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Biomedical subjects

F Kiil

Publications and source records attributed to F Kiil.

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

Filtered bicarbonate and plasma pH as determinants of renal bicarbonate reabsorption.

To examine if bicarbonate reabsorption varies with filtered bicarbonate and plasma pH, we infused anesthetized dogs i.v. with sodium chloride and sodium bicarbonate to alter plasma bicarbonate concentration (PHCO3) without changing hematocrit. Examinations in five dogs over a wide range of glomerular filtration rates (GFR) during ethacrynic acid infusion showed that bicarbonate reabsorption at equal filtered load and equal plasma pH of 7.5 was not significantly changed by increasing PHCO3 from 30.2 +/- 0.4 to 55.2 +/- 0.6 mM and PCO2 from 33.8 +/- 0.7 to 74.1 +/- 2.1 mm Hg. Examinations during respiratory and metabolic alkalosis in five dogs at plasma pH of 7.8 showed that bicarbonate reabsorption at equal filtered load was not significantly different at a PCO2 of 20.2 +/- 0.8 and 36.8 +/- 0.8 mm Hg. Finally, in five dogs that did not receive ethacrynic acid, plasma pH was lowered by inducing respiratory acidosis at a PHCO3 of 30 mM and raised during progressive respiratory and metabolic alkalosis, Bicarbonate reabsorption was linearly related to plasma pH within the range 7.1 to 7.85 (r = 0.92). By altering plasma pH by 0.1 unit, bicarbonate reabsorption was altered by 10 +/- 1%. Thus, filtered bicarbonate rather than GFR and plasma pH rather than PCO2 are important acute regulators of bicarbonate reabsorption. This regulation may be achieved by determining pH and bicarbonate concentration in the luminal fluid along the proximal tubules.

Alkalosis↗
PubMed1981

Mechanism of osmotic diuresis.

Mannitol might inhibit paracellular reabsorption of water and sodium chloride in the proximal tubules by reducing the osmotic driving force. We examined this hypothesis in anesthetized dogs. Bicarbonate reabsorption was kept constant by sodium bicarbonate infusion, and transcellular sodium chloride reabsorption was inhibited by ethacrynic acid. The glomerular filtration rate (GFR) was varied by altering renal perfusion pressure. Mannitol infusion reduced sodium chloride reabsorption from 62 +/- 5% to 33 +/- 5% of the filtered load. The calculated increase in reabsorbate osmolality, averaging 82 +/- 6 mOsm/kg H2O, was due to sodium bicarbonate and equalled the increase in plasma osmolality. Mannitol concentration averaged 81 +/- 7 mM in plasma and 101 +/- 12 mM in urine. A linear relationship between reabsorption and GFR (glomerulo-tubular balance) was maintained over the same range of GFR before and after mannitol infusion. Mannitol infusion reduced sodium chloride reabsorption from 2.6 to 1.4 moles for each mole of sodium bicarbonate reabsorbed. During mannitol infusion, acetazolamide inhibited sodium bicarbonate reabsorption as in control experiments, but reduced sodium chloride reabsorption less. We conclude that reduced water reabsorption increases sodium bicarbonate concentration in the paracellular fluid as much as mannitol concentration is raised in the plasma and glomerular filtrate. Along the proximal tubules, net osmotic force is progressively reduced as mannitol concentration rises, accounting for reduced water and sodium chloride reabsorption.

Acetazolamide↗
PubMed1981

Cardiac effects of splanchnic and non-splanchnic blood volume redistribution during aortic occlusions in dogs.

Translocation of blood from the lower body dilates the left ventricle during occlusion of the descending thoracic aorta and by increased activation of the Frank-Starling mechanism, stroke volume is maintained despite raised aortic blood pressure. The contributions from the splanchnic and non-splanchnic blood volumes to the left ventricular dilation were examined by ultrasonic measurements of myocardial chord length (MCL) in atropinized open-chest dogs. End-diastolic MCL rose by 2.5 +/- 0.9% during abdominal suprarenal aortic occlusion, draining blood from the non-splanchnic region, and by 7.4 +/- 1.7% during thoracic aortic occlusion draining blood from both splanchnic and non-splanchnic regions. Systolic left ventricular pressure rose by 16 +/- 3 mmHg and 76 +/- 12 mmHg, respectively. End-diastolic MCL rose by 6.0 +/- 1.2% during combined thoracic aortic and abdominal infrahepatic vena cava occlusion draining blood solely from the splanchnic region and further by 2.5 +/- 0.8% by blood drained from the non-splanchnic region after release of the vena cava occlusion. Similar results were obtained using a shunt permitting selective drainage first from the non-splanchnic region during thoracic aortic occlusion. Blood translocation from the non-splanchnic region maintains cardiac output during abdominal aortic occlusion. During occlusion of the thoracic aorta, drainage from the splanchnic region accounts for about 70% of the increase in end-diastolic MCL.

