Acute Effect of Parathyroid Hormone on Urine Concentration in the Rat

1995 ◽  
Vol 88 (2) ◽  
pp. 197-201 ◽  
Author(s):  
S. L. Carney ◽  
A. H. B. Gillies
Keyword(s):  
Parathyroid Hormone ◽  
Arginine Vasopressin ◽  
Partial Agonist ◽  
Acute Effect ◽  
Inhibitory Effect ◽  
Urine Concentration ◽  
Antidiuretic Effect ◽  
Plasma Calcium Concentration ◽  
Subsequent Effect

1. It has been demonstrated that parathyroid hormone can increase adenylate cyclase activity in the rat papilla, produce a small antidiuretic effect and in vitro can interfere with the action of arginine vasopressin on water transport. Clearance studies were performed in the anaesthetized water diuretic thyroparathyroidectomized rat to evaluate further the effect of parathyroid hormone on urine concentration in the presence and absence of arginine vasopressin. 2. A maximal phosphaturic concentration of rat parathyroid hormone (2 μg/kg) reduced urine flow from 125 ± 7 to 81 ± 9 μl/min within 10 min (P < 0.01). Addition of a maximal antidiuretic concentration of arginine vasopressin (100 ng/kg) produced a delayed and diminished antidiuretic response when compared with a group of rats not pretreated with parathyroid hormone (47 ± 5 compared with 27 ± 5 μl/min; P < 0.01). However, a supramaximal arginine vasopressin concentration (1000 ng/kg) produced a maximal antidiuretic effect in the presence of parathyroid hormone. 3. To evaluate further the inhibitory effect of parathyroid hormone on arginine vasopressin-induced anti-diuresis, parathyroid hormone (2 μg/kg) was administered to one group of rats and a minimally effective arginine vasopressin concentration (7.5 ng/kg) to another group, which produced a similar antidiuretic effect. However, the subsequent effect of a maximal antidiuretic arginine vasopressin concentration (100 ng/kg) was again significantly blunted in the group pretreated with parathyroid hormone. 4. Parathyroid hormone produced only a small increase in mean plasma calcium concentration, and glomerular filtration rate was not altered by either hormone. 5. These results demonstrate that high physiological concentrations of parathyroid hormone do have a significant antidiuretic effect and can interfere with the action of arginine vasopressin. This suggests that parathyroid hormone may act as a partial agonist to arginine vasopressin in the collecting system.

Effect of calcitonin on urine concentration in the rat

1983 ◽  
Vol 244 (4) ◽  
pp. F432-F435 ◽  
Author(s):  
S. Carney ◽  
T. Morgan ◽  
C. Ray ◽  
L. Thompson
Keyword(s):  
Water Permeability ◽  
Partial Agonist ◽  
Collecting Duct ◽  
Free Water ◽  
Urine Concentration ◽  
Distal Nephron ◽  
Free Water Clearance ◽  
Normal Increase

Because mammalian distal nephron segments with both calcitonin- and antidiuretic hormone- (ADH) sensitive adenylate cyclase activity have been described, in vivo and in vitro experiments were performed to study the effect of calcitonin on rat distal nephron water permeability. Calcitonin 1 and 0.1 U/ml, but not 0.01 U/ml, significantly increased the diffusional water permeability in the isolated papillary collecting duct by 15 and 11%, respectively. However, this effect was small when compared with a 68% increase with a supramaximal concentration of ADH (from 4.0 +/- 0.3 to 6.7 +/- 0.9 microns/s; n = 6, P less than 0.01). The normal increase in water permeability with increasing concentration of ADH (0.02 and 0.2 mU/ml) was depressed by the previous addition of calcitonin (1 U/ml) to the bath but was unaltered with the supramaximal ADH concentration (2 mU/ml). Verapamil, a compound that antagonizes cellular calcium entry, did not alter the effect of calcitonin on diffusional water permeability. Calcitonin in concentrations of 0.05, 0.5, and 5 U/ml produced a significant reduction in urine flow and free water clearance. Pretreatment with calcitonin in these concentrations inhibited the antidiuretic action of ADH. These studies suggest that calcitonin acts as a partial agonist to ADH within the distal nephron. It is unclear whether such an action represents a physiological or a pharmacological effect.

