Effect of deoxycorticosterone on sodium appetite of intact and adrenalectomized rats

1965 ◽  
Vol 208 (6) ◽  
pp. 1281-1285 ◽  
Author(s):  
George Wolf
Keyword(s):  
Sodium Chloride ◽  
Low Doses ◽  
Sodium Appetite ◽  
Self Selection ◽  
Saline Preference ◽  
High Doses ◽  
Adrenalectomized Rats ◽  
Stimulation Of ◽  
Intact Rats

The effect of DOC on sodium chloride (saline) intake was studied in intact and adrenalectomized rats under "two-bottle" self-selection conditions. It was found that in adrenalectomized rats low doses of DOC produced a decrease in saline intake (restoration of sodium-retaining ability), whereas high doses produced an increase in saline intake (stimulation of sodium appetite). At high doses, however, intact rats consumed more saline and manifested a greater preference for it than did similarly treated adrenalectomized rats. Treatment with corticosterone increased both absolute saline intake and saline preference of DOC-treated adrenalectomized rats.

Renin secretion and loop of Henle chloride reabsorption in the adrenalectomized rat

1985 ◽  
Vol 249 (4) ◽  
pp. F596-F602
Author(s):  
W. J. Welch ◽  
C. E. Ott ◽  
G. P. Guthrie ◽  
T. A. Kotchen
Keyword(s):  
Sodium Chloride ◽  
Chloride Transport ◽  
Plasma Renin ◽  
Saline Infusion ◽  
Renin Release ◽  
Loop Of Henle ◽  
Water Drinking ◽  
Before And After ◽  
Adrenalectomized Rats ◽  
Stimulation Of

Renin release is increased in the adrenalectomized rat and is not inhibited by sodium chloride administration. The purpose of this study was to determine whether increased renin release is related to impaired absorptive chloride transport in the loop of Henle. Chloride transport in the loop was measured before and after acute saline infusion in three groups of rats: 1) saline-drinking adrenalectomized rats (Adx); 2) saline-drinking dexamethasone-treated adrenalectomized rats (Dex); and 3) water-drinking sham-operated controls. Unrelated to differences of arterial pressure, glomerular filtration rate, or net sodium chloride balance, chloride reabsorption in the loop of Henle of Adx [836 +/- 172 peq/min (SE)] was less (P less than 0.01) than in controls (1,646 +/- 353) and Dex (1,377 +/- 318) before saline infusion. After saline infusion, chloride delivery to the loop increased (P less than 0.05) in all three groups. However, loop chloride reabsorption increased (P less than 0.01) only in controls and Dex but not in Adx. Before saline infusion, plasma renin concentration (PRC) of Adx (350 +/- 108 U/ml) was greater (P less than 0.01) than that in controls (56 +/- 6) or Dex (108 +/- 36); sodium chloride infusion failed to inhibit PRC in Adx, whereas PRC was suppressed (P less than 0.01) by saline in Dex and controls. Thus stimulation of renin release in adrenalectomized animals was associated with decreased absorptive chloride transport in the loop of Henle. Dexamethasone normalized loop function and renin responsiveness to sodium chloride.

THE SECRETION OF ANTIDIURETIC HORMONE IN RESPONSE TO HAEMORRHAGE AND THE FATE OF VASOPRESSIN IN ADRENALECTOMIZED RATS

1954 ◽  
Vol 11 (2) ◽  
pp. 165-176 ◽  
Author(s):  
M. GINSBURG
Keyword(s):  
Body Weight ◽  
Sodium Chloride ◽  
Antidiuretic Hormone ◽  
Intravenous Injection ◽  
Posterior Pituitary ◽  
Arterial Blood ◽  
Adrenalectomized Rats ◽  
Intact Rats