Animals↗
PubMed1981

Transcellular and intercellular transport of anions in the kidney tubules of dogs.

Fractional reabsorption of 4 anions was measured in anesthetized dogs either during inhibition of bicarbonate-dependent intercellular NaCl transport by acetazolamide or mannitol, or during inhibition of transcellular NaCl reabsorption in the diluting segment by ethacrynic acid or ouabain. When administered subsequent to ethacrynic acid, acetazolamide reduced fractional reabsorption of SCN, Br, Cl and I by 0.28 +/- 0.03, 0.28 +/- 0.02, 0.27 +/- 0.03 and 0.31 +/- 0.03. Mannitol given after ethacrynic acid reduced fractional reabsorptions by 0.23 +/- 0.04, 0.20 +/- 0.04, 0.20 +/- 0.05 and 0.20 +/- 0.05, respectively. Thus, the bicarbonate-dependent reabsorption system does not discriminate between these anions. Ethacrynic acid reduced fractional reabsorption of SCN, Br and Cl by 0.28 +/- 0.05, 0.24 +/- 0.03, 0.22 +/- 0.03 in one group, by 0.32 /+- 0.04, 0.34 +/- 0.03, 0.31 +/- 0.04 in another group, with significantly smaller reductions for I, 0.07 +/- 0.03, in both groups. Ouabain reduced fractional reabsorption of Br, Cl and I by 0.48 +/- 0.04, 0.46 +/- 0.04 and 0.24 +/- 0.03, respectively. Thus, anion permeability or transport affinity for bromide, chloride and iodide are equal both for inter- and transcellular transport, while iodide transport is slow along the transcellular route. No specific transport mechanism for chloride was detected.

Absorption↗
PubMed1981

Effect of low-level renal nerve stimulation on renin release from nonfiltering kidneys.

The mechanism whereby renal nerves influence the renin-release response to aortic constriction was examined in a nonfiltering ureter-occluded kidney preparation in anesthetized dogs. The kidney was rendered nonfiltering by a combination of mannitol infusion and ureteral occlusion. Suprarenal aortic constriction reduced renal perfusion pressure to 61 +/- 7 mmHg and increased renin release from 16.7 +/- 4.1 to 26.1 +/- 6.0 U/min. At normal renal perfusion pressure, low-frequency renal nerve stimulation (0.25 Hz) increased renin release by 11.6 +/- 4.2 to 25.1 +/- 7.6 U/min. The effect of combined low-level renal nerve stimulation and aortic constriction on renin release was additive; renin release increased by 24.6 +/- 6.5 to 39.5 +/- 7.3 U/min. Propranolol or metoprolol, administered intrarenally at 2 microgram . min-1 . kg-1, abolished the renin-release response to low-level renal nerve stimulation at normal renal perfusion pressure. These data provide evidence that low-frequency renal nerve stimulation influences the renin-release response to reduction in renal perfusion pressure in a nonfiltering ureter-occluded kidney with an inoperative macula densa receptor mechanism. The neural effect on renin release at normal renal perfusion pressure is mediated via beta 1-adrenoceptors probably located on the juxtaglomerular granular cells.

Animals↗
PubMed1981

Myocardial function of the interventricular septum. Effects of right and left ventricular pressure loading before and after pericardiotomy in dogs.

We examined the function of the interventricular septum in six open-chest dogs by inserting piezoelectric crystals into the interventricular septum. Continuous ultrasonic recordings showed that the changes in myocardial chord length (MCL) in the septum and free walls of the right and left ventricle were similar during saline infusion and during pericardiotomy. End-diastolic MCL and myocardial shortening during ejection (MS) rose in the septum and free walls of both ventricles during saline infusion as end-diastolic MCL and MS in the septum and free walls of the ventricles, and reduced end-diastolic pressures by 1-2 mm Hg. The responses to aortic and pulmonary artery constrictions were similar before and after pericardiotomy. When aortic constriction had raised free left ventricular systolic pressure by about 60 mm Hg, end-diastolic MCL increased in the septum and free left ventricular wall, whereas end-diastolic MCL and MS of the free right ventricular wall fell. Pulmonary artery constriction increased end-diastolic MCL in the free right ventricular wall and reduced end-diastolic MCL and MS in the septum and free left ventricular wall. Thus, the myocardium, including the interventricular septum, is uniformly expanded during saline infusion and pericardiotomy. The interventricular septum behaves as part of the left ventricle during aortic and pulmonary artery constriction. The pericardium imposes a restraint on the interventricular septum and free walls of the ventricles during volume loading, but not during pressure loadings, because dilation of one ventricle is associated with shrinkage of the other.

