THE URINARY CHANGES INDUCED IN RATS BY HIGH PITCHED SOUND (20 KCYC./SEC.)

1968 ◽  
Vol 42 (2) ◽  
pp. 253-260 ◽  
Author(s):  
C. W. OGLE ◽  
MARY F. LOCKETT
Keyword(s):  
Urinary Excretion ◽  
Antidiuretic Hormone ◽  
Adrenal Medulla ◽  
Urinary Output ◽  
Renal Response ◽  
Adrenalectomized Rats ◽  
Intact Rats

SUMMARY Repeated exposures of intact rats, neurohypophysectomized rats and rats with denervated kidneys to high-pitched sound (20 kcyc./sec.) for 2 sec. with an intensity of 98–100 decibels caused diuresis, natriuresis and kaluresis: the rate of urinary excretion of adrenaline rose very significantly. Adrenal demedullation abolished the natriuresis and kaluresis in response to 20 kcyc./sec. and converted the diuresis to an antidiuresis. The renal response of normal rats to 20 kcyc./sec. was therefore attributed to the release of adrenaline from the adrenal medulla in amounts sufficient to prevent an emotional release of antidiuretic hormone from the neurohypophysis. Since 20 kcyc./sec. caused a significant increase in the urinary output of vasopressin by adrenalectomized rats, an emotional release of vasopressin is assumed to have proceeded, uninhibited, in adrenal-de-medullated rats exposed to 20 kcyc./sec., and to have caused the observed antidiuresis. The diuresis, natriuresis and kaluresis caused by 150 cyc./sec. mimicked by s.c. injection of 4 m-u. oxytocin, was unaffected by demedullation of the adrenals and was not accompanied by increase in urinary adrenaline.

Alteration of Renal Response to Carbonic Anhydrase Inhibitor by Synthetic Adrenal Steroids

1958 ◽  
Vol 195 (1) ◽  
pp. 142-146 ◽  
Author(s):  
Joseph H. Perlmutt ◽  
Donald A. Olewine
Keyword(s):  
Carbonic Anhydrase ◽  
Urine Volume ◽  
Significant Rise ◽  
Carbonic Anhydrase Inhibitor ◽  
Adrenal Steroids ◽  
Renal Response ◽  
Significant Change ◽  
Adrenalectomized Rats ◽  
Intact Rats

The increased urinary Na+ output induced by Diamox in water-loaded adrenalectomized rats was partially antagonized by the mineralocorticoid, desoxycorticosterone glucoside (DCG), the increased K+ excretion was augmented and urine volume was not affected. Intact rats subjected to the same treatment showed only a small, but significant, rise in K+ excretion. Under the same conditions, the glucocorticoid, hydrocortisone hemisuccinate (compound FH), significantly elevated Na+, K+ and H2O excretion in adrenalectomized rats receiving Diamox; intact rats showed an increase in Na+ and H2O excretion with no significant change in K+ output. Of particular interest is the finding that 2.5 mg compound FH alone increased H2O excretion in adrenalectomized rats to a slightly greater extent than Diamox alone with considerably less Na+ loss.

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.

Hormonal factors influencing postirradiation creatinuria and polyuria in the rat

1959 ◽  
Vol 196 (6) ◽  
pp. 1352-1355 ◽  
Author(s):  
G. M. Krise ◽  
C. M. Williams
Keyword(s):  
Gamma Radiation ◽  
Urinary Excretion ◽  
Antidiuretic Hormone ◽  
Intramuscular Injection ◽  
Whole Body ◽  
Albino Rats ◽  
Hormonal Factors ◽  
Factors Influencing ◽  
Adrenalectomized Rats

Normal albino rats exposed to 1500 r of whole-body Co60 gamma radiation were found to have a significant increase in urinary creatine excretion for the first 3 postirradiation days. Adrenalectomized rats, irradiated at 8 days postoperatively, did not show a creatinuria significantly greater than nonirradiated controls. Thyroparathyroidectomized rats, irradiated at 8 days postoperatively, did not have a significant increase in urinary creatine excretion over that of nonirradiated fasted controls. There were no significant increases in polyuria or polydipsia on the 1st postirradiation day in either the adrenalectomized or thyroparathyroidectomized rats. The intramuscular injection of 500 mu of the antidiuretic hormone vasopressin (Pitressin tannate) in oil inhibited postirradiation polydipsia and polyuria in normal rats but significantly increased the urinary excretion of creatine over that of irradiated noninjected controls.

