Perfusion of the Isolated Adrenals <i>in Situ</i>

Hilton, James G.; Weaver, Davis C.; Muelheims, Gerhard H.; Glaviano, Vincent V.; Wégria, René

doi:10.1152/ajplegacy.1958.192.3.525

Cited by 38 publications

(12 citation statements)

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“…The secretion rates of cortisol found immediately after beginning perfusion are in agreement with those found in anaesthetized dogs and in the perfused adrenal preparations of Hilton, Weaver, Muelheims, Glaviano & Wegria (1958). Since this initial rate was not exceeded even after large doses of ACTH, it may represent the maximal secretion rate.…”

Section: The Adrenal Blood Flowsupporting

confidence: 87%

The effect of adrenocorticotrophic hormone on the secretion of corticosteroids by the isolated perfused adrenal gland of the dog

Greenway¹,

Verney²

1962

The Journal of Physiology

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Section: The Adrenal Blood Flowsupporting

confidence: 87%

The effect of adrenocorticotrophic hormone on the secretion of corticosteroids by the isolated perfused adrenal gland of the dog

Greenway¹,

Verney²

1962

The Journal of Physiology

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“…Cross-circulation of blood from normal dogs provided a control on the effect of cross-circulation per se. The recipient's adrenals were isolated in situ with segments of aorta and inferior vena cava by the procedure of Hilton and co-workers (3). Care was taken to include in the arterial circulation to the lower pole of the right adrenal gland a small artery arising from the aorta.…”

Section: Methodsmentioning

confidence: 99%

Evidence That a Humoral Agent Stimulates the Adrenal Cortex to Secrete Aldosterone in Experimental Secondary Hyperaldosteronism *

Yankopoulos¹,

Davis²,

Kliman³

et al. 1959

J. Clin. Invest.

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The mechanisms which effect alterations in the secretion of aldosterone by the adrenal cortex may be nervous, humoral or both. The present study was undertaken to examine the possibility that a humoral agent stimulates the adrenal cortex to secrete aldosterone in dogs with experimental secondary hyperaldosteronism produced by constriction of the thoracic inferior vena cava. These animals secrete large amounts of aldosterone (1) and show almost complete retention of Na (2). To test the hypothesis of a humoral mechanism, the effect on aldosterone secretion was studied in normal recipient animals or in the isolated adrenals of normal dogs during cross-circulation of blood from dogs with constriction of the thoracic inferior vena cava. Corticosterone secretion was also measured to evaluate the possible role of adrenocorticotropic hormone (ACTH) in the aldosterone regulatory system. METHODSThe basic plan of the experiments consisted of crosscirculation of blood from a donor into a recipient animal or into the isolated adrenal glands of a recipient animal. Secondary hyperaldosteronism was produced in the donor animals by either acute or chronic constriction of the thoracic inferior vena cava. Acute caval constriction was performed on normal dogs. In the chronic donor dogs, ascites had been present for one to three weeks, and Na excretion on the day before the experiment was less than 4 mEq. per day; Na and K intakes were 60 and 18 mEq. per day, respectively. Also, aldosterone secretion from the right adrenal gland was measured in a group of eight dogs with chronic thoracic inferior vena cava constriction to determine the magnitude and consistency of hypersecretion. All animals were mongrel dogs which weighed 15 to 20 Kg. Nembutal® anesthesia was used.Each dog received 15,000 I.U. of heparin before collection of adrenal vein blood and before cross-circulation. * A preliminary report was given at the Laurentian Hormone Conference, September, 1958. After control determinations in both animals, the thoracic inferior vena cava was constricted in one of the dogs which became the donor. In the two other experiments of this group, dogs with chronic thoracic caval constriction were the donor animals. Under these circumstances, control observations were made in both the chronic donor and the normal recipient before crosscirculation was established.In the second group of experiments (15 pairs of dogs), blood was circulated from a donor animal with chronic thoracic caval constriction and ascites or from a normal dog into the isolated adrenals of a normal recipient animal (Figure 1). Cross-circulation of blood from normal dogs provided a control on the effect of cross-circulation per se. The recipient's adrenals were isolated in situ with segments of aorta and inferior vena cava by the procedure of Hilton and co-workers (3). Care was taken to include in the arterial circulation to the lower pole of the right adrenal gland a small artery arising from the aorta. Polyethylene tubing was used for all connections. During the control an...

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“…The pituitary gland was removed by a dental drill through a transsphenoidal approach at the beginning of the operation. The adrenal glands were then prepared for perfusion by a technique previously described by Hilton et al (22). In this procedure the circulation of the glands is completely isolated on the arterial and venous sides.…”

mentioning

confidence: 99%

Beta endorphin selectively stimulates aldosterone secretion in hypophysectomized, nephrectomized dogs.

Güllner¹,

Gill²

1983

J. Clin. Invest.

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A B S T R A C T We examined the effects of synthetic human /-endorphin (BEND) and a stable methionine (Met)-enkephalin analogue on aldosterone and cortisol secretion rates in anesthetized, hypophysectomized, and nephrectomized dogs and compared them to those of (1-39) ACTH. The circulation of the adrenal glands was completely isolated on the arterial and venous sides (Hilton Pouch). The peptides were infused to deliver 3 pmol/min into the aortic "pouch." Blood was collected from the vena caval pouch, which received blood only from the adrenal gland. Secretion rates of aldosterone and cortisol were calculated as the product of adrenal blood flow and venous steroid concentration. Duplicate steroid measurements were obtained during a control period, at 10, 30, and 50 min of peptide infusion and during a postcontrol period. BEND increased aldosterone secretion rate from 2.4±0.5 ng/ min (mean±SEM) to 3.2±0.9 ng/min at 10 min (N.S.), 8.2±2.5 ng/min (P < 0.05) at 30 min and 11.0±3.7 ng/ min (P < 0.05) at 50 min of infusion. Cortisol secretion rate was not affected by infusion of SEND. Infusion of the stable Met-enkephalin analogue D-alanine2; Metphenylalanine4, Met(O)-enkephalin-ol or saline alone had no effect on aldosterone or cortisol secretion rates. ACTH infusion increased mean aldosterone secretion rate by -215% and significantly stimulated cortisol secretion rate. These results indicate that BEND selectively stimulates aldosterone secretion with a potency similar to that of an equimolar dose of ACTH. INTRODUCTION There is considerable indirect evidence suggesting that an unidentified pituitary factor other than ACTH

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Perfusion of the Isolated Adrenals in Situ

Cited by 38 publications

References 0 publications

The effect of adrenocorticotrophic hormone on the secretion of corticosteroids by the isolated perfused adrenal gland of the dog

The effect of adrenocorticotrophic hormone on the secretion of corticosteroids by the isolated perfused adrenal gland of the dog

Evidence That a Humoral Agent Stimulates the Adrenal Cortex to Secrete Aldosterone in Experimental Secondary Hyperaldosteronism *

Beta endorphin selectively stimulates aldosterone secretion in hypophysectomized, nephrectomized dogs.

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