Animals↗
PubMed1981

Conditions for humoral alpha-adrenoceptor stimulation of renin release in anaesthetized dogs.

To examine whether an alpha-adrenergic agonist, methoxamine, influences renin release solely by its haemodynamic effect, experiments were performed in anaesthetized dogs with denervated kidneys. Methoxamine was infused intrarenally at rates which reduced renal blood flow (RBF) by 30-40%. At control blood pressure, renin release rose during infusion of methoxamine from 1.4 +/- 0.7 to 31 +/- 11 microgram/min. A beta-adrenergic stimulator, isoproterenol, did not increase renin release significantly when administered alone into the renal artery, but doubled the effect of methoxamine infusion: at control blood pressure renin release rose from 0.5 +/- 0.3 to 71 +/- 17 microgram/min during combined infusion of isoproterenol and methoxamine. Mechanical constriction of the renal artery left RBF unaltered down to a renal perfusion pressure of 90 +/- 4 mmHg during methoxamine infusion, whereas the lowest autoregulating pressure in control experiments averaged 60 +/- 5 mmHg. At renal infusion pressure below the range of autoregulation, renin release was not further increased by intrarenal infusion of methoxamine. Isoproterenol infusion at low renal perfusion pressure doubled renin release, which was not significantly altered by additional infusion of methoxamine. The stimulatory effect of methoxamine on renin release at control blood pressure could be diminished but not prevented by infusing 2.9% NaCl intravenously in large amounts. These data indicate that methoxamine induces autoregulated dilation of afferent arterioles by disproportionate vasoconstriction on pre-afferent arteries. Thereby afferent arterioles are conditioned for stimulation of renin release by isoproterenol.

Animals↗
PubMed1981

Conditions for stimulation of renin release by cyclic AMP in anaesthetized dogs.

Cyclic AMP (cAMP) is the intracellular mediator of beta-adrenergic stimulation in most tissues. Stimulation of beta-adrenoceptors increases renin release much more at low than at control arterial perfusion pressure. If beta-adrenergic stimulation is mediated by cAMP, this nucleotide should also potentiate renin release at low perfusion pressure. In anaesthetized, propranolol treated dogs, the dibutyryl derivative of cAMP (DB-cAMP), which penetrates cell membranes more readily than cAMP, increased renin release significantly during renal arterial constriction at a perfusion pressure below the range of autoregulation, but no significant effect was observed at control blood pressure. A dose-response relationship could be demonstrated in propranolol treated dogs by administering DB-cAMP at 10, 100 and 1000 micrograms/min at low but not at control blood pressure. Since sodium excretion increased, stimulation of a macula densa mechanism is unlikely, whereas arteriolar dilation, caused by autoregulation at low blood pressure, may condition the juxtaglomerular apparatus for renin release. Infusion of cAMP had no effect on renin release either at control or low blood pressure, whereas 5'AMP exerted a marked inhibitory effect at low blood pressure. We conclude that infusion of DB-cAMP rather than cAMP stimulates renin release at low but not at control blood pressure and that this effect is not mediated by beta-adrenergic receptors; cAMP may be an intracellular mediator of renin release.

Adenosine Monophosphate↗
PubMed1981

Mechanism of renin release during renal nerve stimulation in dogs.

