Interaction between antidiuretic and parathyroid hormones on urine concentration

1980 ◽  
Vol 239 (3) ◽  
pp. F244-F249
Author(s):  
H. D. Humes ◽  
C. F. Simmons ◽  
B. M. Brenner
Keyword(s):  
Calcium Ion ◽  
Calcium Concentration ◽  
Urine Concentration ◽  
Sprague Dawley ◽  
Urinary Osmolality ◽  
Group Of Seven ◽  
Parathyroid Hormones ◽  
Sprague Dawley Rats ◽  
Maximum Water ◽  
Solute Excretion

Experiments were performed on 26 acutely thyroparathyroidectomized (TPTX) Sprague-Dawley rats undergoing maximum water diuresis to determine whether the rise in urinary osmolality (Uosmol) in response to a submaximal dose of antidiuretic hormone (ADH) is modified by exogenous administration of parathyroid hormone (PTH). During administration of a submaximal dose of PTH to 11 TPTX rats, the ADH-induced increase in Uosmol averaged 267 +/- 15 mosmol, or twice the average increment of 131 +/- 18 mosmol observed when the same dose of ADH was given prior to PTH infusion (P < 0.001). This difference could not be attributed to changes in endogenous ADH release, renal hemodynamics, or solute excretion, and was not observed in a second group of eight other water-diuretic TPTX rats given sham PTH infusion. A third group of seven water-diuretic TPTX rats were studied with verapamil, a compound known to antagonize calcium ion entry into cells. Pretreatment of these rats with intravenous verapamil abolished the PTH potentiation of the Uosmol response to ADH described above. We conclude, therefore, that PTH enhances the Uosmol response to ADH, perhaps via a mechanism requiring a PTH-mediated change in the cellular calcium concentration or content of cells important in the urinary concentrating process.

Role of arginine vasopressin in medullary thick ascending limb on maximal urinary concentration

1986 ◽  
Vol 251 (2) ◽  
pp. F266-F270 ◽  
Author(s):  
J. K. Kim ◽  
S. N. Summer ◽  
A. E. Erickson ◽  
R. W. Schrier
Keyword(s):  
Adenylate Cyclase ◽  
Arginine Vasopressin ◽  
Urinary Concentration ◽  
Thick Ascending Limb ◽  
Sprague Dawley ◽  
Urinary Osmolality ◽  
Medullary Thick Ascending Limb ◽  
Sprague Dawley Rats ◽  
Collecting Tubules

Two groups of Sprague-Dawley rats, Harlan (H) and Charles River (CR), were discovered in that the medullary thick ascending limb (MAL) had a profoundly different adenylate cyclase response to arginine vasopressin (AVP). Using these two groups of rats, we studied the correlation between AVP action on the MAL and maximal urinary concentration. AVP (10(-6) M) significantly stimulated adenylate cyclase in MAL of H rats (7.4 +/- 0.9 to 43.8 +/- 4.6 fmol cAMP formed X 30 min-1 X mm-1, P less than 0.001) but not in CR rats (10.3 +/- 1.4 to 12.7 +/- 2.0 fmol cAMP formed X 30 min-1 X mm-1, NS). In contrast, AVP significantly stimulated adenylate cyclase of cortical, outer and inner medullary collecting tubules from both H and CR rats. Glucagon (10(-6) M) significantly stimulated adenylate cyclase of MAL from both H and CR rats. After 48 h of fluid deprivation, urinary osmolality was significantly higher (P less than 0.001) in the H (4,504 +/- 399 mosmol/kg H2O, n = 14) than CR (2,840 +/- 176 mosmol/kg H2O, n = rats. This observation was not attributable to differences in creatinine clearance (CR, 1.30 +/- 0.24; H, 1.24 +/- 0.03 ml/min, NS, n = 4) or plasma AVP (CR, 12.75 +/- 1.44; H, 12.38 +/- 1.17 pg/ml, NS, n = 6) levels. These results therefore suggest that the action of AVP on the MAL, in addition to the effect on collecting tubules, is involved in maximal urinary concentration in rats.

