Urinary sodium, phosphate, and hydrogen excretion following unilateral kidney clamping

1978 ◽  
Vol 56 (3) ◽  
pp. 428-434 ◽  
Author(s):  
Gérard E. Plante ◽  
Hubert Hermkens
Keyword(s):  
Sodium Phosphate ◽  
Renal Plasma Flow ◽  
Left Kidney ◽  
Critical Role ◽  
Extracellular Volume ◽  
Urinary Sodium ◽  
Ammonium Excretion ◽  
Titratable Acid ◽  
Group I ◽  
Group Ii

The influence of extracellular volume on compensatory adaptation of sodium, phosphate, and hydrogen excretion after unilateral kidney exclusion was examined in the dog. Ammonium chloride was administered to all animals to raise urinary hydrogen excretion. Eleven dogs (group I) were studied under relative hydropenia and 11 (group II) were volume expanded with isotonic NaCl. Six animals (group III) prepared as group II were sham operated.In groups I and II, plasma bicarbonate decreased by 1.1 and 1.2 mM/ℓ after unilateral kidney clamping, while serum phosphate rose from 5.3 to 6.1 and from 3.6 to 3.9 mg%, respectively. The following parameters are those obtained from the left kidney before and after contralateral clamping. Urinary sodium remained unchanged after clamping in group I but rose from 422 to 681 μequiv./min in group II. In contrast, urinary phosphate increased from 83 to 233 and from 94 to 189 μg/min in groups I and II, respectively.Measured titratable acid and urinary ammonium excretion remained unchanged in group I. A small but significant decrement in ammonium was obtained with time in group II. Glomerular filtration and renal plasma flow were not influenced by contralateral clamping, but filtration fraction was lower in group II than in group I. No change occurred in group III.Extracellular volume appears to play a critical role in the physiological expression of contralateral natriuresis after unilateral clamping whereas compensatory phosphaturia is obtained in both hydropenic and volume-expanded animals.

Effect of parathyroid hormone on renal excretion of sodium and hydrogen ions

1977 ◽  
Vol 55 (3) ◽  
pp. 628-638 ◽  
Author(s):  
Hubert Hermkens ◽  
Tewfik Nawar ◽  
Claude Caron ◽  
Gerard E. Plante
Keyword(s):  
Parathyroid Hormone ◽  
Renal Plasma Flow ◽  
Extracellular Volume ◽  
Phosphate Transport ◽  
Left Renal Artery ◽  
Group Iii ◽  
Titratable Acid ◽  
Group I ◽  
Group Ii ◽  
The Right

The contribution of parathyroid hormone (PTH) to the renal adjustment of phosphate transport has been extensively investigated, whereas the action of this hormone on bicarbonate and hydrogen excretion has not received as much attention.Nineteen dogs were studied before and during a 2-h infusion of PTH in the left renal artery (8 mU/min per kilogram) under slight expansion of extracellular volume (fractional sodium excretion = U/FNa = 3.8 ± 0.3%). Group I (n = 7) was studied under normal acid–base condition while group II (n = 6) was studied during metabolic acidosis. Bicarbonate titration curves were obtained from group III (n = 6) in which the right kidney was used as control. In all studies, plasma pCO2 was kept constant.[Formula: see text] rose from 4.2 ± 1.1 to 15.6 ± 3.0% and from 3.8 ± 0.4 to 25.0 ± 3.5% in groups I and II, respectively. U/FNa was unchanged in both groups. [Formula: see text] rose from 5.8 ± 0.6 to 10.1 ± 0.7% in group I but remained at 1.0 ± 0.2% in group II during PTH. Urinary titratable acid and ammonium were not influenced by PTH in group II. In group III, plasma HCO3 was progressively increased from 15 to 40 mM/litre. For all plasma values exceeding 22 mM/litre, HCO3 reabsorption was 1 mM/litre of filtrate lower in the left than in the right kidney. Glomerular filtration and renal plasma flow remained constant during PTH.The results indicate that PTH affects sodium and hydrogen excretion in a very modest fashion. Bicarbonaturia obtains whenever plasma HCO3 exceeds 22 mM/litre during PTH. This phenomenon is associated with a demonstrable reduction in tubular HCO3 reabsorption per unit of filtrate.