SUMMARY 1. The antidiuretic potency of arterial blood from adrenalectomized rats was greater than that from intact rats, but only if 2 or more ml. of blood were taken from each rat. It is concluded that the amounts of posterior pituitary antidiuretic hormone released during haemorrhage are greater in adrenalectomized than in intact rats. 2. The effect of haemorrhage on the antidiuretic potency of blood in adrenalectomized rats treated with sodium chloride or cortisone was not different from that in intact rats. 3. The disappearance of intravenously injected vasopressin (100 mU/100 g body weight) was retarded after adrenalectomy. Up to 48 hr after adrenalectomy this was due to a reduced capacity of the kidneys to remove vasopressin from the circulation. 4. Treatment with cortisone increased the rate of disappearance of vasopressin in adrenalectomized rats, but the rate was not restored to that observed in intact animals. 5. Treatment with sodium chloride did not affect the rate at which vasopressin was removed from the circulation of adrenalectomized rats. 6. The excretion of an antidiuretic agent in the urine which followed intravenous injection of vasopressin (100 mU/100 g) 48 hr after adrenalectomy was equivalent to 2·1% of the dose. This compared with an excretion of 6·7% of the dose in intact animals.

ANTIDIURETIC ACTIVITY IN THE NEUROHYPOPHYSIS OF RATS AFTER ADRENALECTOMY AND REPLACEMENT THERAPY

1954 ◽  
Vol 10 (3) ◽  
pp. 228-237 ◽  
Author(s):  
C. CAVALLERO ◽  
EMMA DOVA ◽  
L. ROSSI
Keyword(s):  
Sodium Chloride ◽  
Antidiuretic Hormone ◽  
Urine Volume ◽  
Daily Output ◽  
Antidiuretic Activity ◽  
Hormone Content ◽  
Pars Nervosa ◽  
Daily Urine ◽  
Adrenalectomized Rats ◽  
Intact Rats

SUMMARY 1. The content of antidiuretic hormone in the neurohypophysis, the weight of the neurohypophysis and the daily output of urine were studied in the following groups of rats: intact rats which received 2 g NaCl/100 ml. as drinking fluid; adrenalectomized rats; sham-adrenalectomized rats; adrenalectomized rats injected with deoxycorticosterone acetate or aqueous adrenocortical extract, lipo-adrenal extract, cortisone or cortisone and noradrenaline; adrenalectomized rats to which sodium chloride had been administered; and adrenalectomized rats which received both sodium chloride and adrenocortical hormones. 2. The antidiuretic hormone content of the pars nervosa (per mg wet gland) of intact rats to which salt had been given was about half of that of controls without extra salt. There was no significant difference between the mean daily urine volumes of the two series. 3. In adrenalectomized and sham-adrenalectomized rats, 2 days after the operation, the hormone content of the pars nervosa was reduced. In adrenalectomized animals this decrease in antidiuretic activity persisted; in sham-operated rats the antidiuretic activity had increased 5 days after the operation and was fully restored after 7. The daily urine output of the adrenalectomized animals was about one-third of that of intact controls. 4. No significant increase in antidiuretic hormone content of the neurohypophysis occurred when adrenocortical preparations were injected into adrenalectomized rats, but the urine volume of these animals increased. 5. Salt alone, in low or high doses, both orally or subcutaneously administered, increased the amount of antidiuretic principle in the pituitaries of adrenalectomized rats, but control levels were not attained. The daily urine volume of these animals returned to normal. 6. Combined treatment of adrenalectomized rats with salt and adrenocortical extract or cortisone, but not with salt and deoxycorticosterone acetate, led to full restoration of the antidiuretic hormone content of the neurohypophysis. These treatments also produced a rise of the daily urine volume above that of intact controls. 7. In adrenalectomized rats a close relationship was found between the degree to which the various treatments raised the hormone content of the gland and that to which they increased the daily output of urine. 8. The significance of the results is discussed, and the impossibility of drawing conclusions from them about neurohypophysial function in adrenocortical deficiency is stressed.