During renal nerve stimulation, a predominant vasoconstrictory effect on small arteries would lower blood pressure in the afferent arterioles and induce arteriolar dilation and renin release by the autoregulation mechanism. This hypothesis was examined in anaesthetized dogs by stimulating renal nerves at 4 Hz which permitted continuous reduction of renal blood flow (RBF) by 30-40%; renin release increased almost equally at control and low blood pressure, and in the non-filtering kidney during ureteral occlusion. Examinations of the relationship between RBF and arterial perfusion pressure during mechanical constriction of the renal artery showed that the lowest autoregulating pressure was 25-35 mmHg higher during nerve stimulation than in control experiments, consistent with the hypothesis of arteriolar dilation. Phenoxybenzamine, an inhibitor of alpha-adrenoceptors, abolished vasoconstriction and the effect of nerve stimulation on renin release at control blood pressure; renin release rose from 0.9 +/- 0.4 to 17 +/- 5 microgram/min before, and from 1.7 +/- 0.5 to 4.6 +/- 1.4 microgram/min after phenoxybenzamine infusion. At pressures below the range of autoregulation, phenoxybenzamine did not alter renin release response to nerve stimulation. Propranolol, a Beta-adrenergic inhibitor, attenuated the effect of nerve stimulation on renin release both at control and low blood pressure. We conclude that during renal nerve stimulation (1) renin release is caused by beta-adrenergic stimulation provided the afferent arterioles are dilated and (2) that alpha-adrenergic stimulation dilated the afferent arterioles as a consequence of a predominant vasoconstrictory effect on small arteries. Hence, by inhibiting the beta-adrenergic effect by propranolol, renin release does not increase during renal nerve stimulation. Phenoxybenzamine prevents renin release at control blood pressure because afferent arterioles are not dilated during nerve stimulation. In contrast, phenoxybenzamine does not reduce renin release during nerve stimulation at low blood pressure because afferent arterioles are dilated by the autoregulating mechanism.

Animals↗
PubMed1981

Ethacrynic acid inhibits transcellular NaCl reabsorption in dog kidneys in doses of 1 to 10 mg.kg-1 and proximal bicarbonate-dependent reabsorption at higher doses.

In anesthetized dogs, sodium reabsorption in the kidney tubule was continuously reduced with increasing dosage of ethacrynic acid until 59% of the filtered load was excreted with 25 mg.kg-1 at constant glomerular filtration rate. With 50 mg.kg-1, glomerular filtration rate fell, but fractional sodium reabsorption was further reduced by 7%. In the dosage range of 1 to 10 mg.kg-1, ethacrynic acid inhibited chloride but not bicarbonate reabsorption, and the ratio between reductions in sodium reabsorption and oxygen consumption (delta Na/delta O2) averaged 25.5 +/- 5.2. With doses of 25 and 50 mg.kg-1, ethacrynic acid further reduced chloride reabsorption, reduced fractional bicarbonate reabsorption by 17% and almost halved phosphate reabsorption, whereas delta Na/delta O2 rose significantly to 65.3 +/- 12.2. Renal cortical carbonic anhydrase activity was normal and the inhibitory effect of acetazolamide, a carbonic anhydrase inhibitor, on bicarbonate reabsorption was unimpaired. We conclude that ethacrynic acid in doses up to 10 mg.kg-1 exclusively inhibits transcellular NaCl reabsorption, but in higher doses interferes with bicarbonate reabsorption and bicarbonate-dependent passive reabsorption of NaCl in the proximal tubules without inhibiting carbonic anhydrase activity.

Absorption↗
PubMed1980

Renal bicarbonate reabsorption during bicarbonate loading.

To examine bicarbonate reabsorption at different GFR's, we varied the renal perfusion pressure in anesthetized dogs after inhibiting autoregulation by expanding extracellular volume and infusing ethacrynic acid. At a plasma bicarbonate concentration (PHCO3) of 28 +/- 1 mM, bicarbonate reabsorption varied in proportion to GFR (glomerulotubular balance). When PHCO3 was raised to 52 +/- 2 mM at constant PCO2 and hematocrit, bicarbonate reabsorption was reduced at all levels of filtered load. When plotted against GFR, different results were obtained dependent on the GFR level examined. At the control GFR,. bicarbonate loading reduced bicarbonate reabsorption by 30 +/- 5%. At a GFR level about 50% below the control GFR, bicarbonate loading increased reabsorption by about one third because the inhibitory effect of raising PHCO3 and extracellular pH was not sufficient to counteract the stimulatory effect of a higher filtered load. At intermediate levels of GFR, a rise in PHCO3 did not alter bicarbonate reabsorption. The finding that acetazolamide (30 mg/kg of body wt) at high PHCO3 failed to reduce bicarbonate reabsorption supports the hypothesis that the depressive effect of high extracellular pH on bicarbonate reabsorption may be attributed to reduced net tubular hydrogen ion secretion.

Absorption↗
PubMed1980

Mechanism of hemodynamic responses to occlusion of the descending thoracic aorta.

