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Biomedical subjects

F Kiil

Publications and source records attributed to F Kiil.

At least 37 records · Page 2Linked to original sources
PubMed1990

Loop diuretics reduce lithium reabsorption without affecting bicarbonate and phosphate reabsorption.

The effects of the loop diuretics ethacrynic acid and bumetanide on lithium, bicarbonate and phosphate reabsorption were compared in 16 anaesthetized, normovolaemic dogs. In six dogs, ethacrynic acid (3 mg kg-1 body wt) significantly reduced absolute lithium reabsorption from 29.3 +/- 4.1 to 19.0 +/- 3.4 mumol min-1, fractional lithium reabsorption from 0.65 +/- 0.04 to 0.37 +/- 0.04 and fractional chloride reabsorption from 1.00 +/- 0.00 to 0.65 +/- 0.02. Bicarbonate and phosphate reabsorption did not decrease significantly. In six other dogs, bumetanide (30 micrograms kg-1 body wt) gave similar results. Absolute lithium reabsorption significantly decreased from 34.0 +/- 2.2 to 18.1 +/- 2.6 mumol min-1 and fractional lithium reabsorption decreased from 0.50 +/- 0.03 to 0.25 +/- 0.03. Fractional chloride reabsorption decreased from 0.98 +/- 0.00 to 0.61 +/- 0.05, whereas bicarbonate and phosphate reabsorption were not significantly altered. Thus, both loop diuretics greatly reduced lithium reabsorption. We propose that loop diuretics inhibit passive lithium reabsorption in the thick ascending limb of Henle's loop by reducing the lumen-positive electrical potential that drives passive cation transport.

Absorption↗
PubMed1989

Effect of increased alpha-adrenergic activity on the blood pressure/cardiac output relationship in dogs.

The relationship between mean aortic blood pressure (MAP) and cardiac output (CO) was examined in anaesthesized, open-chest dogs during variations in pre-load with and without alpha-adrenergic stimulation with phenylephrine. When phenylephrine increased MAP to 200 mmHg, CO fell greatly and could not be increased by volume expansion. Left ventricular ultrasonic measurements and pressure recordings showed that the Frank-Starling mechanism was maximally activated. During vena cava obstruction CO and MAP fell proportionally. At a lower infusion rate of phenylephrine, MAP increased to 160 mmHg without a great reduction of CO. As in control experiments without phenylephrine infusion, CO could be increased by dextran/saline infusion and lowered about 20% below control by vena cava obstruction with no significant change in MAP; by further caval obstruction CO and MAP fell in proportion. Phenylephrine did not alter the relationship between aortic baroreceptor activity and MAP. The same MAP/CO relationships were obtained before and after bilateral vagotomy and nephrectomy. Caval obstruction and pacing tachycardia resulted in similar MAP/CO relationships despite different effects on left ventricular end-diastolic pressure. Thus, phenylephrine infusion may raise MAP to 200 mmHg but no cardiac reserve is left. During reduction of CO by caval obstruction, peripheral vascular resistance remains constant despite varying baroreceptor activity. At the lower infusion rate of phenylephrine, raising MAP to 160 mmHg, peripheral vascular resistance is constant at low CO, but at high CO the vasoconstrictive effect of phenylephrine is counteracted by a vasodilatory mechanism which seems to be flow-dependent.

Adrenergic alpha-Agonists↗
PubMed1989

Difference between hypertonic NaCl and NaHCO3 as osmotic diuretics in dog kidneys.