Toll-Like Receptor Triggering Modulates Factor VIII-Specific Immune Memory in Murine Hemophilia A with Factor VIII Inhibitors.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 214-214 ◽  
Author(s):  
Peter Allacher ◽  
Christina Hausl ◽  
Rafi U. Ahmad ◽  
Hans Peter Schwarz ◽  
Peter L. Turecek ◽  
...  
Keyword(s):  
B Cells ◽  
Factor Viii ◽  
B Cell ◽  
Hemophilia A ◽  
Memory B Cells ◽  
Immune Memory ◽  
Low Doses ◽  
Specific Memory ◽  
High Doses ◽  
Stimulation Of

Abstract The development of inhibitory antibodies against factor VIII (FVIII) is the major complication in the treatment of hemophilia A patients with FVIII products. Immune Tolerance Induction (ITI) therapy using long-term application of high doses of FVIII has evolved as an effective therapy to eradicate the antibodies and induce long-lasting immune tolerance. It is a common observation that infections, particularly central venous catheter infections during ITI cause a rise in anti-FVIII antibody titers that can prolong the course of ITI or possibly even lead to failure of ITI. Based on this observation, we asked the question whether microbial components derived from viruses or bacteria modulate the re-stimulation of FVIII-specific immune memory and disturb the recently described inhibition of memory-B-cell-re-stimulation by high doses of FVIII (Hausl et al.: Blood2005; in press). Microbial components are recognized by toll-like receptors (TLRs) that serve as an important link between innate and adaptive immunity. TLRs can discriminate various microbial components such as lipopeptides derived from bacteria or zymosan derived from yeast (recognized by TLR1/2 or TLR2/6), double-stranded RNA derived from viruses (recognized by TLR3), lipopolysaccharide (LPS) derived from gram-negative bacteria (recognized by TLR4), flagellin derived from bacterial flagella (recognized by TLR5), single-stranded RNA derived from viruses (recognized by TLR7/8) or bacterial DNA containing the unmethylated CpG motif (recognized by TLR9). We analyzed the re-stimulation of FVIII-specific memory-B cells using a murine model of hemophilia A as described previously (Hausl et al.: Blood2004; 104:115–22; Hausl et al.: Blood2005, in press). The following TLR ligands were tested: zymosan for TLR2 (0.1–10,000 ng/ml), poly I:C for TLR3 (1.0–50,000 ng/ml), LPS for TLR4 (0.1–10,000 ng/ml), Flagellin for TLR5 (0.01–1,000 ng/ml), Loxoribine for TLR7 (1.0–50,000 ng/ml) and CpG oligonucleotides for TLR9 (0.1–10,000 ng/ml). Our results indicate that none of the TLR ligands at the concentrations tested induced a significant re-stimulation of FVIII-specific memory B cells in the complete absence of either FVIII or T cells. However, ligands for TLR3, TLR4, TLR7 and TLR9 were able to disturb the inhibition of memory-B-cell-re-stimulation by high doses of FVIII and amplified the re-stimulation induced by low doses of FVIII substantially. We conclude that triggering of TLRs by microbial components that are present during infections amplify the re-stimulation of FVIII-specific memory B-cells induced by low doses of FVIII and disturb the inhibition induced by high doses of FVIII.

Response of rat jejunum to angiotensin II: role of norepinephrine and prostaglandins

1981 ◽  
Vol 240 (1) ◽  
pp. G17-G24 ◽  
Author(s):  
N. R. Levens ◽  
M. J. Peach ◽  
R. M. Carey ◽  
J. A. Poat ◽  
K. A. Munday
Keyword(s):  
Angiotensin Ii ◽  
Water Absorption ◽  
Rapid Onset ◽  
Inhibitory Response ◽  
High Dose ◽  
Low Doses ◽  
Slow Decay ◽  
High Doses ◽  
Stimulation Of