scholarly journals Chronic use of chloroquine disrupts the urine concentration mechanism by lowering cAMP levels in the inner medulla

2012 ◽  
Vol 303 (6) ◽  
pp. F900-F905 ◽  
Author(s):  
Tobias N. von Bergen ◽  
Mitsi A. Blount
Keyword(s):  
Lupus Erythematosus ◽  
Urine Analysis ◽  
Water Channel ◽  
Chronic Administration ◽  
Urine Osmolality ◽  
Urine Concentration ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Chloroquine Treatment ◽  
Camp Levels

Chloroquine, a widely used anti-malaria drug, has gained popularity for the treatment of rheumatoid arthritis, systemic lupus erythematosus (SLE), and human immunodeficiency virus (HIV). Unfortunately, chloroquine may also negatively impact renal function for patients whose fluid and electrolyte homeostasis is already compromised by diseases. Chronic administration of chloroquine also results in polyuria, which may be explained by suppression of the antidiuretic response of vasopressin. Several of the transporters responsible for concentrating urine are vasopressin-sensitive including the urea transporters UT-A1 and UT-A3, the water channel aquaporin-2 (AQP2), and the Na+-K+-2Cl−cotransporter (NKCC2). To examine the effect of chloroquine on these transporters, Sprague-Dawley rats received daily subcutaneous injections of 80 mg·kg−1·day−1of chloroquine for 4 days. Twenty-four hour urine output was twofold higher, and urine osmolality was decreased by twofold in chloroquine-treated rats compared with controls. Urine analysis of treated rats detected the presence chloroquine as well as decreased urine urea and cAMP levels compared with control rats. Western blot analysis showed a downregulation of AQP2 and NKCC2 transporters; however, UT-A1 and UT-A3 abundances were unaffected by chloroquine treatment. Immunohistochemistry showed a marked reduction of UT-A1 and AQP2 in the apical membrane in inner medullary collecting ducts of chloroquine-treated rats. In conclusion, chloroquine-induced polyuria likely occurs as a result of lowered cAMP production. These findings suggest that chronic chloroquine treatment would exacerbate the already compromised fluid homeostasis observed in diseases like chronic kidney disease.

Oxytocin resistance in Brattleboro rat adipocytes and comparative studies on insulin or oxytocin responsiveness in normal rat adipocytes

1983 ◽  
Vol 61 (11) ◽  
pp. 1418-1425 ◽  
Author(s):  
K. Hanif ◽  
H. J. Goren ◽  
R. M. Geonzon ◽  
K. Lederis ◽  
M. D. Hollenberg
Keyword(s):  
Calcium Concentration ◽  
Maximal Response ◽  
Sprague Dawley ◽  
Assay Medium ◽  
Rat Adipocytes ◽  
Sprague Dawley Rats ◽  
Normal Rat ◽  
Increased Sensitivity ◽  
Long Evans ◽  
Treatment Use

We have evaluated factors, other than genetic, which might be related to the lack of an oxytocin-mediated insulinlike response (glucose oxidation; lipogenesis) in adipocytes from Brattleboro rats, homozygous for the diabetes insipidus trait (HoDI rats). The manoeuvres used in an attempt to restore the glucoregulatory responses to oxytocin in HoDI cells (increased glucose in the fat pad digestion medium; increased calcium concentration in the oxidation assay; estrogen treatment; use of [1-14C]glucose as substrate; inclusion of adenosine in the assay medium; vasopressin replacement therapy) uniformly failed to result in oxytocin activation of HoDI adipocytes, in contrast, the contractile responses of estrogenized HoDI rat uteri were indistinguishable from those of estrogenized normal rats. We conclude that the nonresponsiveness of the Brattleboro adipocytes to the glucoregulatory actions of oxytocin is not due to factors related to the conditions of the bioassay. On the other hand, in normal fat cells (from Sprague–Dawley and Long Evans rats), oxytocin responsiveness was augmented by a number of the manoeuvres mentioned above, most notably by the inclusion of either calcium (10 mM) or adenosine (10 μM) in the assay medium. Nonetheless, the maximum oxytocin responsiveness of adipocytes from Long Evans or Sprague–Dawley rats, under all conditions of assay, was still only a fraction (less than 20%) of the maximal response to insulin. The effect of adenosine on oxytocin action (increased sensitivity, without an effect on the maximum response) is in keeping with the previously observed effects of this nucleoside on the action of insulin; our results thus pointed to a new parallel in the action of insulin and oxytocin.