Effect of renal vein pressure on urinary sodium and bicarbonate ions

1978 ◽  
Vol 56 (1) ◽  
pp. 30-38 ◽  
Author(s):  
J. Jobin ◽  
R. Hemmings ◽  
G. E. Plante
Keyword(s):  
Carbonic Anhydrase ◽  
Renal Vein ◽  
Renal Plasma Flow ◽  
Carbonic Anhydrase Activity ◽  
Urinary Sodium ◽  
Bicarbonate Transport ◽  
Group Iii ◽  
Titratable Acid ◽  
Group I ◽  
Group Ii

The present study was undertaken to assess the effect of renal vein pressure on sodium and bicarbonate transport under two opposite conditions of bicarbonate filtered loads. Unilateral partial occlusion of the renal vein (RVO) was induced in 17 mongrel dogs: renal vein pressure rose from 9 to 20, 25, and 30 mmHg in a stepwise fashion. Seven of these animals (group I) were studied during bicarbonate loading [Formula: see text] and six others (group II) were studied during metabolic acidosis, induced with ammonium chloride [Formula: see text]. In the four remaining dogs (group III), administered bicarbonate in the manner described for group I, acetazolamide was given in a bolus and sustained infusion to inhibit the carbonic-anhydrase-mediated fraction of bicarbonate reabsorption while renal vein pressure was being kept at 30 mmHg. Plasma pCO2 was maintained at constant levels in all studies.In group I, urinary sodium (UNaV) decreased from 203 ± 32 to 110 ± 17 μEquiv./min, and bicarbonaturia [Formula: see text] from 131 ± 21 to 79 ± 18 μEquiv./min during RVO. In group II, UNaV) dropped from 132 ± 32 to 81 ± 20 μEquiv./min while [Formula: see text] remained at 2 μEquiv./min. Urinary ammonium and titratable acid decreased from 12.6 ± 1.7 to 8.7 ± 1.2 and from 8.0 ± 1.6 to 5.5 ± 1.1 μEquiv./min, respectively, during RVO. In group III, UNaV averaged 208 ± 42, 132 ± 29, and 203 ± 37 μEquiv./min during control, RVO, and RVO plus acetazolamide, respectively. During these same periods, [Formula: see text] was 144 ± 22, 72 ± 23, and 155 ± 30 μEquiv./min. All the above changes observed in the experimental kidney were significant (p < 0.05). In contrast, the same parameters measured in the opposite control kidney remained unaffected. Glomerular filtration and renal plasma flow remained stable in group I but decreased slightly in groups II and III. Filtration fraction was unaffected, however.The data indicate that RVO influences Na and HCO3 excretion through mechanisms not obviously related to peritubular physical forces. Since acetazolamide abolishes the effect of RVO, the mechanism(s) of antinatriuresis could be related to renal carbonic anhydrase activity.

Functional adaptation to reduced renal mass in early development

1982 ◽  
Vol 242 (2) ◽  
pp. F190-F196 ◽  
Author(s):  
R. L. Chevalier
Keyword(s):  
Renal Mass ◽  
Left Kidney ◽  
Extracellular Fluid ◽  
Functional Adaptation ◽  
Fluid Loss ◽  
Group Iii ◽  
Arterial Blood ◽  
India Ink ◽  
Group I ◽  
Group Ii