At low doses, angiotensin II (AII) stimulates jejunal sodium and water absorption in the pentobarbital sodium-anesthetized rat. This response to the hormone can be blocked by cycloheximide and has a rapid onset and decay, indicating that any protein involved must have a short half-life and/or fast turnover. At high doses, AII inhibits jejunal absorption by a process that does not involve protein synthesis and has a rapid onset but slow decay. The AII-induced inhibition of water absorption can be abolished, and a net stimulation ensues after pretreatment of the animals with meclofenamate or indomethacin, suggesting that at high doses AII stimulates intestinal prostaglandin biosynthesis. The AII analogue, [Sar1,Leu8]AII, significantly stimulated jejunal water absorption and was devoid of any inhibitory response at any dose administered. Simultaneous infusion of low doses of [Sar1,Leu8]AII and AII resulted in a stimulation of water transport, while simultaneous infusion of high dose [Sar1,Leu8]AII and AII also stimulated water absorption. It is suggested that the AII analogue is a full agonist with regard to stimulation of jejunal transfer but antagonizes the inhibitory response to high doses of AII. A model consistent with these data is discussed.

Nycthemeral rhythms and sodium chloride appetite in rats

1985 ◽  
Vol 249 (3) ◽  
pp. R375-R378 ◽  
Author(s):  
N. E. Rowland ◽  
L. L. Bellush ◽  
M. J. Fregly
Keyword(s):  
Polyethylene Glycol ◽  
Sodium Chloride ◽  
Nacl Solution ◽  
Dark Cycle ◽  
Adrenalectomized Rats ◽  
Intact Rats

Adrenalectomized rats maintained on a 12:12 light-dark cycle drank large amounts of 0.3 M NaCl solution during the night. They showed virtually no NaCl appetite during the day. As a result of their high day natriuresis, the adrenalectomized rats sustained a negative Na+ balance during the day about three times that of controls. This was offset by a correspondingly higher positive Na+ balance at night. In a second experiment in intact rats, the latency to exhibit NaCl appetite during polyethylene glycol-induced hypovolemia was shorter when the treatment was administered in the evening than in the morning. This again demonstrates a relative facilitation of NaCl intake at night and suggests a major nycthemeral interaction with putative physiological stimuli of NaCl appetite.

ANALYSIS OF THE ROLE OF ENDOGENOUS PROLACTIN ON FLUID AND SODIUM CHLORIDE ABSORPTION BY THE RAT JEJUNUM

1975 ◽  
Vol 67 (3) ◽  
pp. 343-349 ◽  
Author(s):  
J. R. MAINOYA
Keyword(s):  
Sodium Chloride ◽  
Adverse Effects ◽  
Intestinal Absorption ◽  
Rat Jejunum ◽  
Chloride Absorption ◽  
Adrenalectomized Rats ◽  
Intact Rats

SUMMARY Intestinal absorption of fluid and NaCl in rats is significantly decreased after hypophysectomy and increased in rats with pituitary implants. Oestrogen and reserpine significantly stimulate mucosal fluid and NaCl transfer in both normal and adrenalectomized rats, comparable to the effects of administration of prolactin. In intact rats, ergocryptine enhanced intestinal absorption of fluid and NaCl; however, it failed to exert any effects in adrenalectomized rats. Adrenalectomy alone had no adverse effects on intestinal absorption in saline-compensated rats. The administration of corticosterone alone or together with prolactin significantly enhanced intestinal absorption, although the effect of corticosterone alone was more variable. These data strongly suggest that increased endogenous prolactin levels produce stimulatory effects on intestinal absorption of fluid and NaCl by the rat jejunum.

