fall in collecting duct pH. The NH3 concentration gradient favoring diffusion of NH3 into the collecting ducts increased during acidosis because [NH3] in the loop of Henle and medullary interstitium increased more than [NH3] in the collecting duct. These findings indicate that transport processes involved in medullary ammonia accumulation play an important role in regulating ammonia secretion into the inner medullary collecting duct in vivo and that a fall in inner medullary collecting duct pH is not necessarily required for ammonia secretion by this segment to increase during chronic metabolic acidosis.

Acidosis↗
PubMed1987

Ammonia transport by early and late proximal convoluted tubule of the rat.

Free-flow micropuncture experiments were performed to examine ammonia transport separately in early and late proximal convoluted tubule (PCT) of the rat. In control rats, ammonia was secreted along the early PCT but was reabsorbed along the late PCT. In rats with chronic metabolic acidosis, ammonia secretion along the early PCT was increased compared with controls, and ammonia absorption by the late PCT was converted to small net ammonia secretion. In the acidotic rats, ammonia secretion rate in the early PCT was six times higher than that in the late PCT. Thus, most or all of ammonia secretion by the PCT occurred along its early portion. In control and acidotic rats, luminal NH3 concentration in the early PCT was significantly higher than that in the late PCT, indicating that ammonia is not in diffusion equilibrium throughout the renal cortex. It is proposed that differences in ammonia transport rate in early vs. late PCT may be due to differences in ammonia production rate and/or to differences in the rate of an ammonia backflux that detracts from net ammonia secretion.

Acidosis↗
PubMed1987

Effects of potassium on ammonia transport by medullary thick ascending limb of the rat.

Renal ammonium excretion is increased by potassium depletion and reduced by potassium loading. To determine whether changes in potassium concentration would alter ammonia transport in the medullary thick ascending limb (MAL), tubules from rats were perfused in vitro and effects of changes in K concentration within the physiological range (4-24 mM) were evaluated. Increasing K concentration from 4 to 24 mM in perfusate and bath inhibited total ammonia absorption by 50% and reduced the steady-state transepithelial NH+4 concentration gradient. The inhibition of total ammonia absorption was reversible and occurred when K replaced either Na or N-methyl-D-glucamine. Increasing K concentration in the luminal perfusate alone gave similar inhibition of total ammonia absorption. At 1-2 nl/min per mm perfusion rate, increasing K concentration in perfusion and bathing solutions had no significant effect on transepithelial voltage. With either 4 or 24 mM K in perfusate and bath, an increase in luminal perfusion rate markedly increased total ammonia absorption. Thus, both potassium concentration and luminal flow rate are important factors capable of regulating total ammonia transport by the MAL. Changes in systemic potassium balance may influence renal ammonium excretion by affecting NH+4 absorption in the MAL and altering the transfer of ammonia from loops of Henle to medullary collecting ducts.

Absorption↗
PubMed1985

Ammonia transport in the mammalian kidney.

Ammonia, an important urinary buffer in mammals, is synthesized primarily in the proximal tubules and is transferred to the final urine by a sequence of specialized transport processes. The pathway of ammonia transfer to the urine involves secretion into the proximal tubules, absorption from the loops of Henle, accumulation in the renal medullary interstitium, and secretion into the collecting ducts. Ammonia is transported as NH3 at some nephron sites and as NH+4 at others. In this paper, we discuss the physical basis of NH3 and NH+4 transport in epithelia and then describe ammonia transport mechanisms in individual nephron segments. Information about ammonia transport in individual nephron segments from isolated perfused tubule studies is integrated with data from in vivo studies to obtain an expanded overall model of renal ammonia handling.

Acids↗
PubMed1985

Sodium-dependent bicarbonate absorption by cortical thick ascending limb of rat kidney.

In vitro microperfusion experiments were performed to investigate the mechanism of bicarbonate absorption in the cortical thick ascending limb of the rat. Tubules were perfused at 1.0-1.5 nl X min-1 X mm-1 and bicarbonate concentration was 25 mM in the perfusate and bath. Bicarbonate absorption rates were determined by microcalorimetry. Control tubules absorbed bicarbonate at a mean rate of 9.5 +/- 0.6 pmol X min-1 X mm-1. The limiting luminal bicarbonate concentration was approximately 5 mM for tubules perfused at slow rates with 25 mM bicarbonate in the bath. Acetazolamide (10(-4)M) in the bath reduced bicarbonate absorption by 76% without significant effect on transepithelial voltage. Removing sodium from the perfusate and bath or removing potassium from the bath reduced bicarbonate absorption and transepithelial voltage to near zero. Adding amiloride (5 X 10(-4) or 10(-3) M) to the perfusate reduced bicarbonate absorption by 60-75% without detectable effect on transepithelial voltage. Adding furosemide (10(-4)M) to the perfusate increased bicarbonate absorption significantly by 40-50% while decreasing transepithelial voltage from 17 to 1.8 mV. Thus, bicarbonate absorption by cortical thick ascending limbs requires carbonic anhydrase activity and sodium transport but is not dependent on transepithelial voltage. When considered together, the results are consistent with mediation of the bicarbonate absorption by apical membrane sodium-hydrogen exchange.