Central actions of parathyroid hormone on blood calcium and hypothalamic neuronal activity in the rat

1995 ◽  
Vol 268 (1) ◽  
pp. R21-R27 ◽  
Author(s):  
H. Matsui ◽  
S. Aou ◽  
J. Ma ◽  
T. Hori
Keyword(s):  
Parathyroid Hormone ◽  
Neuronal Activity ◽  
Inhibitory Effect ◽  
Dependent Manner ◽  
Blood Calcium ◽  
Bath Application ◽  
Central Actions ◽  
Dose Dependent ◽  
Postsynaptic Mechanism

The central actions of parathyroid hormone (PTH) on the blood ionized calcium level in anesthetized rats and the neuronal activity of the ventromedial nucleus of the hypothalamus (VMH) in vitro were investigated. An intracerebroventricular injection of PTH (0.01, 0.1, and 1 microgram) prevented urethan-induced hypocalcemia in a dose-dependent manner, whereas either an intravenous or an intracisternal injection of PTH (1 microgram) was ineffective. Eighty-three of 177 VMH neurons responded to a bath application of PTH (10(-7) or 3 x 10(-7) M): a majority (72, 83%) of the responsive cells decreased, whereas 11 increased their activity. This inhibitory effect of PTH on neuronal activity still persisted after synaptic blocking in a Ca(2+)-free/high-Mg2+ medium. A PTH receptor antagonist, [Tyr34]bPTH-(7-34)-NH2, suppressed the effect of PTH on the neuronal activity. These findings thus suggest that brain PTH has a calciotropic function and that one of the possible target sites is the VMH, where PTH inhibits its neuronal activity through a postsynaptic mechanism mediated by PTH receptors.

Interleukin-6 Induced Suppression of Bovine Parathyroid Hormone Secretion

1999 ◽  
Vol 19 (1) ◽  
pp. 35-42 ◽  
Author(s):  
E. Carlstedt ◽  
P. Ridefelt ◽  
L. Lind ◽  
J. Rastad
Keyword(s):  
Parathyroid Hormone ◽  
Critically Ill ◽  
Interleukin 6 ◽  
Hormone Secretion ◽  
Acute Effect ◽  
Tnf Α ◽  
Strong Stimulation ◽  
Factor Α ◽  
Necrosis Factor

Calcium disturbances in the critically ill coincide with elevations of proinflammatory cytokines. The effects of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) on parathyroid hormone (PTH) secretion were investigated. IL-6 and TNF-α had no acute effect on PTH secretion in extracellular Ca2+ concentrations of 0.5, 1.25 and 3.0 mM. In contrast to TNF-α, cultures for 24 h in the presence of 10 ng/mL of IL-6 showed decreased PTH secretion by 51% and 29% in 0.5 mM and 1.25 mMCa2+ respectively. Neither IL-6 nor TNF-α, affected cytoplasmic Ca2+ of the cells. We conclude that PTH secretion in vitro can be suppressed by IL-6 at clinically relevant concentrations. This suppression may aggravate hypocalcemia of the critically ill and attenuate the conventionally strong stimulation of the PTH release by reduction in serum calcium.

Calcitonin causes a sustained inhibition of protein kinase C-stimulated bone resorption in contrast to the transient inhibition of parathyroid hormone-induced bone resorption

1990 ◽  
Vol 123 (3) ◽  
pp. 251-256 ◽  
Author(s):  
Maria Ransjö ◽  
Ulf H. Lerner
Keyword(s):  
Protein Kinase C ◽  
Parathyroid Hormone ◽  
Protein Kinase ◽  
Bone Resorption ◽  
Phorbol Esters ◽  
Inhibitory Effect ◽  
Prostaglandin E ◽  
Kinase C

Abstract. Calcitonin is a well known inhibitor of osteoclastic bone resorption, both in vivo and in vitro. However, it is also known that calcitonin has only a transient inhibitory effect on bone resorption. The mechanism for this so-called "escape from inhibition" phenomenon is not clear. In the present study, the inhibitory effect of calcitonin on phorbol ester-induced bone resorption was examined in cultured neonatal mouse calvaria. Bone resorption was assessed as the release of radioactivity from bones prelabelled in vivo with 45Ca. Two protein kinase C-activating phorbol esters, phorbol-12-myristate-13-acetate and phorbol-12,13-dibutyrate, both stimulated 45Ca release in 120-h cultures at a concentration of 10 nmol/l. Calcitonin (30 nmol/l) inhibited phorbol esterstimulated bone resorption without any "escape from inhibition". This was in contrast to the transient inhibitory effect of calcitonin on bone resorption stimulated by parathyroid hormone (10 nmol/l), prostaglandin E2 (2 μmol/l), and bradykinin (1 μmol/l). Our results suggest that activation of protein kinase C produces a sustained inhibitory effect of calcitonin on bone resorption.