To compare the osmotic inhibitory effects of NaCl and NaHCO3 on proximal tubular fluid reabsorption, plasma osmolality was raised by 40 mosmol kg-1 H2O by infusing hypertonic NaCl and NaHCO3 in volume-expanded dogs receiving ethacrynic acid. In five dogs studied at constant plasma pH 7.5, both NaCl and NaHCO3 reduced water reabsorption by 29 +/- 2%. However, NaCl infusion reduced bicarbonate reabsorption by 31 +/- 2%, whereas bicarbonate reabsorption remained unchanged during NaHCO3 infusion. In six dogs, bicarbonate reabsorption was kept constant during NaCl and NaHCO3 infusion by adjustments of plasma pH. At similar glomerular filtration rates (42.4 +/- 2.9 ml min-1), water reabsorption was 28.7 +/- 1.7 ml min-1 in the control period, 29.4 +/- 2.5 ml min-1 during hypertonic NaCl infusion and 20.6 +/- 1.2 ml min-1 during hypertonic NaHCO3 infusion. Therefore, NaCl did not reduce proximal tubular water reabsorption by a direct osmotic effect. By calculating the regression coefficient for the relationship between measured chloride reabsorption and maximal convective chloride flux, the effective reflection coefficient for NaCl averaged 0.11 +/- 0.01. The combination of a low reflection coefficient and high permeability may explain why hypertonic NaCl is not an osmotic diuretic.

Animals↗
PubMed1989

Low oxygen cost of carbonic anhydrase-dependent sodium reabsorption in the dog kidney.

To examine the oxygen requirement of carbonic anhydrase-dependent sodium reabsorption in the proximal tubule, 18 anaesthetized dogs were studied under conditions of saturated distal NaCl reabsorption; the latter was accomplished by volume expansion (all groups) combined with infusion of loop diuretics (groups 1 and 3). Acetazolamide reduced HCO3- reabsorption by 602 +/- 32 mumol min-1 (55%, group 1) and by 777 +/- 103 mumol min-1 (66%, group 2). This was accompanied with a reduction in sodium reabsorption and oxygen consumption in a molar delta Na/delta O2 ratio of about 45 in both groups of dogs. The delta HCO3/delta O2 ratio averaged 16 +/- 1, which was not significantly different from the theoretical value of 18 expected for transcellular sodium transport by Na+, K+-ATPase. Mannitol (group 3) reduced NaCl reabsorption by 37 +/- 2% without affecting NaHCO3 reabsorption or oxygen consumption significantly. We conclude that carbonic anhydrase-dependent NaCl reabsorption in the proximal tubules is passive, and that NaHCO3 reabsorption is the only important active sodium transport which is sensitive to inhibition of carbonic anhydrase.

Acetazolamide↗
PubMed1989

Molecular mechanisms of osmosis.

Osmosis across a semipermeable membrane is usually treated in terms of thermodynamics, but the equations for osmosis can also be derived from kinetic considerations. Since fewer solvent molecules bombard the semipermeable membrane from the solution side, a kinetic pressure difference (osmotic potential) is generated into pore openings. Intermolecular forces cancel each other and do not affect the osmotic potential. On the other hand, osmotic flow is dependent on intermolecular cohesive forces permitting the generation of large negative pressures in the membrane pores. Osmosis is therefore a unique property of liquids, whereas intermolecular cohesive forces do not affect diffusion. Osmotic pressure up to 180 atm can be correctly determined from the reduction in saturated vapor pressure above the solution because osmotic pressure and reduction in vapor pressure to some extent are analogous phenomena. Osmotic pressures up to 180 atm may also be correctly determined from kinetic considerations by accounting for binding between solvent and solute molecules (4-5 water molecules per solute molecule for sucrose solutions).

Animals↗
PubMed1989

Atrial natriuretic factor induces natriuresis during pacing tachycardia in dogs.