Absorption↗
PubMed1985

Deoxycorticosterone-stimulated bicarbonate secretion in rabbit cortical collecting ducts: effects of luminal chloride removal and in vivo acid loading.

To assess the role of cortical collecting duct bicarbonate secretion in the regulation of net acid excretion, we have sought to identify what factors influence the secretion rate. Net and unidirectional bicarbonate fluxes were measured in isolated perfused cortical collecting ducts from deoxycorticosterone-treated rabbits. The collecting ducts secreted bicarbonate at 11-24 pmol X mm-1 X min-1, confirming the high rate seen in earlier studies. Oral acid loading (50 mM NH4Cl drinking water) completely inhibited the net bicarbonate secretion. The bath-to-lumen flux was markedly reduced with acid loading, but the lumen-to-bath flux changed very little. In tubules from rabbits treated with deoxycorticosterone (but not NH4Cl), luminal chloride replacement with either sulfate or gluconate completely and reversibly inhibited the net bicarbonate secretion. The bath-to-lumen flux was greatly inhibited, but there was little change in the lumen-to-bath flux. We conclude: 1) High rates of bicarbonate secretion can be induced in rabbit cortical collecting ducts by chronic treatment of the animals with deoxycorticosterone. 2) When deoxycorticosterone-treated rabbits were made acidotic by oral administration of NH4Cl, the bicarbonate secretion was prevented, indicating that the systemic acid-base state of the animal may be an important factor regulating bicarbonate secretion. 3) Replacement of chloride in the lumen with sulfate inhibits bicarbonate secretion in the cortical collecting duct, an effect which may explain in part the decrease in urinary pH in response to sulfate infusions in mineralocorticoid-stimulated animals.

Acid-Base Equilibrium↗
PubMed1985

Ammonia and bicarbonate transport by rat cortical collecting ducts perfused in vitro.

We measured bicarbonate and ammonia transport by isolated perfused cortical collecting ducts from deoxycorticosterone-treated rats. With no ammonia in the perfusate and bath solutions, the collecting ducts secreted bicarbonate. The bicarbonate secretion was prevented when the rats were given 40 mM NH4Cl to drink. When 4 mM total ammonia was added to the perfusate and bath, the collecting ducts secreted ammonia and the direction of bicarbonate transport reversed toward absorption. Under those conditions the collected total ammonia concentration exceeded the value predicted by the diffusion-trapping model, assuming pH equilibrium. However, when carbonic anhydrase was added to the perfusate (to assure pH equilibrium), the collected total ammonia concentration decreased to the level predicted by the diffusion-trapping model. We conclude that rat cortical collecting ducts can secrete bicarbonate at substantial rates; the rate of bicarbonate secretion is modified by changes in the acid-base intake of the rats; ammonia secretion occurs by simple nonionic diffusion in this segment; the ammonia secretion is enhanced by the presence of acidic pH disequilibrium in the lumen; and ammonia in the perfusion and bath solutions inhibits bicarbonate secretion by rat cortical collecting ducts, a response that may be important for the regulation of renal bicarbonate excretion.

Ammonia↗
PubMed1984

Luminal influences on potassium secretion: low sodium concentration.

In vivo microperfusion techniques were employed in anesthetized rats to determine whether K secretion by renal distal tubules requires the presence of Na in luminal fluid, and, if it does, in what concentration range do changes in Na concentration have the most effect. In a first series of experiments Na in perfusion fluid was replaced at constant Cl with tetramethylammonium (TMA). When the perfusion fluid Na concentration was reduced from 96 or 34 mM to 10 or 3 mM, K secretion was reduced by 50-60% and transepithelial voltage ( VTE ) was reduced by 40-60%. In a second series of experiments, in which NaCl was replaced with urea, perfusion fluid Na concentration again was reduced to 3 mM, and K secretion and VTE were reduced. In a third series of experiments, Na was replaced with rubidium. The reduced K secretion could not be explained solely by changes in electrical driving forces. The results indicate that some luminal Na (half-maximal concentration approx 10 mM) is necessary to permit K secretion to proceed at a normal rate. Considering prior measurements of luminal Na concentration in rat distal tubules, it is unlikely that changes in luminal Na concentration play an important role in regulating the rate of distal K secretion.