To examine left ventricular responses to aortic occlusion, changes in end-diastolic volume (EDV) and end-systolic volume (ESV) were estimated by ultrasonic recordings of myocardial distances in atropinized open-chest dogs. During aortic occlusion EDV and ESV increased equally, systolic left ventricular pressure (LVP) rose by 86 +/- 8 mmHg, and blood flow more than doubled in the superior vena cava and fell by 90% in the inferior vena cava. During combined occlusion of aorta and inferior vena cava, systolic LVP and superior vena cava flow did not rise above control and EDV declined. By infusing 25 +/- 2 ml/kg body wt of blood during combined occlusion, the effects of aortic occlusion could be reproduced; control values before blood infusion were reestablished by withdrawal of only one-third of the infused volume, indicating a shunt line along the spinal column. Thus during aortic occlusion, transfer of blood accounts for the rise in EDV and increased activation of the Frank-Starling mechanism; increased afterload raises ESV as much as EDV in anesthetized dogs not subjected to sympathetic stimulation. Consequently, stroke volume is maintained and systolic LVP increased.

Animals↗
PubMed1980

Left ventricular asynergy during intracoronary isoproterenol infusion in dogs.

Myocardial contractions were examined in the left ventricle of anesthetized, open-chest dogs during infusion of a beta-adrenergic agent, isoproterenol (0.1-0.5 micrograms/min) into a shunt line to the left anterior descending coronary artery. Myocardial chord lengths were continuously monitored by pairs of ultrasonic elements inserted into the isoproterenol-infused and control regions. Heart rate remained constant, but isoproterenol altered contraction patterns in both control and infused regions. Contraction in the infused region started before ejection and stretched the control myocardium in early systole. Because of early relaxation, however, the infusion region was stretched at the end of ejection and in early diastole, while the control myocardium continued to shorten. Thus, isoproterenol infusion to a part of the left ventricle induces asynergic muscle contractions and despite localized inotropic stimulation stroke volume may not be significantly increased.

Animals↗
PubMed1980

Oxygen requirement of bicarbonate-dependent sodium reabsorption in the dog kidney.

The ratio between changes in sodium reabsorption and renal oxygen consumption (Na/O2) was measured in anesthetized dogs at high plasma bicarbonate concentration (32 +/- 1 mM); ethacrynic acid was infused continuously to prevent variations in transcellular NaCl reabsorption when sodium reabsorption was altered by varying plasma PCO2 and glomerular filtration rate (GFR). At high plasma PCO2 (110 mmHg) sodium reabsorption varied in proportion to GRF between 50 and 125% of control GFR (glomerulotubular balance). By reducing PCO2 to 20 mmHg, sodium reabsorption was reduced by 50-60% at constant GFR. The Na/O2 ratio was not significantly different during the two procedures and averaged 48 +/- 2. The ratio between changes in NaHCO3 reabsorption and oxygen consumption averaged 17 +/- 1, which is not significantly different from the Na/O2 ratio of Na-K-ATPase-dependent sodium transport. We propose that NaHCO3 is admitted to the cell by Na+/H+ exchange and that sodium is actively transported by Na-K-ATPase across the peritubular cell membrane; NaHCO3 provides the osmotic force for paracellular reabsorption of water and NaCl (bicarbonate-dependent reabsorption) without additional energy requirement.

Absorption↗
PubMed1979

Renal metabolic rate during changes in bicarbonate-dependent sodium reabsorption in the proximal tubules.

Previous studies indicate that water and at least 2 mol NaCl are reabsorbed in the proximal tubules for each mol NaHCO3 reabsorbed. To examine the effect on cortical energy metabolism of variations in this bicarbonate-dependent sodium reabsorption, the cortical metabolic rate was examined in anaesthetized dogs by the heat production technique during continuous infusion of saline and ethacrynic acid. Sodium reabsorption was altered either by intravenous infusion of a large dose of acetazolamide (500 mg/kg body wt) or by changing plasma Pco2 during metabolic alkalosis. Acetazolamide reduced bicarbonate reabsorption by 71 +/- 2%, sodium reabsorption by 54 +/- 2% and cortical heat production by 21 +/- 3%. A rise in Pco2 to 16.4 +/- 1.3 kPa during metabolic alkalosis increased sodium reabsorption by 25 +/- 3% and cortical heat production by 14 +/- 2%. A similar elevation of plasma Pco2 during metabolic acidosis had no effect on electrolyte reabsorption or the cortical metabolic rate. A reduction in Pco2 to 2.3 +/- 0.3 kPa reduced sodium reabsorption by 40 +/- 3% and cortical heat production by 19 +/- 2%. We conclude that a rise in proximal tubular reabsorption requires energy. However, the changes in energy requirement are small, accounting for previous failures to observe significant changes in cortical energy metabolism during less extensive changes of sodium reabsorption in the proximal tubules.

Acetazolamide↗