To examine whether release of atrial natriuretic factor (ANF) can explain the increase in sodium excretion during supraventricular tachycardia, we compared the natriuretic responses with right atrial pacing tachycardia and ANF infusion in six barbiturate-anesthetized dogs. When we raised the dogs' heart rates from 148 +/- 12 to 263 +/- 12 beats/min for 30 min, plasma immunoreactive (IR) ANF rose from 42.1 +/- 3.4 to 139.0 +/- 25.6 pg/ml. Sodium excretion increased from 36.2 +/- 12.8 to 132.4 +/- 40.8 mumol/min in the exposed denervated kidney. When we infused 12.5 ng.min-1.kg body wt-1 of ANF at a spontaneous heart rate of 146 +/- 12 beats/min, plasma IR-ANF rose from 46.0 +/- 5.1 to 121.7 +/- 17.5 pg/ml, which was similar to that observed during pacing tachycardia. Sodium excretion increased from 40.6 +/- 11.3 to 193.6 +/- 46.0 mumol/min, which was higher than that observed during pacing tachycardia. Renal blood flow was lower during pacing tachycardia than during ANF infusion, but glomerular filtration rate and aortic blood pressure were not significantly different during the two procedures. Because sodium excretion was 30% lower during pacing tachycardia, even though plasma IR-ANF was as high as during ANF infusion, we conclude that ANF induces the acute rise in sodium excretion during pacing tachycardia but that hemodynamic changes may attenuate the natriuretic response.

Animals↗
PubMed1989

Release of atrial natriuretic factor during infusion of isoproterenol and angiotensin II.

Release of atrial natriuretic factor (ANF) is related to atrial pressure and heart rate and may be influenced by beta-adrenergic stimulation and angiotensin II. Experiments in five closed-chest dogs showed lower plasma immunoreactive (ir) ANF during intravenous (iv) isoproterenol (0.2-0.3 micrograms.kg-1.min-1) and higher plasma ir-ANF during iv angiotensin II (0.2-0.3 micrograms.kg-1.min-1) than during blood volume expansion measured at equal mean right atrial pressure (RAP) and heart rate. This indicated that the agents may affect ANF release differently, possibly through their effects on left atrial pressure (LAP). In five open-chest dogs with right atrial pacing at 216 +/- 1 beats/min, blood volume was expanded until mean RAP was 9 mmHg. Mean LAP rose to 16.8 +/- 2.0 mmHg, and plasma ir-ANF rose from 57 +/- 6 to 219 +/- 39 pg/ml. At a constant mean RAP of 9 mmHg, iv isoproterenol infusion reduced mean LAP to 12.6 +/- 1.4 mmHg and reduced plasma ir-ANF by 115 +/- 31 to 105 +/- 13 pg/ml. During iv angiotensin II infusion at a mean RAP of 9 mmHg, mean LAP rose to 23.2 +/- 2.2 mmHg and plasma ir-ANF averaged 281 +/- 77 pg/ml. The correlation between plasma ir-ANF and LAP (r = 0.83) indicates that the different effects of isoproterenol and angiotensin II on ANF release can be accounted for by the effects on LAP.

Angiotensin II↗
PubMed1989

Essentials of glomerulotubular balance.