To determine whether reduced renal mass in the newborn results in acceleration of normal renal development, the response to unilateral nephrectomy (N) before 36 h of age was compared with sham-operated (S) guinea pigs during the period of most rapid nephron maturation. Studies were performed at 7-13 days (group I) and 19-25 days (group II). Mean arterial blood pressure (AP), left kidney glomerular filtration rate (LKGFR), and urine sodium excretion (UNaV) were measured. Superficial single nephron GFR (sSNGFR) and proximal fractional water reabsorption (FRH2O) were measured by micropuncture, and the number of glomeruli (NG) was determined by India ink perfusion. In view of the susceptibility of the neonate to extracellular fluid loss, groups I and II were plasma infused to maintain euvolemia and group II was compared with 19- to 25-day-old hydropenic animals (group III). Increase in body weight with age was unaffected by neonatal N. In group IN, the compensatory increase in sSNGFR was greater than SNGFR for deeper nephrons, which normally contribute most to GFR at this age. In group IIN there was an 80% adaptive increase in LKGFR that could not be entirely explained by the rise in SNGFR. Since NG in group IIN was greater than in group IIS and similar to that in adulthood, the enhanced adaptation in LKGFR in group IIN may be due in part to earlier recruitment of a population of underperfused glomeruli. FRH2O did not change significantly with age and did not differ in N and S groups. Animals in group III developed a rise in hematocrit during the experiment, and AP, LKGFR, and UNaV were lower in group IIIN than in group IIN. It is concluded that following N at birth, the sequence of renal functional maturation is accelerated while glomerulotubular balance is preserved. As a result of these adaptative changes, homeostasis is maintained and body growth proceeds without impairment.

Effect of aortic clamping on proximal reabsorption and sodium excretion in the rat

1977 ◽  
Vol 232 (2) ◽  
pp. F92-F96 ◽  
Author(s):  
R. W. Osgood ◽  
N. H. Lameire ◽  
M. I. Sorkin ◽  
J. H. Stein
Keyword(s):  
Sodium Excretion ◽  
Perfusion Pressure ◽  
Left Kidney ◽  
Extracellular Volume ◽  
Extracellular Fluid ◽  
Renal Perfusion ◽  
Ringer Solution ◽  
Aortic Clamping ◽  
Group I ◽  
Before And After

It has been suggested that aortic clamping prior to expansion of the extracellular fluid volume prevents the natriuretic response normally seen in this setting. To further evaluate this finding, two groups of re-collection micropuncture studies were performed before and after 7.5% body wt expansion with Ringer solution. Group I, immediate-clamp studies, n, 11. After control collections, perfusion pressure to the left kidney was decreased to 75 mmHg followed by Ringer loading. Group II, delayed-clamp studies, n, 8. After control collections, Ringer solution was given for 40 min. Then the left renal perfusion pressure was reduced to 75 mmHg and the Ringer infusion was continued at the same rate. In the immediate-clamp group, there was no change in total kidney glomerular filtration rate (GFR) (1.16 vs. 1.11 ml/min), nephron GFR (40 vs. 39 nl/min), tubular fluid-to-plasma inulin ratio (2.40 vs. 2.28), or filtrate delivery out of the proximal tubule (18 vs. 18 ndium excretion were not significantly altered. In the delayed-clamp studies, there was also no change in total or nephron GFR, but the tubular fluid-to-plasma inulin ratio fell from 2.52 to 1.65 (P less than .001) and distal delivery rose 9 nl/min after expansion (P less than .001). Sodium excretion increased 3.83 mueq/min and fractional sodium excretion rose 2.28%, both values being markedly greater than in the immediate-clamp studies (P less than .005 for both). These results demonstrate that immediate clamping obviates the fall in proximal reabsorption and the natriuretic response to Ringer loading and suggests that intrarenal adjustments are a major determinant of the magnitude of the natriuretic response to expansion of the extracellular volume

Association Between Ligand-Induced Conformational Changes of Integrin IIbβ3 and IIbβ3-Mediated Intracellular Ca2+ Signaling

Blood ◽  
1998 ◽  
Vol 92 (10) ◽  
pp. 3675-3683 ◽  
Author(s):  
Shigenori Honda ◽  
Yoshiaki Tomiyama ◽  
Toshiaki Aoki ◽  
Masamichi Shiraga ◽  
Yoshiyuki Kurata ◽  
...  
Keyword(s):  
Monoclonal Antibodies ◽  
Platelet Aggregation ◽  
Conformational Changes ◽  
Binding Sites ◽  
Critical Role ◽  
Thromboxane A2 ◽  
Fibrinogen Binding ◽  
Group I ◽  
Group Ii ◽  
Inhibition Studies