Stimulation of steroidogenesis by forskolin in rat adrenal zona glomerulosa cell preparations

1991 ◽  
Vol 129 (3) ◽  
pp. 391-397 ◽  
Author(s):  
S. J. Purdy ◽  
B. J. Whitehouse ◽  
D. R. E. Abayasekara
Keyword(s):  
Cyclic Amp ◽  
Adenylate Cyclase ◽  
Zona Glomerulosa ◽  
Zona Fasciculata ◽  
Low Doses ◽  
Significant Stimulation ◽  
Glomerulosa Cells ◽  
High Doses ◽  
Zona Glomerulosa Cells ◽  
Stimulation Of

ABSTRACT The actions of forskolin have been investigated to determine to what extent its effects on steroidogenesis in rat adrenal preparations are dependent on activation of adenylate cyclase. In zona glomerulosa preparations, stimulation of both aldosterone and corticosterone production was obtained at concentrations of forskolin between 1 and 10 μmol/l. The effects of 10 μmol forskolin/l were additive with those of low doses (1 pmol/l) of corticotrophin (ACTH), but not with those of high doses (1 nmol/l) of ACTH. In contrast, in zona fasciculata/reticularis cells, doses of forskolin up to 10 μmol/l produced no significant stimulation of corticosterone production either alone or in the presence of ACTH (1 pmol/l and 1 nmol/l). The response to 1 nmol ACTH/l was attenuated in the presence of forskolin (10 μmol/l) in both zona glomerulosa and zona fasciculata/reticularis cell preparations. Cyclic AMP production increased progressively with dose up to 100 μmol forskolin/l in zona glomerulosa cells, whereas corticosterone production was maximal between 10 and 30 μmol forskolin/l and decreased at 100 μmol forskolin/l. In zona fasciculata/reticularis cells, cyclic AMP production was also increased by forskolin (1 and 10 μmol/l). The stimulation of zona glomerulosa steroido-genesis by forskolin (1–10 μmol/l) and ACTH (1–100 pmol/l) were both reduced by the adenylate cyclase inhibitor, N6-phenylisopropyladenosine (100 μmol/l). The calcium channel inhibitor, nifedipine, only reduced the steroidogenic response to forskolin (3 μmol/l) at doses of 300 μmol/l whereas the response to 8·4 mmol K+/l was inhibited at 10 μmol nifedipine/1. Although there is some dissociation between the effects of forskolin on cyclic AMP and steroidogenesis, the results are generally consistent with the view that the effects of forskolin in rat zona glomerulosa cells are mainly dependent on activation of adenylate cyclase. This contrasts with the effects of forskolin in bovine fasciculata cells which are reported to be mediated by activation of voltage-regulated calcium channels. Journal of Endocrinology (1991) 129, 391–397

THE EFFECT OF ALDOSTERONE ON THE ELECTRICAL ACTIVITY OF RAT COLON

1969 ◽  
Vol 44 (3) ◽  
pp. 363-377 ◽  
Author(s):  
C. J. EDMONDS ◽  
JANE C. MARRIOTT
Keyword(s):  
Large Dose ◽  
Low Dose ◽  
Dose Range ◽  
Rat Colon ◽  
Low Doses ◽  
Continuous Intravenous Infusion ◽  
Submucosal Injection ◽  
High Doses ◽  
Conscious Animals ◽  
Adrenalectomized Rats

SUMMARY The effect of aldosterone on the colonic transmucosal potential difference (p.d.) was examined in normal, adrenalectomized and Na+ depleted rats. Continuous intravenous infusion of aldosterone in conscious animals was more effective than single i.v. injection and over the dose range 0·5–50 μg./hr. for 6 hr., p.d. increased linearly with log dose and returned to the pre-infusion levels 16–24 hr. after stopping infusion. Only a region 2–4 cm. from the anus responded to low doses, but with high doses an increasing length of colon responded. Cortisone (250 μg. daily) intramuscularly maintained adrenalectomized rats even when severely Na+ depleted without affecting the p.d. Cortisone (2·5 mg. daily, i.m.) raised the p.d. but the effect of low doses of aldosterone was unchanged. Neither Na+ depletion nor pentobarbitone anaesthesia affected the action of aldosterone but large doses of spironolactone reduced it. Aldosterone was effective when applied locally by submucosal injection in very low dose but was almost ineffective even in very large dose in the lumen. Again the most sensitive region was 2–4 cm. from the anus. Ouabain (10-3m) injected into the submucosa rapidly reduced the increased p.d. but was ineffective in the lumen.

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