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

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.

1954 ◽  
Vol 10 (3) ◽  
pp. 228-237 ◽  
Author(s):  
C. CAVALLERO ◽  
EMMA DOVA ◽  
L. ROSSI

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.


1980 ◽  
Vol 87 (1) ◽  
pp. 65-71 ◽  
Author(s):  
MASAYOSHI KUMEGAWA ◽  
NORIHIKO MAEDA ◽  
TOSHIHIKO YAJIMA ◽  
TAISHIN TAKUMA ◽  
EIKO IKEDA ◽  
...  

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.


1989 ◽  
Vol 256 (5) ◽  
pp. H1274-H1281 ◽  
Author(s):  
D. N. Darlington ◽  
K. Kaship ◽  
L. C. Keil ◽  
M. F. Dallman

To determine under resting, unstressed conditions the circulating glucocorticoid concentrations that best maintain sensitivity of the vascular smooth muscle and baroreceptor responses to vasoactive agents, rats with vascular cannulas were sham-adrenalectomized (sham) or adrenalectomized (ADRX) and provided with four levels of corticosterone replacement (approximately 100 mg fused pellets of corticosterone: cholesterol 0, 20, 40, and 80% implanted subcutaneously at the time of adrenal surgery). Changes in vascular and baroreflex responses were determined after intravenous injection of varying doses of phenylephrine and nitroglycerin with measurement of arterial blood pressure and heart rate in the conscious, chronically cannulated rats. Vascular sensitivity was decreased, and resting arterial blood pressure tended to be decreased in the adrenalectomized rats; both were restored to normal with levels of corticosterone (40%), which also maintained body weight gain, thymus weight, and plasma corticosteroid binding globulin concentrations at normal values. The baroreflex curve generated from the sham group was different from the curves generated from the ADRX+0, 20, and 40% groups, but not different from that of the ADRX+80% group, suggesting that the baroreflex is maintained by higher levels of corticosterone than are necessary for the maintenance of the other variables. These data demonstrate that physiological levels of corticosterone (40% pellet) restore vascular responsiveness, body weight, thymus weight, and transcortin levels to normal in ADRX rats, whereas higher levels (80% pellet) are necessary for restoration of the baroreflex.


1968 ◽  
Vol 42 (2) ◽  
pp. 253-260 ◽  
Author(s):  
C. W. OGLE ◽  
MARY F. LOCKETT

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.


1965 ◽  
Vol 208 (6) ◽  
pp. 1281-1285 ◽  
Author(s):  
George Wolf

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.


1960 ◽  
Vol 199 (2) ◽  
pp. 221-225 ◽  
Author(s):  
Kathryn Ballard ◽  
Allan Lefer ◽  
George Sayers

Heart-lungs from intact rats were perfused with blood from intact rats (intact-intact preparations) or with blood from adrenalectomized rats (intact-adrenalectomized preparations). Left ventricular work index (LVWI) was employed to evaluate performance of the heart-lung and calculated as the product of cardiac output and mean arterial blood pressure. In confirmation of a previous report from this laboratory, LVWI was less for intact-adrenalectomized preparations than for intact-intact preparations. Aldosterone, added to perfusion blood from adrenalectomized rats to make a concentration of 2 x 10–3, 8 x 10–3 or 3.2 x 10–2 µg/100 ml, increased LVWI of the intact-adrenalectomized preparation to that of the intact-intact preparation. Extracts of plasma from intact rats, which may be expected to contain corticosteroids, were also capable of increasing LVWI of the intact-adrenalectomized preparation. Extracts of plasma from adrenalectomized rats were inactive.