Group VIA phospholipase A2 is a target for vasopressin signaling in the thick ascending limb

2012 ◽  
Vol 302 (7) ◽  
pp. F865-F874 ◽  
Author(s):  
A. Paliege ◽  
T. Roeschel ◽  
H. Neymeyer ◽  
S. Seidel ◽  
T. Kahl ◽  
...  
Keyword(s):  
Gene Expression Analysis ◽  
Urine Concentration ◽  
Prostaglandin E ◽  
Thick Ascending Limb ◽  
Sprague Dawley ◽  
Outer Medulla ◽  
Sprague Dawley Rats ◽  
Β Protein ◽  
Bromoenol Lactone ◽  
V2 Receptor

Na+-K+-2Cl− cotransporter (NKCC2)-mediated NaCl reabsorption in the thick ascending limb (TAL) is stimulated by AVP via V2 receptor/PKA/cAMP signaling. This process is antagonized by locally produced eicosanoids such as 20-HETE or prostaglandin E2, which are synthesized in a phospholipase A2-dependent reaction cascade. Using microarray-based gene expression analysis, we found evidence for an AVP-dependent downregulation of the calcium-independent isoform of PLA2, iPLA2β, in the outer medulla of rats. In the present study, we therefore examined the contribution of iPLA2β to NKCC2 regulation. Immunoreactive iPLA2β protein was detected in cultured mTAL cells as well as in the entire TAL of rodents and humans with the exception of the macula densa. Administration of the V2 receptor-selective agonist desmopressin (5 ng/h; 3 days) to AVP-deficient diabetes insipidus rats increased outer medullary phosphorylated NKCC2 (pNKCC2) levels more than twofold in association with a marked reduction in iPLA2β abundance (−65%; P < 0.05), thus confirming microarray results. Inhibition of iPLA2β in Sprague-Dawley rats with FKGK 11 (0.5 μM) or in mTAL cells with FKGK 11 (10 μM) or ( S)-bromoenol lactone (5 μM) for 1 h markedly increased pNKCC2 levels without affecting total NKCC2 expression. Collectively, these data indicate that iPLA2β acts as an inhibitory modulator of NKCC2 activity and suggest that downregulation of iPLA2β may be a relevant step in AVP-mediated urine concentration.

Indomethacin impairs water diuresis in the DI rat: role of prostaglandins independent of ADH

1981 ◽  
Vol 241 (3) ◽  
pp. F231-F237 ◽  
Author(s):  
J. S. Stoff ◽  
R. M. Rosa ◽  
P. Silva ◽  
F. H. Epstein
Keyword(s):  
Renal Tubules ◽  
Sprague Dawley ◽  
Water Diuresis ◽  
Water Excretion ◽  
Sprague Dawley Rats ◽  
Endogenous Prostaglandins ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Hereditary Diabetes ◽  
Solute Excretion

The mechanisms by which endogenous renal prostaglandins regulate water excretion were investigated in these studies. Inhibition of prostaglandin synthesis slowed water diuresis in water-loaded unanesthetized Sprague-Dawley rats and in Brattleboro rats with hereditary diabetes insipidus owing to absence of endogenous vasopressin. In both strains, treatment with indomethacin or meclofenamate increased the osmolality of the renal papilla by raising sodium and urea content, and also increased the osmolality of the urine. Endogenous creatinine clearance and solute excretion were unchanged. The data are consistent with an effect of prostaglandins on solute transport by renal tubules and demonstrate that endogenous prostaglandins influence water excretion by a mechanism independent of the presence of antidiuretic hormone.