In the proximal tubules, fractional reabsorption remains essentially unchanged during variations in glomerular filtration rate (GFR). Glomerulotubular balance (GTB), defined as the linear relationship between proximal tubular reabsorption and GFR, is quantitatively the most important regulator of tubular reabsorption, which may be stopped by inhibiting Na, K-ATPase activity completely. However, ouabain in doses inhibiting 80% of the Na, K-ATPases, exerts no effect on proximal reabsorption of water, NaCl and NaHCO3. At constant plasma pH, the same relationship between filtered and reabsorbed bicarbonate is obtained whether bicarbonate reabsorption is altered by varying GFR or plasma concentration of bicarbonate. In contrast, a selective rise in plasma NaCl concentration at constant plasma pH (hypernatremia) reduces NaHCO3 reabsorption and fails to stimulate NaCl reabsorption. Other characteristics of proximal tubular reabsorption are that nonreabsorbable solutes, such as mannitol, inhibit water and NaCl reabsorption with little or no change in NaHCO3 reabsorption and renal oxygen consumption. Mannitol reduces the slope of the GTB curve for NaCl but not for NaHCO3. Hypertonic NaHCO3 exerts an osmotic effect on proximal water and NaCl reabsorption comparable to that of mannitol, whereas hypertonic NaCl is without osmotic effect. By reducing plasma pH (hypercapnia at high plasma bicarbonate concentration), the slope of the GTB curves for NaCl and NaHCO3 can be greatly increased. By raising plasma pH either by hypocapnia or bicarbonate loading, proximal reabsorption of NaHCO3 and NaCl is greatly depressed and remains almost unaltered during variations of GFR (abolished GTB). Similarly, carbonic anhydrase inhibitors, such as acetazolamide, reduce the reabsorption of NaCl and NaHCO3 in the same proportion as a rise in plasma pH, and abolish GTB. Examinations of proximal tubular oxygen consumption indicate that the energy requirement for NaHCO3 reabsorption is as expected for transcellular transport by Na, K-ATPases, whereas proximal NaCl reabsorption requires no additional energy. These data indicate that transcellular energy-requiring NaHCO3 reabsorption provides the main osmotic force across the tight junction for paracellular reabsorption of proximal tubular fluid containing NaCl and other solutes of low reflection coefficient. The main factors influencing GTB are the filtered load of bicarbonate, plasma pH and nonreabsorbable solutes in the proximal tubular fluid.

Animals↗
PubMed1988

Properties of the macula densa mechanism for renin release in the dog.

To study the macula densa mechanism for renin release, both the macula densa and the haemodynamic mechanisms were activated in anaesthetized dogs with denervated kidneys, either by renal arterial constriction to a renal arterial pressure (RAP) of 52 +/- 2 mmHg or by ureteral occlusion to a ureteral pressure of 95-105 mmHg, 20-25 mmHg below RAP. Renal arterial constriction increased renin release from 0.3 +/- 0.2 to 16 +/- 4 micrograms AI min-1. At low RAP, renin release was subsequently reduced to 7 +/- 3 micrograms AI min-1 when sodium excretion was raised far above control values by plasma volume expansion and acetazolamide infusion. Ethacrynic acid (3 mg kg-1 body wt.) restored renin release to pre-expansion values, and a large dose (25 mg kg-1 body wt.) prevented renin release from falling even after unclamping the artery. During ureteral occlusion with stopped glomerular filtration, plasma volume expansion, acetazolamide and ethacrynic acid infusion did not alter renin release. On the other hand, beta-adrenergic stimulation by isoproterenol raised renin release equally (by 30-40 micrograms AI min-1) before and after plasma volume expansion, during both renal arterial constriction and ureteral occlusion. Indomethacin (10 mg kg-1 body wt.) abolished renin release induced by ethacrynic acid infusion and ureteral occlusion. We conclude that the macula densa mechanism for renin release is inactivated by high NaCl reabsorption during plasma volume expansion and acetazolamide infusion, reactivated by inhibition of NaCl reabsorption with ethacrynic acid and completely inhibited by indomethacin. The degree of activation does not influence the renin release induced by beta-adrenergic stimulation.

Acetazolamide↗
PubMed1988

Myocardial oxygen consumption during atrial pacing at various inotropic levels.

In anaesthetized open-chest pigs (n = 15) we examined whether myocardial oxygen consumption (MVO2) per min increased in proportion to heart rate during right atrial pacing at control, high and low inotropy. By modulating aortic constriction and the circulating blood volume, left ventricular (LV) systolic blood pressure, stroke volume and LV dimensions were kept constant. Examinations at control inotropy (n = 7) showed a linear relationship between increments in MVO2 beat-1 and LV dP/dt when heart rate was increased in four steps, each of 10 beats min-1 from 130 +/- 3 beats min-1 (r = 0.76 +/- 0.08). In a second series (n = 8) heart rate was increased by 36-37 beats min-1 in control experiments, during intracoronary isoproterenol infusion (high inotropy) and after propranolol administration (low inotropy). The increments in MVO2 min-1 during pacing tachycardia were not significantly different at control, high or low inotropy. At high inotropy MVO2 beat-1 and LV dP/dt did not rise significantly during pacing tachycardia. Myocardial oxygen consumption beat-1 increased more at control (6.3 +/- 2.0%) than at high inotropy (diff: P less than 0.02). At low inotropy MVO2 beat-1 increased even more (17.4 +/- 2.8%) than at control inotropy (diff: P less than 0.05). Thus, the increase in MVO2 beat-1 during pacing tachycardia is related to the increase in LVdP/dt and is dependent on the level of inotropy; great increments during tachycardia after propranolol administration and no changes during intracoronary isoproterenol infusion.