1965 ◽  
Vol 43 (2) ◽  
pp. 269-278 ◽  
Author(s):  
John Hunter ◽  
R. E. Haist

The removal of the posterior part of the pituitary gland in the rat leads to an elevation in blood pressure. The production of an anterior–posterior pituitary imbalance in hypophysectomized animals by the administration of certain hormones of target glands influenced by the anterior pituitary (thyroxine, testosterone, cortisone (TTC)) also produces an increase in mean arterial blood pressure. In the intact animal, too, the administration of the hormones of the target organs (TTC) will lead to an elevation of blood pressure, and 1 week after the cessation of this treatment the blood pressure is as high or higher than at the end of the administration period. Administration of anterior pituitary hormones TSH, LH, and ACTH both in hypophysectomized and in intact rats also produced elevations in blood pressure. In two female dogs, administration of pituitary target-organ hormones (TTC) consistently produced an elevation of blood pressure associated with a direct effect of the injected hormones, followed by a depression of blood pressure below previous resting values after hormone withdrawal, presumably because of an associated inhibition of anterior pituitary effects. When certain hormones of the posterior pituitary gland are administered along with TTC, in both hypophysectomized and intact rats, the blood pressure elevation is not as great as with TTC alone, though, by themselves, the posterior pituitary factors caused some elevation in blood pressure. It is concluded that an imbalance between the influences of the anterior and posterior parts of the pituitary gland can lead to a significant elevation in blood pressure. It seems likely that, depending on the dose, the effects observed after the injection of the agent is discontinued may be due to persistence of the action of the agent or, in some instances, to inhibition of the activity of part of the pituitary gland.


1995 ◽  
Vol 82 (6) ◽  
pp. 1396-1405. ◽  
Author(s):  
Maieli Kasner ◽  
Jochen Grosse ◽  
Martin Krebs ◽  
Gabriele Kaczmarczyk

Background Anesthetic agents influence central regulations. This study investigated the effects of methohexital anesthesia on renal and hormonal responses to acute sodium and water loading in dogs in the absence of surgical stress. Methods Fourteen experiments (two in each dog) were performed in seven well-trained, chronically tracheotomized beagle dogs kept in highly standardized environmental and dietary conditions (2.5 mmol sodium and 91 ml water/kg body weight daily). Experiments lasted 3 h, while the dogs were conscious (7 experiments) or, after 1 h control, while they were anesthetized (7 experiments) with methohexital (initial dose 6.6 mg/kg body weight and maintenance infusion 0.34 mg.min-1.kg-1 body weight) over a period of 2 h. In both experiments, extracellular volume expansion was performed by intravenous infusion of a balanced isoosmolar electrolyte solution (0.5 ml.min-1.kg-1 body weight). Normal arterial blood gases were maintained by controlled mechanical ventilation. In another five dogs the same protocol was used, and vasopressin (0.05 mU.min-1.kg-1 body weight) was infused intravenously during methohexital anesthesia. Results Values are given as means. During methohexital anesthesia, mean arterial pressure decreased from 108 to 101 mmHg, and heart rate increased from 95 to 146 beats/min. Renal sodium excretion decreased; urine volume increased; and urine osmolarity decreased from 233 to 155 mosm/l, whereas plasma osmolarity increased from 301 to 312 mosm/l because of an increase in plasma sodium concentration from 148 to 154 mmol/l. Plasma renin activity, plasma aldosterone concentration, plasma atrial natriuretic peptide, and plasma antidiuretic hormone concentrations (range 1.8-2.8 pg/ml) did not change in either protocol. In the presence of exogenous vasopressin (antidiuretic hormone 3.3 pg/ml), water diuresis did not occur, and neither plasma osmolarity nor the plasma concentration of sodium changed. Conclusions Methohexital may impair osmoregulation by inhibiting adequate pituitary antidiuretic hormone release in response to an osmotic challenge.


1985 ◽  
Vol 249 (3) ◽  
pp. R375-R378 ◽  
Author(s):  
N. E. Rowland ◽  
L. L. Bellush ◽  
M. J. Fregly

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.


1975 ◽  
Vol 67 (3) ◽  
pp. 343-349 ◽  
Author(s):  
J. R. MAINOYA

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.


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