Effect of methylation of the hydroxyl group of tyrosine in [1-β-mercaptopropionic acid, 8-D-arginine]vasopressin on its biological effects

1979 ◽  
Vol 44 (5) ◽  
pp. 1642-1644 ◽  
Author(s):  
Viktor Krchňák ◽  
Milan Zaoral
Keyword(s):  
Arginine Vasopressin ◽  
Solid Phase Synthesis ◽  
Solid Phase ◽  
Biological Effects ◽  
Hydroxyl Group ◽  
Rat Uterus ◽  
Phase Synthesis ◽  
Mercaptopropionic Acid ◽  
Antidiuretic Effect

Using the method of solid-phase synthesis, S-benzyl-β-mercaptopropionyl-O-methyltyrosyl-phenylalanyl-glutaminyl-asparaginyl-S-benzylcysteinyl-prolyl-NG-p-toluenesulfonyl-D-arginyl-glycine amide (I) was prepared which after removal of the protecting groups, oxidation, and purification afforded [1-β-mercaptopropionic acid, 2-O-methyltyrosine, 8-D-arginine]vasopressin (II). II shows a low antidiuretic effect, c. 10 I.U./mg. It is without effect on rat uterus in vitro and on the blood pressure of rat in vitro.

The effects of corticotrophin-releasing hormone, arginine vasopressin and their antagonists on ACTH release from perifused horse anterior pituitary cells

1994 ◽  
Vol 143 (1) ◽  
pp. 85-93 ◽  
Author(s):  
M J Ellis ◽  
R S Mulligan ◽  
M J Evans ◽  
R A Donald
Keyword(s):  
Arginine Vasopressin ◽  
Anterior Pituitary ◽  
Dose Range ◽  
Inhibitory Effect ◽  
Pituitary Cells ◽  
Releasing Hormone ◽  
Anterior Pituitary Cells ◽  
The Individual ◽  
Acth Release

Abstract Antagonists are useful for probing hormone action and receptor characteristics. In this study we have investigated the inhibitory effects of analogues of arginine vasopressin (AVP) and corticotrophin-releasing hormone (CRH) on stimulated release of immunoreactive ACTH from perifused equine anterior pituitary cells in vitro. Our aims were to gain some insight into the characteristics of the CRH and AVP receptors of the horse pituitary and to establish whether the response induced by AVP and CRH together could be blocked by combining antagonists. Experimental design included 5-min pulses of AVP (12·5 nmol/l), CRH (0·3 nmol/l) or CRH plus AVP given every 40 min alternately with pulses of secretagogue(s) plus appropriate antagonist(s). The effect of combined antagonists on the response to lower secretagogue concentrations (CRH, 0·03 nmol/l plus AVP, 2·5 nmol/l) was also tested. Response in the presence of an antagonist was compared with the mean response to secretagogue in the immediately preceding and following pulse and was expressed as per cent expected ACTH. The ACTH response to AVP was inhibited over the dose range 0·4–50 μmol/l by Phaa-d-Tyr(Et)2Lys6Arg3VP (P<0·002; ANOVA) and by d(CH2)5[Tyr(Me)2]AVP (P<0·001). Suppression of the expected ACTH response to AVP by these two antagonists was most effectively achieved by antagonist concentrations of 10 μmol/l (to 28±2·1%) and 25 μmol/l (to 22±5·1%) respectively. Inhibition was not improved by preinfusion compared with a bolus pulse. Aaa-d-Tyr(Et)2Val4Abu6Arg8·9VP and the non-peptide antagonist OPC-21268 had no inhibitory effect. Two α-helical (α-h) analogues of CRH, (α-hCRH(12–41) and α-hCRH(9–41) tested over the dose range 0·5–5 μmol/l, suppressed CRH-induced ACTH secretion (P<0·001) but CRH(23–41) had no significant effect. The α-hCRH(12–41) achieved greater suppression of ACTH release than the (9–41) derivative (8·7±4·2% compared with 19·3±3·5% of the expected ACTH response). Combination of d(CH2)5[Tyr(Me)2]AVP (25 μmol/l) plus α-hCRH (12–41) (5·0 μmol/l) achieved suppression to −0·5±1·3% and 0·8±1·5% of the expected response to CRH+AVP at 0·3+12·5 nmol/l and 0·03+2·5 nmol/l respectively. These effects were greater than seen by the individual antagonists alone. The antagonist effects suggest that the CRH and AVP receptors of the equine pituitary have similar properties to those from other species and are consistent with the pituitary AVP receptor being unlike the V2 receptor and resembling but not being identical to the V1 type. We also conclude that α-hCRH(12–41) and d(CH2)5[Tyr(Me)2]AVP can together block the ACTH response to CRH plus AVP and suggest that these antagonists should provide a means of investigating additional secretagogues involved in ACTH release in the horse. Journal of Endocrinology (1994) 143, 85–93

Effect of Dipyridamole on Spontaneous Platelet Aggregation in Whole Blood Decreases with the Time After Venepuncture: Evidence for the Role of ADP

1987 ◽  
Vol 58 (02) ◽  
pp. 744-748 ◽  
Author(s):  
A R Saniabadi ◽  
G D O Lowe ◽  
J C Barbenel ◽  
C D Forbes
Keyword(s):  
Platelet Aggregation ◽  
Correlation Coefficient ◽  
Whole Blood ◽  
Blood Platelet ◽  
Inhibitory Effect ◽  
Time Interval ◽  
Adp Receptor ◽  
Spontaneous Platelet Aggregation