Animals↗
PubMed1988

Effects of ureteral occlusion and ethacrynic acid infusion on renal prostaglandin degradation in the dog.

The two major renal prostaglandins PGE2 and PGI2 are partly metabolized during a single passage of the kidney. To examine whether stopping glomerular filtration affected the renal degradation, PGE2 and PGI2 were infused into the suprarenal aorta of dogs during ureteral occlusion. Prostaglandin synthesis was blocked by indomethacin, 10 mg kg-1 b.w. i.v. About 20% of PGI2 and 80-90% of PGE2 were metabolized during one passage through the kidney. Prostaglandin degradation and arterial input were proportional (r greater than 0.95). Compared to control conditions at free urine flow, PGI2 degradation was not changed, whereas the degradation of PGE2 was slightly increased by ureteral occlusion. Ethacrynic acid might reduce degradation of PGE2 by inhibiting two degradation enzymes. To examine the influence of ethacrynic acid, PGE2 was infused in different doses into the suprarenal aorta of dogs before and after administration of ethacrynic acid 3 mg kg-1 b.w. i.v. At all dose levels of PGE2, 75-80% was degraded by one passage through the kidney, whether ethacrynic acid was administered or not. However, although ethacrynic acid did not alter the total renal output, the urinary fraction was reduced from 20-30% to 10-15%. We conclude that degradation of both PGE2 and PGI2 is mainly confined to the blood vessels, and that ethacrynic acid in conventional doses does not prevent degradation of PGE2, but redistributes PGE2 output from urine to renal venous blood.

Animals↗
PubMed1988

Haemodynamic regulation of renal prostaglandin and renin release.

To examine the relationship between renal release of the prostaglandins E2 (PGE2) and I2 (PGI2) and renin during autoregulatory vasodilation, experiments were performed in anaesthetized dogs with denervated kidneys. Autoregulatory vasodilation was induced by reducing renal arterial pressure (RAP) or by raising ureteral pressure in steps. During progressive renal arterial constriction, PGE2 and PGI2 release reached maximal values (10.6 +/- 1.7 for PGE2 and 6.6 +/- 1.1 pmol min-1 for PGI2 release) at RAP of 70-80 mmHg, associated with almost no increase in renin release. By further reduction of RAP, prostaglandin release was not significantly altered, whereas renin release reached maximal values (18.7 +/- 2.4 micrograms AI min-1) when autoregulatory vasodilation was complete at RAP below 55-60 mmHg. During progressive elevation of ureteral pressure, the release of PGE2, PGI2 and renin increased in concert in a curvilinear fashion, reaching maximal values at a ureteral pressure of 85 mmHg. There was no further increase during ureteral occlusion and the plateau values averaged 23.6 +/- 3.7 pmol min-1 for PGE2, 8.0 +/- 1.6 pmol min-1 for PGI2 and 16.6 +/- 3.4 micrograms AI min-1 for renin. We conclude that vascular dilation enhances both prostaglandin and renin release. During reduction of RAP, preglomerular arteries are dilated at higher RAP than are afferent arterioles. Release of prostaglandins synthetized in arteries consequently occurs at higher RAP than release of renin, which is not enhanced until afferent arterioles ultimately dilate at RAP approaching 60 mmHg. In contrast, elevation of ureteral pressure provides nearly uniform enhancement of prostaglandin and renin release, indicating a more uniform dilation of the whole preglomerular vascular tree.

