63Ni Complexes in Rabbit Serum and Urine after Injection of 63NiCl2

1972 ◽  
Vol 18 (12) ◽  
pp. 1478-1484 ◽  
Author(s):  
Maria Van Soestbergen ◽  
F William Sunderman

Abstract Radioactive nickel chloride (63NiCl2) was injected i.v. into rabbits in dosage of 0.24 mg Ni/kg body wt. 63Ni was rapidly cleared from the serum (T1/2 ≃ 8.2 h) during the period from 1 h to 2 days after the injection, but slowly (T1/2 ≃ 95 h) during the period from 4 to 7 days after the injection. During 24 h after injection of 63NiCl2, an average of 90% of serum 63Ni was bound to albumin and 10% was ultrafiltrable. Chromatography on Sephadex G-25 demonstrated the presence of five distinct 63Ni complexes (Fractions I to V) in serum ultrafiltrates. During 24 h after injection of 63NiCl2, an average of 78% of the administered dose of 63Ni was excreted in the urine. Chromatography of the urine on Sephadex G-25 separated three 63Ni complexes, which appeared to have identical chromatographic mobilities as serum Fractions II, III, and V. The chemical identities of the ultrafiltrable 63Ni complexes in serum and urine have not been established, although one (Fraction V) resembles Ni histidine in its chromatographic mobility on Sephadex G-25. This study demonstrates that ultrafiltrable nickel in serum and urine does not exist primarily as free Ni(II), but instead as Ni complexes, and suggests that ultrafiltrable Ni receptors play an important physiological role in nickel homeostasis by serving as diffusible vehicles for the extracellular transport and renal excretion of nickel.

2001 ◽  
Vol 280 (5) ◽  
pp. R1510-R1517 ◽  
Author(s):  
John R. Dietz ◽  
Dionne Y. Scott ◽  
Carol S. Landon ◽  
Stanley J. Nazian

The experiments, performed in pentobarbital sodium-anesthetized rats, consisted of a 1-h equilibration period followed by two 30-min control periods. Subsequently, synthetic rat pro atrial natriuretic peptide (ANP) [proANP-(1–30)] ( n = 8) was given as a bolus of 10 μg in 1 ml of 0.9% saline followed by an infusion at 30 ng/min (20 μl/min) for six additional periods. Control rats ( n = 6) received only 0.45% saline in the appropriate volumes. Mean arterial pressure, renal blood flow, and glomerular filtration rate did not change significantly in either group during the proANP-(1–30) infusion. Urine flow and potassium excretion increased ∼50% in the proANP-(1–30)-infused group only ( P < 0.05). Sodium excretion and fractional excretion of sodium, expressed as the change from their own baselines, were significantly increased by the proANP-(1–30) infusion ( P < 0.05), whereas cGMP excretion was similar in both groups. These results suggest that the rat sequence of proANP-(1–30) produces a natriuresis in the rat independent of changes in hemodynamics and renal cGMP production. In a second study, rats ( n = 8) were prepared as above and pretreated with 0.4 ml iv of rabbit serum containing an antibody directed against proANP-(1–30) (anti-proANP group). The rats were volume expanded with 3 ml of 6% albumin in Krebs and observed for 3 h to determine if the anti-proANP would attenuate the responses to volume expansion. Control rats ( n = 7) received 0.4 ml of normal rabbit serum. The elevation in potassium excretion in response to volume expansion was significantly attenuated in the anti-proANP group ( P < 0.05). Sodium excretion and urine flow responses also tended to be reduced but not significantly. These results suggest that in the rat, proANP-(1–30) plays a physiological role in regulating renal excretion.


1972 ◽  
Vol 55 (2) ◽  
pp. 245-252 ◽  
Author(s):  
D. N. KALU ◽  
CARMEL HILLYARD ◽  
G. V. FOSTER

SUMMARY The effect of glucagon on bone was studied in rats. Urinary hydroxyproline excretion and incorporation of [3H]proline into bone hydroxyproline were used as indices of bone collagen breakdown and formation respectively. Parathyroid extract (15 USP units/rat/h, i.v.), infused into thyroparathyroidectomized animals, increased urinary hydroxyproline excretion. This increase was nullified by simultaneous administration of glucagon (50 μg/rat/h, i.v.). Rats treated with glucagon for 12 days (30 μg/100 g/day, s.c.) excreted slightly less hydroxyproline in their urine than controls. In both intact and thyroparathyroidectomized rats, glucagon (10 μg/100 g/h, s.c.) decreased incorporation of [3H]proline into bone. Similar results were obtained in nephrectomized rats, evidence that changes produced by glucagon were not solely due to alterations in proline pool size caused by increased renal excretion. From these data it is concluded that: (1) glucagon can inhibit bone resorption (the effect being slight in normal rats, but easily demonstrable in parathyroid hormone-treated thyroparathyroidectomized rats), (2) release of endogenous calcitonin is not required to produce this effect, (3) parathyroid hormone and glucagon may act on the same target cell in bone, (4) inhibition of skeletal resorption may contribute to glucagon-induced hypocalcaemia, and (5) the hormone possibly decreases bone formation. Since pharmacological doses of glucagon were used in our studies, the relationship of the observations made to the physiological role of glucagon is unknown.