Platelet IIbβ3 is a prototypic integrin and plays a critical role in platelet aggregation. Occupancy of IIbβ3 with multivalent RGD ligands, such as fibrinogen, induces both expression of ligand-induced binding sites (LIBS) and IIbβ3 clustering, which are thought to be necessary for outside-in signaling. However, the association between LIBS expression and outside-in signaling remains elusive. In this study, we used various IIbβ3-specific peptidomimetic compounds as a monovalent ligand instead of fibrinogen and examined the association between LIBS expression and outside-in signaling such as IIbβ3-mediated intracellular Ca2+ signaling. Using a set of monoclonal antibodies (MoAbs) against LIBS, we showed that antagonists can be divided into two groups. In group I, antagonists can induce LIBS on both IIb and β3 subunits. In group II, antagonists can induce LIBS on the IIb subunit, but not on the β3 subunit. Inhibition studies suggested that group I and group II antagonists interact with distinct but mutually exclusive sites on IIbβ3. Neither group I nor group II antagonist increased intracellular Ca2+concentrations ([Ca2+]i) in nonactivated platelets. All antagonists at nanomolar concentrations abolished the increase in [Ca2+]i in 0.03 U/mL thrombin-stimulated platelets, which is dependent on both fibrinogen-binding to IIbβ3 and platelet-aggregation. However, only group I antagonists at higher concentrations dose-dependently augmented the [Ca2+]i increase, which is due to aggregation-independent thromboxane A2 production. This increase in [Ca2+]i was not observed in thrombasthenic platelets, which express no detectable IIbβ3. Thus, only the group I antagonists, albeit a monovalent ligand, can initiate IIbβ3-mediated intracellular Ca2+ signaling in the presence of thrombin stimulation. Our findings strongly suggest the association between β3LIBS expression and IIbβ3-mediated intracellular Ca2+ signaling in platelets.

The Antinatriuretic Effect of Dopaminergic Blockade during Volume Expansion is Independent of Circulating Atrial Natriuretic Factor

1989 ◽  
Vol 77 (5) ◽  
pp. 479-484 ◽  
Author(s):  
Paolo Coruzzi ◽  
Almerico Novarini ◽  
Luisa Musiari ◽  
Carlo Ravanetti ◽  
Salvatore Ghielmi ◽  
...  
Keyword(s):  
Sodium Excretion ◽  
Atrial Natriuretic Factor ◽  
Water Immersion ◽  
Urinary Sodium Excretion ◽  
Plasma Aldosterone ◽  
Urinary Sodium ◽  
Natriuretic Factor ◽  
Group I ◽  
Group Ii ◽  
Atrial Natriuretic

1. Ten normal subjects were subjected to 2 h water immersion with and without pharmacological dopaminergic blockade with either metoclopramide (group I) or domperidone (group II). 2. In group I, urinary sodium excretion showed a marked increase during water immersion alone, whereas it was blunted during water immersion plus dopaminergic blockade with metoclopramide (P < 0.05 vs water immersion alone, n = 5). Plasma aldosterone was significantly suppressed by water immersion alone (P < 0.05), but remained unchanged during water immersion plus metoclopramide. Plasma atrial natriuretic factor showed similar augmentation during water immersion alone and during water immersion plus metoclopramide. 3. Another five subjects (group II) were studied during water immersion alone and during water immersion plus dopaminergic blockade with domperidone. In this group the increase in urinary sodium excretion was similarly blunted by dopaminergic blockade. Plasma atrial natriuretic factor was equally elevated during water immersion alone and during water immersion plus domperidone, but aldosterone was suppressed by both water immersion alone and water immersion plus domperidone. 4. Our findings suggest that water immersion-induced atrial natriuretic factor release is independent of dopaminergic activity. Dopamine blockade is able to blunt significantly both water immersion-induced natriuresis and plasma aldosterone suppression, independently of the marked elevation of circulating atrial natriuretic factor, via a mechanism involving type 2 dopaminergic receptors.

scholarly journals Anatomy of Inferior Mesenteric Artery in Fetuses

Scientifica ◽  
2016 ◽  
Vol 2016 ◽  
pp. 1-5
Author(s):  
Ayesha Nuzhat
Keyword(s):  
Renal Artery ◽  
Mesenteric Artery ◽  
Inferior Mesenteric Artery ◽  
Left Kidney ◽  
Lumbar Vertebra ◽  
Left Renal Artery ◽  
Accessory Renal Artery ◽  
Medical College ◽  
Group I ◽  
Group Ii