Specific alterations in sodium chloride intake after hypothalamic lesions in the rat

1963 ◽  
Vol 205 (5) ◽  
pp. 922-926 ◽  
Author(s):  
Miguel R. Covian ◽  
José Antunes-Rodrigues
Keyword(s):  
Sodium Chloride ◽  
Urinary Excretion ◽  
The Other ◽  
Urinary Output ◽  
Water Ingestion ◽  
Hypothalamic Lesions ◽  
Paraventricular Nuclei ◽  
Electrolytic Lesions ◽  
Specific Increase ◽  
Sodium Chloride Intake

Bilateral electrolytic lesions in the hypothalamus of the rat elicited either a decrease or increase in 2% NaCl intake, without a significant change in water ingestion. Lesions placed in the anterior hypothalamus involving supraoptic or paraventricular nuclei, or both, resulted in a conspicuous fall (as much as 93%) of NaCl intake. The decreased consumption remained to the end of the experiments which in some rats lasted 105 days and was accompanied by a decrease in NaCl urinary output. On the contrary, lesions placed in the central hypothalamus determined a specific increase of NaCl intake together with an augmented urinary excretion. The increased ingestion was permanent and lasted to the end of the experiment, attaining in one rat the value of 290%. To account for these results two provisional explanations are advanced, one of them considering the possibility of the existence of two areas of opposite effects regarding NaCl ingestion and the other claiming a neurohumoral mechanism in which oxytocin and aldosterone could be the two responsible hormones.

Role of the Splanchnic Nerve and the Adrenal Medulla in the Genesis of ‘Preoptic Pulmonary Edema’

1956 ◽  
Vol 184 (2) ◽  
pp. 351-355 ◽  
Author(s):  
Frederick W. Maire ◽  
Harry D. Patton
Keyword(s):  
Body Weight ◽  
Protective Effect ◽  
Pulmonary Edema ◽  
Adrenal Medulla ◽  
Adrenal Glands ◽  
Splanchnic Nerve ◽  
Lung Edema ◽  
Splanchnic Nerves ◽  
Intact Rats

The pulmonary edema which follows preoptic lesions in rats is prevented by antecedent bilateral section of the splanchnic nerves. Intravenous epinephrine in doses exceeding 0.0125 mg/100 gm body weight causes fatal lung edema in rats comparable to that produced by preoptic lesions. Moreover, extracted pressor amines from rat adrenal glands cause lung edema, often fatal, when injected into the donor or into intact rats. However, adrenal demedullation does not prevent lung edema following preoptic lesions. Hence the protective effect of splanchnectomy against preoptic lesions is not wholly due to adrenal denervation. It is tentatively suggested that preoptic lung edema results from overloading of the pulmonary circuit owing to splanchnic mediated constriction of visceral venous reservoirs. Liver and spleen weights of animals dying from preoptic lung edema were significantly less than normal.

Renal Response to Carbonic Anhydrase Inhibitor in Water-Loaded Intact and Adrenalectomized Rats

1958 ◽  
Vol 192 (3) ◽  
pp. 592-596 ◽  
Author(s):  
Donald A. Olewine ◽  
Joseph H. Perlmutt
Keyword(s):  
Carbonic Anhydrase ◽  
Carbonic Anhydrase Inhibitor ◽  
Water Intoxication ◽  
Exchange Mechanism ◽  
Male Rats ◽  
Water Reabsorption ◽  
Intact Group ◽  
Renal Response ◽  
The Absolute ◽  
Adrenalectomized Rats

Renal excretions of water, Na+ and K+ were determined over a 5-hour period in sham-operated and adrenalectomized male rats injected intraperitoneally with water (5% body wt.) at postoperative intervals of 3, 14, 21 and 28 days. Intact animals maintained fairly constant outputs. In the adrenalectomized group: decreased excretion of water was apparent by 3 days, but was not maximal until after this interval; Na+ excretion increased after 14 days and rose progressively; and K+ excretion was maximally depressed by 3 days. Diamox (25 mg/100 gm body wt.) increased these values in both groups. The absolute increases in water and K+ excretion for the adrenalectomized animals were less than those for the intact animals, while Na+ excretion exceeded that of the intact group at the 14-day and subsequent intervals. These data indicate that the diuretic does not completely overcome the increased water reabsorption occurring after adrenalectomy and that the Na+—K+ exchange mechanism operates at a reduced capacity. Diamox was ineffective in protecting adrenalectomized rats against water intoxication.