1988 ◽  
Vol 255 (5) ◽  
pp. F811-F822 ◽  
Author(s):  
D. B. Young

Aldosterone is part of a complex system that regulates plasma potassium concentration by affecting the renal excretion of the ion as well as its distribution within the body. Because there are other components of the system, it has been difficult to determine the physiological significance of aldosterone in potassium regulation by attempting to study the hormone's effects in isolation. In this presentation a quantitative analysis of the potassium control system is used to provide information concerning the physiological role of aldosterone in potassium regulation under normal and pathological conditions, as well as during pharmacological interventions.


1989 ◽  
Vol 257 (4) ◽  
pp. H1104-H1109 ◽  
Author(s):  
A. Sasaki ◽  
O. Kida ◽  
T. Kita ◽  
J. Kato ◽  
S. Nakamura ◽  
...  

To clarify the physiological role of endogenous atrial natriuretic polypeptide (ANP), we investigated the effects of specific rabbit antiserum against alpha-rat ANP (alpha-rANP) on hemodynamics, diuresis, and natriuresis in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). Intravenous administration of anti-alpha-rANP antiserum caused an obvious rise of mean blood pressure and cardiac output in both SHR and WKY compared with rats administered with normal rabbit serum. Although there was no significant difference in increments of mean blood pressure between SHR and WKY, the increment of cardiac output in SHR was significantly higher than that in WKY. On the other hand, significant reductions in urine output and urinary sodium and potassium excretion lasted for approximately 20 min after administration of the antiserum in both SHR and WKY compared with rats administered with normal rabbit serum. There was no significant difference in these initial maximal decrements between SHR and WKY. These results indicate that endogenous ANP has an important physiological role in the regulation of hemodynamics and water-electrolyte balance in both SHR and WKY. The greater increment of cardiac output in SHR in response to the antiserum suggests that endogenous ANP in SHR may have a stronger cardiosuppressive action that it does in WKY.


1989 ◽  
Vol 257 (1) ◽  
pp. 291-292 ◽  
Author(s):  
Y Nagata ◽  
R Konno ◽  
Y Yasumura ◽  
T Akino

The physiological role of D-amino acid oxidase was investigated by using mutant ddY/DAO- mice lacking the enzyme. Free D-amino acid concentrations in the mutant mice were significantly higher than those of control ddY/DAO+ mice in kidney, liver, lung, heart, brain, erythrocytes, serum and urine. The results suggest that the enzyme is involved in the catabolism of free D-amino acids in the body, and that free D-amino acids are also excreted into urine.


1990 ◽  
Vol 258 (2) ◽  
pp. G268-G274 ◽  
Author(s):  
K. Y. Lee ◽  
L. Zhou ◽  
X. S. Ren ◽  
T. M. Chang ◽  
W. Y. Chey

We have investigated a physiological role of endogenous insulin on exocrine pancreatic secretion stimulated by a liquid meal as well as exogenous secretin and cholecystokinin octapeptide (CCK-8) in conscious rats. Each rat was prepared with a chronic pancreatic fistula and an indwelling catheter in a jugular vein. Oral ingestion of a liquid meal (5 ml) resulted in significant increases in pancreatic secretion, including volume, bicarbonate, and amylase output, in these rats. A rabbit anti-insulin serum (1.0 ml) given intravenously completely blocked the postprandial exocrine pancreatic secretion, whereas a normal rabbit serum did not influence the pancreatic secretion in the same rats. When pancreatic secretion was stimulated by intravenous administration of both secretin and CCK-8 in three different doses, including 0.015, 0.03, and 0.06 clinical unit and microgram.kg-1.h-1, respectively, volume, bicarbonate, and amylase output increased significantly in a dose-dependent manner. This increase in pancreatic secretion was also completely blocked by a rabbit anti-insulin serum, whereas it was not influenced by a normal rabbit serum. The amount of the antiserum employed abolished the postprandial increases in plasma insulin concentration. We conclude that endogenous insulin plays an important role on the regulation of postprandial pancreatic secretion in rats. Furthermore, for the stimulatory action of the two intestinal hormones secretin and CCK-8 on the pancreatic exocrine secretion, endogenous insulin is need.