Location of epicardial pacemaker electrodes and myocardial contractility

1969 ◽  
Vol 47 (3) ◽  
pp. 267-271 ◽  
Author(s):  
G. M. Tremblay ◽  
M. Nahas
Keyword(s):  
Rat Heart ◽  
Myocardial Contractility ◽  
Calcium Concentration ◽  
Cardiac Contractility ◽  
Sprague Dawley ◽  
Perfused Rat Heart ◽  
Isolated Perfused Rat Heart ◽  
Sprague Dawley Rats ◽  
Significant Difference ◽  
Pacemaker Electrodes

Effects of pacing from different epicardial sites on cardiac contractility were studied in the isolated perfused rat heart. An indwelling balloon containing a known volume of saline was used to record intracavitary pressure (LVP), force, and maximum dp/dt during isovolumic paced contraction. Coronary flow was kept constant, and the adequacy of oxygenation was verified by lactate extraction. Forty male Sprague–Dawley rats weighing 250–300 g were divided into two groups, according to the rate of pacing, and stimulated. Pacing from four different epicardial sites failed to show any statistically significant difference in LVP, force, or maximum dp/dt at either different heart rate or calcium concentration. The present study suggests that myocardial contractility in the isolated perfused rat heart is not affected by the pacing site of the epicardial pacemaker.

Contrasting effects of vasopressin on baroreflex inhibition of lumbar sympathetic nerve activity

1985 ◽  
Vol 249 (5) ◽  
pp. H922-H928 ◽  
Author(s):  
F. M. Sharabi ◽  
G. B. Guo ◽  
F. M. Abboud ◽  
M. D. Thames ◽  
P. G. Schmid
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Sprague Dawley ◽  
Nerve Activity ◽  
Urinary Osmolality ◽  
Arterial Baroreceptors ◽  
Sprague Dawley Rats ◽  
The Difference ◽  
High Level

Baroreflex inhibition of lumbar sympathetic nerve activity (LSNA) during intravenous infusions of phenylephrine and vasopressin is contrasted in rats and rabbits. In rabbits, vasopressin caused smaller increases in arterial pressure and greater inhibition of LSNA than phenylephrine. In Sprague-Dawley rats, however, both vasopressin and phenylephrine caused equivalent increases in arterial pressure and reflex reductions in LSNA. The inhibition of LSNA was mediated through the arterial baroreceptors in both species because it was abolished by sinoaortic denervation. In rats, the possibility that a high level of endogenous vasopressin may have prevented the demonstration of a facilitated baroreflex with the infusion of exogenous vasopressin is unlikely since vasopressin also did not facilitate the reflex in Brattleboro rats, which lack circulating vasopressin. Further, Sprague-Dawley rats were responsive to exogenous vasopressin since infusion of increasing doses of vasopressin caused significant increases in urinary osmolality as well as progressive increments in arterial pressure. The results indicate that intravenous vasopressin given for a period of 6 min facilitates the reflex inhibition of LSNA mediated through arterial baroreceptors in rabbits, but not in rats. Vasopressin given for a period of up to 45 min to rats also fails to facilitate baroreflexes, emphasizing the difference from rabbits. In rabbits, this facilitation appears to involve a central mechanism.

scholarly journals Expression of transporters involved in urine concentration recovers differently after cessation of lithium treatment

2010 ◽  
Vol 298 (3) ◽  
pp. F601-F608 ◽  
Author(s):  
Mitsi A. Blount ◽  
Jae H. Sim ◽  
Rong Zhou ◽  
Christopher F. Martin ◽  
Wei Lu ◽  
...  
Keyword(s):  
Lithium Treatment ◽  
Urine Volume ◽  
Urine Osmolality ◽  
Urine Concentration ◽  
Lithium Therapy ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Rapid Restoration ◽  
Critical Components ◽  
Immunohistochemical Analyses