Animals↗
PubMed1988

The release mechanism for atrial natriuretic factor during blood volume expansion and tachycardia in dogs.

Atrial natriuretic factor (ANF) is released during blood volume expansion and tachycardia, but only blood volume expansion causes atrial distension, which presumably promotes ANF release. Our study was undertaken to search for a common release mechanism. In five anaesthetized, closed-chest dogs, plasma immunoreactive (IR) ANF was measured at three levels of blood volume, which were obtained by infusing a Ringer's solution. At each level of blood volume, plasma IR-ANF was measured at three pacing frequencies. Plasma IR-ANF increased as mean right atrial pressure (mRAP) was raised from 2 to 10 mmHg by volume expansion, whereas pacing tachycardia (at heart rates (HR) 50 +/- 3 and 98 +/- 1 beats min-1 above control) at each level of blood volume expansion increased plasma IR-ANF and systolic RAP (sRAP) at constant mRAP. Plasma IR-ANF was more strongly correlated to sRAP (r = 0.83) than to mRAP (r = 0.69), but the product sRAP x HR had the highest correlation coefficient (r = 0.86). According to the multiple regression equation: plasma IR-ANF = k1 + k2mRAP + k3sRAP + k4sRAP x HR, the product sRAP x HR had the highest coefficient of determination (r2 = 0.75) and was the only significant determinant. We conclude that atrial tension or stress, developing during each atrial systole, is an important determinant of ANF release. Since atrial diastolic and systolic dimensions do not increase during pacing tachycardia, ANF release is not dependent on atrial distension.

Animals↗
PubMed1988

Effect of maleate on tubular protein reabsorption in dog kidneys.

To examine the effects on protein and electrolyte reabsorption of reducing the energy supply to the proximal tubules, an inhibitor of the citric acid cycle, maleate (600 mg.kg-1), was administered to anesthetized dogs during continuous ethacrynic acid infusion. One hour after infusion, maleate reduced renal oxygen consumption from 128 +/- 3 to 48 +/- 6 mumol.min-1. Comparisons at similar GFR showed that maleate reduced bicarbonate reabsorption by 65%, chloride reabsorption by 60% and phosphate reabsorption by 90%. Tubular reabsorption of lysozyme, determined by the 'trapped-label' method, was reduced by 97%. Total protein excretion in urine increased from 0.12 to 1.0 mg.min-1 and was not associated with a significant increase in brush border and lysosome marker enzymes. However, by superimposing a carbonic anhydrase inhibitor, acetazolamide (100 mg.kg-1), electrolyte reabsorption was slightly further reduced but protein excretion increased to 2.7 mg.min-1, coincidentally with a dramatic increase in enzyme excretion: approximately 20-fold in the brush border enzymes, alanine aminopeptidase and alkaline phosphatase, and 10-fold in the lysosomal enzymes, acid phosphatase and N-acetyl-beta-glucosaminidase. Our data indicate that maleate stops protein reabsorption without signs of acute tubular damage, whereas subsequent administration of acetazolamide results in tubular desquamation and albumin leakage.

Absorption↗
PubMed1987

How bicarbonate loading inhibits tubular reabsorption of NaCl in dog kidneys.