1990 ◽  
Vol 258 (3) ◽  
pp. R690-R696 ◽  
Author(s):  
G. Wakabayashi ◽  
M. Ueda ◽  
N. Aikawa ◽  
M. Naruse ◽  
O. Abe

The effect of pulmonary injury induced by aspiration of HCl on plasma atrial natriuretic polypeptide (ANP) level was examined in rats given a constant infusion of water and electrolytes. In addition, using specific antiserum against ANP, we investigated the physiological role of ANP in rats after HCl aspiration. Rats were housed individually in metabolic cages and were given a constant infusion of sodium solution via catheters chronically inserted into the jugular vein. Plasma ANP levels were elevated at 3 and 24 h after tracheal injection of 0.2 ml of 0.1 N HCl via the cricothyroid membrane. Urine volume and urinary sodium excretion increased during the first 24 h after acid aspiration. However, this increase was reduced by the injection of anti-ANP serum. Furthermore, the injection of anti-ANP serum resulted in a significant (P less than 0.05) increase in wet lung weight from a value of 0.74 +/- 0.06 (HCl aspiration with normal rabbit serum injection) to 0.83 +/- 0.07% of body weight. These results indicate that ANP plays a physiological role in the regulation of urinary water and sodium excretion after pulmonary acid injury and suggest that ANP elevated in plasma after pulmonary injury may prevent pulmonary edema with its diuretic action and/or some direct action on water movement in the lung.


1990 ◽  
Vol 259 (6) ◽  
pp. E792-E796 ◽  
Author(s):  
M. E. Melton ◽  
J. J. D'Anza ◽  
S. A. Wimbiscus ◽  
V. Grill ◽  
T. J. Martin ◽  
...  

Parathyroid hormone (PTH)-related protein has been shown to be a factor responsible for hypercalcemia of malignancy. Recent studies have shown the presence of mRNA for PTH-related protein in lactating breast tissue, suggesting a physiological role for this peptide during lactation. In the present study, we evaluated the effect of neutralization of PTH-related protein activity in lactating mice (by passive immunization) on various parameters of maternal and neonatal calcium homeostasis. PTH-related protein bioactivity, as tested in the adenylate cyclase assay, was present in mouse milk, and this activity was completely neutralized by the antisera used in the present study. In lactating mice, the effects of injection of PTH-related protein antisera on maternal serum calcium concentrations, milk calcium and phosphorus concentration, pup growth, dam femur calcium content, and pup calcium content were similar to those of the injection of normal rabbit serum. Therefore, maternal PTH-related protein does not appear to have a role in calcium homeostasis during lactation.


1987 ◽  
Vol 73 (5) ◽  
pp. 479-487 ◽  
Author(s):  
J. S. Hunt ◽  
Anne Groufsky ◽  
K. L. Lynn

1. A role has been suggested for anti-Tamm–Horsfall protein (THP) antibodies in renal disease based on the results of immunoassays of pathological sera. The putative autoantibodies have not been isolated from such sera nor have definitive inhibition studies of their binding been carried out. We have carried out such studies using rabbit anti-THP antibodies as control reagents. 2. Urinary THP prepared by salt precipitation was used to prepare four immunoabsorbent columns by covalent coupling to CNBr-activated Sepharose 4B. After washing with a variety of dissociating agents to remove any non-covalently bound subunit THP, each column was incubated with normal and immune rabbit serum. Fractions washed and eluted from columns were tested for anti-THP antibodies by enzyme-linked immunosorbent assay (ELISA) and THP antigen by radioimmunoassay, and showed NH4SCN (3 mol/l) and guanidine hydrochloride (GuHCl) (6 mol/l) equivalent and sodium dodecyl sulphate (20 g/l) to be inferior in their capacity to produce immunoabsorbent THP capable of isolating specific antibodies from immune rabbit serum. 3. The column treated with GuHCl (6 mol/l) was used further in attempts to isolate putative anti-THP antibodies from five patients, who had a history of urinary tract infections and whose sera showed strong binding by ELISA. 4. Results from direct and inhibition ELISA experiments on fractions collected after washing and elution with all sera suggested that the putative human anti-THP antibodies were of very low affinity and/or directed against non-subunit THP. 5. The pathological relevance of human anti-THP antibodies measured by ELISA remains to be established.


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