Aim. To analyze Inferior Mesenteric Artery in fetuses through its site of origin, length, diameter, and variation of its branches.Method. 100 fetuses were collected from various hospitals in Warangal at Kakatiya Medical College in Andhra Pradesh, India, and were divided into two groups, group I (second-trimester fetuses) and group II (third-trimester fetuses), followed by dissection.Result.(1) Site of Origin. In group I fetuses, origin of Inferior Mesenteric Artery was at third lumbar vertebra in 33 out of 34 fetuses (97.2%). In one fetus it was at first lumbar vertebra, 2.8%. In all group II fetuses, origin of Inferior Mesenteric Artery was at third lumbar vertebra.(2) Length. In group I fetuses it ranged between 18 and 30 mm, average being 24 mm except in one fetus where it was 48 mm. In group II fetuses the length ranged from 30 to 34 mm, average being 32 mm.(3) Diameter. In group I fetuses it ranged from 0.5 to 1 mm, and in group II fetuses it ranged from 1 to 2 mm, average being 1.5 mm.(4) Branches. Out of 34 fetuses of group I, 4 fetuses showed variation. In one fetus left colic artery was arising from abdominal aorta, 2.9%. In 3 fetuses, Inferior Mesenteric Artery was giving a branch to left kidney, 8.8%. Out of 66 fetuses in group II, 64 had normal branching. In one fetus left renal artery was arising from Inferior Mesenteric Artery, 1.5%, and in another fetus one accessory renal artery was arising from Inferior Mesenteric Artery and entering the lower pole of left kidney.Conclusion. Formation, course, and branching pattern of an artery depend on development and origin of organs to attain the actual adult position.

Association Between Ligand-Induced Conformational Changes of Integrin IIbβ3 and IIbβ3-Mediated Intracellular Ca2+ Signaling

Blood ◽  
1998 ◽  
Vol 92 (10) ◽  
pp. 3675-3683 ◽  
Author(s):  
Shigenori Honda ◽  
Yoshiaki Tomiyama ◽  
Toshiaki Aoki ◽  
Masamichi Shiraga ◽  
Yoshiyuki Kurata ◽  
...  
Keyword(s):  
Monoclonal Antibodies ◽  
Platelet Aggregation ◽  
Conformational Changes ◽  
Binding Sites ◽  
Critical Role ◽  
Thromboxane A2 ◽  
Fibrinogen Binding ◽  
Group I ◽  
Group Ii ◽  
Inhibition Studies

Abstract Platelet IIbβ3 is a prototypic integrin and plays a critical role in platelet aggregation. Occupancy of IIbβ3 with multivalent RGD ligands, such as fibrinogen, induces both expression of ligand-induced binding sites (LIBS) and IIbβ3 clustering, which are thought to be necessary for outside-in signaling. However, the association between LIBS expression and outside-in signaling remains elusive. In this study, we used various IIbβ3-specific peptidomimetic compounds as a monovalent ligand instead of fibrinogen and examined the association between LIBS expression and outside-in signaling such as IIbβ3-mediated intracellular Ca2+ signaling. Using a set of monoclonal antibodies (MoAbs) against LIBS, we showed that antagonists can be divided into two groups. In group I, antagonists can induce LIBS on both IIb and β3 subunits. In group II, antagonists can induce LIBS on the IIb subunit, but not on the β3 subunit. Inhibition studies suggested that group I and group II antagonists interact with distinct but mutually exclusive sites on IIbβ3. Neither group I nor group II antagonist increased intracellular Ca2+concentrations ([Ca2+]i) in nonactivated platelets. All antagonists at nanomolar concentrations abolished the increase in [Ca2+]i in 0.03 U/mL thrombin-stimulated platelets, which is dependent on both fibrinogen-binding to IIbβ3 and platelet-aggregation. However, only group I antagonists at higher concentrations dose-dependently augmented the [Ca2+]i increase, which is due to aggregation-independent thromboxane A2 production. This increase in [Ca2+]i was not observed in thrombasthenic platelets, which express no detectable IIbβ3. Thus, only the group I antagonists, albeit a monovalent ligand, can initiate IIbβ3-mediated intracellular Ca2+ signaling in the presence of thrombin stimulation. Our findings strongly suggest the association between β3LIBS expression and IIbβ3-mediated intracellular Ca2+ signaling in platelets.