SummarySpontaneous platelet aggregation (SPA) was studied in human whole blood at 3, 5, 10, 20, 30, 40 and 60 minutes after venepuncture. Using a whole blood platelet counter, SPA was quantified by measuring the fall in single platelet count upon rollermixing aliquots of citrated blood at 37° C. The extent of SPA increased with the time after venepuncture, with a correlation coefficient of 0.819. The inhibitory effect of dipyridamole (Dipy) on SPA was studied: (a) 10 μM at each time interval; (b) 0.5-100 μM at 3 and 30 minutes and (c) 15 μM in combination with 100 μM adenosine, 8 μM 2-chloroadenosine (2ClAd, an ADP receptor blocker) and 50 μM aspirin. There was a rapid decrease in the inhibitory effect of Dipy with the time after venepuncture; the correlation coefficient was -0.533. At all the concentrations studied, Dipy was more effective at 3 minutes than at 30 minutes after venepuncture. A combination of Dipy with adenosine, 2ClAd or aspirin was a more effective inhibitor of SPA than either drug alone. However, when 15 μM Dipy and 10 μM Ad were added together, the inhibitory effect of Dipy was not increased significantly, suggesting that Dipy inhibits platelet aggregation independent of Ad. The increase in SPA with the time after venepuncture was abolished when blood was taken directly into the anticoagulant containing 5 μM 2ClAd. It is suggested that ADP released from the red blood cells is responsible for the increased platelet aggregability with the time after venepuncture and makes a serious contribution to the artifacts of in vitro platelet function studies.

In Vitro Effects of Ethanol on Rabbit Platelet Aggregation, Secretion of Granule Contents, and Cyclic AMP Levels in the Presence of Prostacyclin

1989 ◽  
Vol 61 (02) ◽  
pp. 254-258 ◽  
Author(s):  
Margaret L Rand ◽  
Peter L Gross ◽  
Donna M Jakowec ◽  
Marian A Packham ◽  
J Fraser Mustard
Keyword(s):  
Cyclic Amp ◽  
Inhibitory Effect ◽  
Rabbit Platelet ◽  
Inhibitory Effects ◽  
Low Concentrations ◽  
Rabbit Platelets ◽  
High Concentrations ◽  
In Vitro Effects ◽  
Aggregation Of Platelets

SummaryEthanol, at physiologically tolerable concentrations, inhibits platelet responses to low concentrations of collagen or thrombin, but does not inhibit responses of washed rabbit platelets stimulated with high concentrations of ADP, collagen, or thrombin. However, when platelet responses to high concentrations of collagen or thrombin had been partially inhibited by prostacyclin (PGI2), ethanol had additional inhibitory effects on aggregation and secretion. These effects were also observed with aspirin- treated platelets stimulated with thrombin. Ethanol had no further inhibitory effect on aggregation of platelets stimulated with ADP, or the combination of ADP and epinephrine. Thus, the inhibitory effects of ethanol on platelet responses in the presence of PGI2 were very similar to its inhibitory effects in the absence of PGI2, when platelets were stimulated with lower concentrations of collagen or thrombin. Ethanol did not appear to exert its inhibitory effects by increasing cyclic AMP above basal levels and the additional inhibitory effects of ethanol in the presence of PGI2 did not appear to be brought about by further increases in platelet cyclic AMP levels.

The Effect of Barbituric Acid Derivatives on Platelet Function in Vitro and in Vivo

1973 ◽  
Vol 30 (02) ◽  
pp. 315-326
Author(s):  
J. Heinz Joist ◽  
Jean-Pierre Cazenave ◽  
J. Fraser Mustard
Keyword(s):  
Platelet Aggregation ◽  
Platelet Function ◽  
Barbituric Acid ◽  
Platelet Rich Plasma ◽  
Inhibitory Effect ◽  
Primary Response ◽  
Sodium Pentobarbital ◽  
Barbituric Acid Derivatives

SummarySodium pentobarbital (SPB) and three other barbituric acid derivatives were found to inhibit platelet function in vitro. SPB had no effect on the primary response to ADP of platelets in platelet-rich plasma (PRP) or washed platelets but inhibited secondary aggregation induced by ADP in human PRP. The drug inhibited both phases of aggregation induced by epinephrine. SPB suppressed aggregation and the release reaction induced by collagen or low concentrations of thrombin, and platelet adherence to collagen-coated glass tubes. The inhibition by SPB of platelet aggregation was readily reversible and isotopically labeled SPB did not become firmly bound to platelets. No inhibitory effect on platelet aggregation induced by ADP, collagen, or thrombin could be detected in PRP obtained from rabbits after induction of SPB-anesthesia.

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