During continuous infusion of ethacrynic acid in dogs, changes in glomerular filtration rate (GFR) and PCO2 at constant plasma bicarbonate concentration (PHCO3) alter bicarbonate and chloride reabsorption in a ratio of 1:2. This ratio did not apply when PHCO3 was raised by bicarbonate loading in 11 anaesthetized volume-expanded dogs. A rise in PHCO3 from 30 to 54 mM at constant PCO2 and GFR reduced sodium reabsorption during ethacrynic acid infusion from 3586 +/- 725 to 2449 +/- 403 mumol min-1. Bicarbonate and chloride reabsorption were reduced in a ratio of 1:10. When plasma pH was restored from 7.8 to 7.5 by raising PCO2, the inhibitory effect on chloride reabsorption was halved. At constant plasma pH 7.5 a rise in PHCO3 from 20 to 30 mM reduced chloride reabsorption by 20%. A further 30% inhibition was caused by raising PHCO3 from 30 to 54 mM. Bicarbonate reabsorption was highest at PHCO3 54 mM, suggesting a large capacity for bicarbonate reabsorption if PHCO3 is raised at constant plasma pH 7.5. Water and NaCl reabsorption remaining during ethacrynic acid infusion is almost equally inhibited by alkalosis and by an osmotic effect of unreabsorbed NaHCO3.

Animals↗
PubMed1987

Renal degradation and distribution between urinary and venous output of prostaglandins E2 and I2.

To examine renal degradation and distribution between urine and renal venous blood, prostaglandins E2 and I2 (PGE2 and PGI2), and a metabolite of PGI2, 6-keto-PGF1 alpha, were infused into the suprarenal aorta of anaesthetized dogs after blocking prostaglandin synthesis by indomethacin, 10 mg kg-1 body wt iv. During one passage through the kidney 80% of PGE2 and only 25% of PGI2 and 6-keto-PGF1 alpha were metabolized. Prostaglandin degradation and arterial input were proportional (r greater than 0.90). To stimulate the intrarenal prostaglandin synthesis in unblocked kidneys, arachidonic acid was infused at rates ranging from 24 to 160 micrograms min-1 kg-1 body wt. During arachidonic acid and PGE2 infusion the urinary excretion of PGE2 was about 20% of the renal venous output over a wide range of infusion rates. During arachidonic acid and PGI2 infusion urinary excretion of 6-keto-PGF1 alpha was about 10% of total renal output, but failed to increase further when total renal output exceeded 70 pmol min-1. Further increase in output occurred only in the renal vein. In contrast, during 6-keto-PGF1 alpha infusion the urinary excretion and the renal venous output of this metabolite were related as 1:2 over a wide range of infusion rates. Thus, PGI2 is much less degraded by renal tissue than PGE2, and the distribution patterns differ. Similar distributions between urine and renal venous blood during aortic infusion and stimulated intrarenal synthesis suggest a pre-glomerular vascular origin of both prostaglandins.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Mechanism of osmotic diuresis studied by infusion of NaHCO3 and mannitol in dogs.

To examine whether mannitol and NaHCO3 are equally potent inhibitors of proximal tubular fluid reabsorption, experiments were performed in 10 anaesthetized volume-expanded dogs during continuous infusion of ethacrynic acid. At plasma pH 7.5, a rise in plasma osmolality of 40 mosmol kg-1 reduced the remaining tubular fluid reabsorption in five dogs by 14 +/- 3% during NaHCO3 infusion and by 28 +/- 1% during mannitol infusion. Bicarbonate reabsorption increased by 25 +/- 5% during NaHCO3 infusion and decreased by 14 +/- 1% during mannitol infusion. At equal rates of bicarbonate reabsorption the inhibitory effects on tubular fluid and NaCl reabsorption were slightly less during mannitol than during NaHCO3 infusion. In five other dogs studied at constant plasma concentration of sodium, changes in bicarbonate reabsorption were avoided by raising plasma pH to 7.7 during NaHCO3 infusion and by reducing plasma pH to 7.4 during mannitol infusion. Tubular fluid reabsorption was reduced 32 +/- 4% by NaHCO3 and 34 +/- 4% by mannitol infusion, indicating equal inhibitory effects. The mechanism may be that the osmotic force for paracellular reabsorption of water and NaCl across the tight junction is equally reduced by equiosmolal increments in the NaHCO3 and mannitol concentration of the proximal tubular fluid.

Animals↗