Hyperfiltration in remnant nephrons: a potentially adverse response to renal ablation

1981 ◽  
Vol 241 (1) ◽  
pp. F85-F93 ◽  
Author(s):  
T. H. Hostetter ◽  
J. L. Olson ◽  
H. G. Rennke ◽  
M. A. Venkatachalam ◽  
B. M. Brenner
Keyword(s):  
Left Kidney ◽  
Diet Group ◽  
Normal Diet ◽  
Cell Protein ◽  
Hydraulic Pressure ◽  
Group Iii ◽  
Group I ◽  
Renal Ablation ◽  
Single Nephron ◽  
Group Ii

Micropuncture studies were performed in three groups of male Munich-Wistar rats 1 wk after surgery: group I, eight control rats that underwent laparotomy and were fed a normal diet; group II, nine rats that underwent right nephrectomy and segmental infarction of five-sixths of the left kidney and were fed a normal diet; and group III, seven rats that underwent the same renal ablative procedure and were fed a low protein diet. Single nephron glomerular filtration rate (SNGFR) was higher in the remnant kidney of group II rats compared with group I rats due to higher average values for mean glomerular transcapillary hydraulic pressure difference (delta P) and initial glomerular plasma flow rate (QA) in group II. Glomeruli in remnant kidneys of group II showed striking alterations in morphology, including epithelial cell protein reabsorption droplets, foot process fusion, and mesangial expansion. Group III rats demonstrated a mean SNGFR not statistically different from that of group I, but significantly less than that of group II rats. This lack of absolute hyperfiltration in remnant glomeruli of group III rats relative to group I obtained because QA and delta P did not increase above values found in group I. The glomerular structural lesions seen in group II were also largely attenuated in group III. These studies demonstrate that alterations in glomerular hemodynamics associated with renal ablation are accompanied by structural lesions and suggest that sustained single nephron hyperfiltration may have maladaptive consequences by damaging remnant glomeruli.

scholarly journals The role of a complement regulatory protein in rat mesangial glomerulonephritis.

1995 ◽  
Vol 6 (2) ◽  
pp. 234-241 ◽  
Author(s):  
H Nishikage ◽  
L Baranyi ◽  
H Okada ◽  
N Okada ◽  
K Isobe ◽  
...  
Keyword(s):  
Left Kidney ◽  
Regulatory Protein ◽  
Protein A ◽  
Systemic Circulation ◽  
Host Cells ◽  
Complement Regulatory Protein ◽  
Glomerular Injury ◽  
Group I ◽  
Group Ii

The host cells are protected from the indiscriminate attack of homologous complement by the membrane-associated complement regulatory proteins. A mouse monoclonal antibody (mAb) 512 (immunoglobulin G1 subclass) has recently been described that recognizes and inhibits the function of a rat complement regulatory protein, a rat homologue of mouse Crry/p65. The aim of this work is to assess the role of a complement regulatory protein (512Ag) recognized by mAb 512 in the complement-dependent glomerular injury induced by mAb OX7 against rat Thy-1.1. For the induction of mesangial injury, the left kidney of a rat was perfused with a combination of OX7 and 512 and the perfusate was discarded from the renal vein (Group I). After the renal artery and vein were restored, the left kidney was connected to the systemic circulation. Rats were euthanized 3 h, 2 days, and 14 days later. Rats perfused either with OX7 (Group II) or with 512 (Group III) or with vehicle only (Group IV) were used as controls. At 3 h, rats of Group I showed more prominent cellular infiltration and mesangial lysis and more C3 deposition in the glomeruli than rats of Group II. Rats of Groups III and IV showed no significant changes. At Day 2, there was still significant mesangial lysis and leukocyte infiltration in Group I rats, whereas rats in other groups showed an almost normal appearance. Glomerular injury in Group I rats returned to normal by Day 14.

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