Animals↗
PubMed1984

Ammonia and bicarbonate transport by thick ascending limb of rat kidney.

Ammonia and bicarbonate transport by the thick ascending limb of rat kidney was studied to determine whether this segment contributes to the regulation of renal ammonia and net acid excretion. Cortical and medullary thick ascending limbs were perfused in vitro at 1.0-1.5 nl X min-1 X mm-1 with HCO3-buffered solutions. There was no significant net fluid transport. With 4 mM ammonia in bath and perfusate, transepithelial voltage averaged 6-9 mV, lumen positive, and did not differ between the two segments. The mean ammonia concentration in collected tubule fluid was 2.8 mM with cortical segments and 2.3 mM with medullary segments, indicating net absorption of ammonia. Furosemide (10(-4) M) in the perfusate eliminated ammonia absorption in medullary thick ascending limbs and converted net absorption to net secretion in cortical thick ascending limbs. Furosemide reduced transepithelial voltage to near zero in every tubule. Cortical and medullary thick ascending limbs also absorbed bicarbonate, indicating that their tubule fluid was acidified relative to the bath. Therefore, absorption of ammonia could not have occurred by nonionic diffusion. The absorption most likely was due to direct transport of NH4+. The possible mechanisms involved are discussed, and it is proposed that absorption of ammonia by thick ascending limbs provides a source for its accumulation in the renal medulla and secretion into the collecting ducts.

Acid-Base Equilibrium↗
PubMed1984

Mechanism of ammonia secretion by cortical collecting ducts of rabbits.

The collecting duct system is a major site of ammonia addition to the tubule fluid. To study the mechanisms involved, we measured total ammonia and total CO2 transport in isolated, perfused cortical collecting ducts (CCD) from deoxycorticosterone-(DOC) treated rabbits. Perfusate and bath solutions contained 25 meq/liter HCO3 and 4 mM total ammonia. Net fluid transport was not significantly different from zero. Net secretion of total CO2 occurred in all tubules (mean collected concentration, 44.2 mM). Despite bicarbonate secretion, there was net secretion of total ammonia (mean collected concentration, 6.4 mM). There was no detectable ammonia addition to the collected fluid when ammonia was excluded from the perfusate and bath, ruling out a major contribution from synthesis. Ouabain did not significantly affect net transport of total ammonia or total CO2. To test the hypothesis that an acid pH disequilibrium may lower the luminal pH enough to drive ammonia secretion by nonionic diffusion, we perfused CCD from DOC-treated rabbits with carbonic anhydrase (CA) (0.1 mg/ml). Without CA, there was net total ammonia secretion (-2.2 pmol X min-1 X mm-1) and net total CO2 secretion (-16.6 pmol X min-1 X mm-1). Luminal CA converted the net total ammonia secretion to net absorption (1.0 pmol X min-1 X mm-1) while the bicarbonate secretion persisted (-11.2 pmol X min X mm-1). We conclude that total ammonia secretion in these tubules occurs primarily by diffusion of NH3 and is dependent on a luminal acid pH disequilibrium.

Ammonia↗
PubMed1984

Mutual dependence of sodium and chloride absorption by renal distal tubule.

Sodium transport and chloride transport by the renal distal tubule of rats were studied by in vivo continuous microperfusion to determine the effects of separately altering luminal sodium and chloride concentrations. Results showed that sodium absorption depends on luminal sodium concentration and chloride absorption depends on luminal chloride concentration; both relations are linear between approximately 10 and 100 mM and have slopes of approximately 2.5 pmol X min-1 X mM-1. Sodium absorption is also a saturable function of luminal chloride concentration, and chloride absorption is a saturable function of luminal sodium concentration; the half-maximal chloride and sodium concentrations are approximately 10 mM. Furosemide, 10(-4) M, when added to the fluid used to perfuse this segment inhibited sodium absorption and chloride absorption to a similar extent. Removal of chloride from luminal fluid (replaced with sulfate) and addition of furosemide to the perfusion fluid had little or no effect on the measured transepithelial voltage. The results are consistent with the presence of a mechanism in the luminal membrane of distal tubule cells that couples the absorptive transport of sodium and chloride.

Absorption↗