Patients receiving lithium therapy, an effective treatment for bipolar disorder, often present with acquired nephrogenic diabetes insipidus. The nephrotoxic effects of lithium can be detected 3 wk after the start of treatment and many of these symptoms may disappear in a few weeks after lithium use is stopped. Most patients, however, still have a urine-concentrating defect years after ending treatment. This prompted an investigation of the transporters involved in the urine concentration mechanism, UT-A1, UT-A3, aquaporin-2 (AQP2), and NKCC2, after discontinuing lithium therapy. Sprague-Dawley rats fed a Li2CO3-supplemented diet produced large volumes of dilute urine after 14 days. After lithium treatment was discontinued, urine osmolality returned to normal within 14 days but urine volume and urine urea failed to reach basal levels. Western blot and immunohistochemical analyses revealed that both urea transporters UT-A1 and UT-A3 were reduced at 7 and 14 days of lithium treatment and both transporters recovered to basal levels 14 days after discontinuing lithium administration. Similar analyses demonstrated a decrease in AQP2 expression after 7 and 14 days of lithium therapy. AQP2 expression increased over the 7 and 14 days following the cessation of lithium but failed to recover to normal levels. NKCC2 expression was unaltered during the 14-day lithium regimen but did increase 14 days after the treatment was stopped. In summary, the rapid restoration of UT-A1 and UT-A3 as well as the increased expression of NKCC2 are critical components to the reestablishment of urine concentration after lithium treatment.

Functional differences of six forms of renin in rats

1988 ◽  
Vol 254 (3) ◽  
pp. F432-F439
Author(s):  
S. H. Kim ◽  
M. C. Lloyd ◽  
F. M. Sessler ◽  
J. Q. Feng ◽  
R. L. Malvin
Keyword(s):  
Enzyme Inhibitor ◽  
Biological Activities ◽  
Urine Flow ◽  
Sprague Dawley ◽  
Water Excretion ◽  
Urinary Osmolality ◽  
Pentobarbital Sodium ◽  
Functional Differences ◽  
Sprague Dawley Rats ◽  
Isoelectric Points

Six forms of renin with different isoelectric points (pIs) have been described in rats. This study was designed to determine if any of the renin forms have different biological activities. Each form of rat renin was semipurified and injected intravenously or intraventricularly in Sprague-Dawley rats anesthetized with pentobarbital sodium or Inactin. Changes in blood pressure (BP), renal function, sodium, and water excretion were observed, before and following equipressor doses; the peak response of BP was similar for all forms. However, the half-lives were significantly different. Form 4 (pI = 5.2) caused a significant increase in urine flow, Na, and K excretion, and urinary osmolality when given intravenously. The other forms were without significant effect. Infusion of converting enzyme inhibitor not only completely blocked the BP response, but also prevented the natriuresis and diuresis. This was observed in rats anesthetized with pentobarbital sodium or Inactin. Intraventricular infusions resulted in a diuresis and natriuresis when form 6 (pI = 4.8) was infused, but not with other forms. BP remained unchanged throughout. This study presents evidence that functional differences exist between renin forms.

Ultrastructural Investigation of Spontaneous Pituitary Adenomas in Aging Sprague-Dawley Rats

1982 ◽  
Vol 40 ◽  
pp. 216-217
Author(s):  
D. J. McComb ◽  
J. Beri ◽  
F. Zak ◽  
K. Kovacs
Keyword(s):  
Microscopic Study ◽  
Pituitary Adenomas ◽  
Wistar Rats ◽  
Microscopic Level ◽  
Sprague Dawley ◽  
Prolactin Cells ◽  
Light Microscopic Level ◽  
Ultrastructural Investigation ◽  
Sprague Dawley Rats ◽  
Long Evans

Investigation of the spontaneous pituitary adenomas in rat have been limited mainly to light microscopic study. Furth et al. (1973) described them as chromophobic, secreting prolactin. Kovacs et al. (1977) in an ul trastructural investigation of adenomas of old female Long-Evans rats, found that they were composed of prolactin cells. Berkvens et al. (1980) using immunocytochemistry at the light microscopic level, demonstrated that some spontaneous tumors of old Wistar rats could contain GH, TSH or ACTH as well as PRL.

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