Effects of thyroid hormones on urinary and renal kallikreins

1992 ◽  
Vol 263 (3) ◽  
pp. E430-E434
Author(s):  
S. Avigdor ◽  
F. Alhenc-Gelas ◽  
J. Bouhnik
Keyword(s):  
Thyroid Hormones ◽  
Urinary Excretion ◽  
Plasma Aldosterone ◽  
Urinary Kallikrein ◽  
Single Measurement ◽  
Kidney Weight ◽  
Plasma Aldosterone Concentration ◽  
Renal Kallikrein ◽  
Enzyme Changes ◽  
Intact Rats

The effects of thyroid hormones on the urinary excretion of kallikrein and on renal kallikrein were studied in rats. Total and active urinary kallikrein was decreased after thyroidectomy, but renal kallikrein content remained unchanged. Diuresis increased, and kidney weight and plasma aldosterone concentration decreased. Treatment with 3,5,3'-triiodo-L-thyronine restored the urinary kallikrein in thyroidectomized rats to normal and increased it in intact rats. It also produced increases in kidney weight and plasma aldosterone and a decrease in diuresis. The effect of thyroid hormones on the urinary kallikrein response to mineralocorticoids was also tested. Deoxycorticosterone acetate increased urinary kallikrein more in normal than in thyroidectomized rats. These results suggest that thyroidectomy decreases renal kallikrein synthesis and lowers the turnover rate of the enzyme, changes not detectable by a single measurement of the renal kallikrein content but reflected by an alteration in the urinary excretion of the enzyme. Thyroid hormones participate in the control of urinary kallikrein. This effect, however, is probably indirect and may be mediated by mineralocorticoids since thyroid function affects both the plasma level of aldosterone, which is known to influence renal kallikrein, and the kallikrein response to exogenous mineralocorticoids.

l-THYROXINE, CORTISOL AND DIET AFFECT THE LEVEL OF AMYLASE IN THE PAROTID GLAND OF DEVELOPING RATS

1980 ◽  
Vol 87 (1) ◽  
pp. 65-71 ◽  
Author(s):  
MASAYOSHI KUMEGAWA ◽  
NORIHIKO MAEDA ◽  
TOSHIHIKO YAJIMA ◽  
TAISHIN TAKUMA ◽  
EIKO IKEDA ◽  
...  
Keyword(s):  
Body Weight ◽  
Enzyme Activity ◽  
Parotid Gland ◽  
Amylase Activity ◽  
Synergistic Effects ◽  
Dietary Factors ◽  
Adult Rats ◽  
Early Increase ◽  
Adrenalectomized Rats ◽  
Intact Rats

The effects of cortisol (10 μg/g body weight) and l-thyroxine (T4; 0·2 μg/g body weight) on the activity of parotid gland amylase in young rats were investigated. Administration of cortisol or T4 for 5 consecutive days from day 5 after birth caused the precocious appearance of amylase, T4 having almost twice the effect of cortisol. Cortisol and T4 did not have synergistic effects. In thyroidectomized-adrenalectomized rats, T4 increased amylase activity but cortisol did not. The increase in enzyme activity after day 20 was much less in rats thyroidectomized on day 10 than in rats adrenalectomized on day 10. These results suggest that T4 has a direct effect on the early increase of amylase activity (days 15–25) and that the action of glucocorticoid requires the presence of endogenous thyroid hormones. The hormone-induced level of amylase in intact rats was less than that of normal adult rats. Forced weaning of intact rats resulted in a further increase in amylase activity, suggesting that further amylase accumulation (after day 25) may be due to dietary factors.

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