Adrenocortical metabolism of angiotensin in sheep with adrenal transplants.

Conscious trained sheep with adrenal gland autotransplants in cervical skin loops were used to study adrenocortical metabolism and clearance of angiotensin (AII) administered by constant systemic infusion. For comparative purposes similar experiments were undertaken in five control sheep with skin loops but no cervical adrenal tissue. During AII infusions (0.33 microgram/min for 30 min), loop venous-arterial AII ratios (0.42--0.62 were similar in both groups of sheep. Measured AII clearances across the skin loop in sheep with and without adrenal transplants were 400--600 and 100--150 pg/min, respectively, which correlated with blood flow (r = 0.79), but showed no relation to aldosterone secretion rate. Analysis of AII immunoreactive fragments showed similar proportions of octa-, hepta-, and hexapeptide fractions (64, 26, and 5%, respectively) in adrenal arterial, adrenal venous, and systemic venous plasma. These studies do not support selective heptapeptide uptake or metabolism by adrenal tissue in vivo and indicate that specific adrenal binding of AII is likely to be less than 400 pg/min at arterial AII concentrations approximating 120 pg/ml.

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IN VITRO AND IN VIVO EFFECT OF GROWTH HORMONE ON ALDOSTERONE SECRETION

Canadian Journal of Biochemistry and Physiology ◽

10.1139/y60-133 ◽

1960 ◽

Vol 38 (1) ◽

pp. 1069-1075

Author(s):

O. J. Lucis ◽

E. H. Venning

Keyword(s):

Growth Hormone ◽

Adrenal Gland ◽

Human Growth Hormone ◽

Human Growth ◽

Secretion Rate ◽

Aldosterone Secretion ◽

Hypophysectomized Rats

Porcine, monkey, and human growth hormone have no effect on the in vitro secretion of aldosterone by the rat adrenal gland. When monkey growth hormone is injected into hypophysectomized rats, the adrenals of these animals secrete, under in vitro conditions, increased amounts of aldosterone with no change in the secretion rate of corticosterone. The plasma of these rats contains a substance which appears to stimulate the secretion of aldosterone in the adrenals of normal rats.

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Local inhibition of nitric oxide temporarily stimulates aldosterone secretion in conscious sheep in vivo

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.2001.280.4.e584 ◽

2001 ◽

Vol 280 (4) ◽

pp. E584-E590 ◽

Cited By ~ 3

Author(s):

Renato Salemi ◽

John G. McDougall ◽

Kenneth J. Hardy ◽

E. Marelyn Wintour

Keyword(s):

Nitric Oxide ◽

Blood Flow ◽

Secretion Rate ◽

Aldosterone Secretion ◽

Local Inhibition ◽

Negative Effect ◽

Endogenous Nitric Oxide ◽

Conscious Sheep ◽

Time Point

The effect of localized blockage of endogenous nitric oxide (NO) on basal aldosterone secretion was studied in conscious sheep with autotransplanted adrenal glands. We have shown that infusion of the NO synthase (NOS) inhibitor N G-nitro-l-arginine methyl ester (l-NAME; 130 μg/l blood flow) significantly stimulated basal aldosterone secretion rate (ASR). This stimulatory effect was seen up to 4 h of infusion. Beyond this time point, however, the elevated ASR level was not sustained, and it was seen to drop markedly to lower than control values at 5 h. l-NAME had no effect on cortisol secretion rate (FSR) during the first 4 h of infusion, but a significant reduction in FSR was seen by the 8-h time point. Adrenal blood flow was consistently decreased in association with long l-NAME infusion. Additionally, l-NAME was shown to have no effect on aldosterone secretion when infused systemically. We conclude that the relationship between NO and aldosterone secretion is an inhibitory one, in which NO seems to have a negative effect on basal aldosterone secretion.

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IN VITRO AND IN VIVO EFFECT OF GROWTH HORMONE ON ALDOSTERONE SECRETION

Canadian Journal of Biochemistry and Physiology ◽

10.1139/o60-133 ◽

1960 ◽

Vol 38 (10) ◽

pp. 1069-1075 ◽

Cited By ~ 7

Author(s):

O. J. Lucis ◽

E. H. Venning

Keyword(s):

Growth Hormone ◽

Adrenal Gland ◽

Human Growth Hormone ◽

Human Growth ◽

Secretion Rate ◽

Aldosterone Secretion ◽

Hypophysectomized Rats

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DECREASED ALDOSTERONE PRODUCTION BY RAT ADRENAL TISSUE IN VITRO DUE TO TREATMENT WITH 9α-FLUOROCORTISOL, DEXAMETHASONE AND ADRENOCORTICOTROPHIN IN VIVO

Acta Endocrinologica ◽

10.1530/acta.0.0630001 ◽

1970 ◽

Vol 63 (1) ◽

pp. 1-10 ◽

Cited By ~ 12

Author(s):

Jürg Müller

Keyword(s):

Sodium Intake ◽

Sodium Balance ◽

Potassium Ions ◽

Aldosterone Secretion ◽

Deficient Diet ◽

Adrenal Tissue ◽

Aldosterone Production ◽

Unknown Control

ABSTRACT Quartered adrenal glands of rats treated with 9α-fluorocortisol, dexamethasone or adrenocorticotrophin (ACTH) for two weeks were found to produce 70–90% less aldosterone in vitro than the adrenal tissue of untreated animals. The same fractional decreases in aldosterone production were observed when the adrenal tissue was incubated under basal conditions or was stimulated by serotonin, potassium ions or ACTH. In rats kept on a sodium-deficient diet, treatment with dexamethasone and ACTH, respectively, impaired aldosterone production to the same extent as in rats on a normal sodium intake, whereas treatment with 9α-fluorocortisol was almost completely ineffective. These results indicate that inhibition of aldosterone secretion by an exogenous mineralocorticosteroid is mediated by changes in sodium balance. On the other hand, high levels of exogenous or endogenous glucocorticosteroids apparently decrease aldosterone production by a yet unknown control mechanism which is independent of sodium intake.

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Renal 131I-hippurate clearance overestimates true renal blood flow in the instrumented conscious dog

AJP Renal Physiology ◽

10.1152/ajprenal.1996.271.2.f269 ◽

1996 ◽

Vol 271 (2) ◽

pp. F269-F274 ◽

Cited By ~ 1

Author(s):

C. A. Visscher ◽

D. De Zeeuw ◽

G. Navis ◽

A. K. Van Zanten ◽

P. E. De Jong ◽

...

Keyword(s):

Blood Flow ◽

Renal Blood Flow ◽

Artery Blood Flow ◽

Venous Outflow ◽

Flow Probe ◽

The Difference ◽

Probe Calibration ◽

Clearance Technique ◽

Venous Plasma

We evaluated renal 131I-hippurate clearance (ERPFhip) as a measure of renal blood flow (RBF) in chronically instrumented conscious dogs. When adjusted for renal hippurate extraction (Ehip, 0.77 +/- 0.01) and hematocrit (Hct, 39.7 +/- 1%), calculated RBFhip (656 +/- 37 ml/min) markedly exceeded renal blood flow measured with renal artery blood flow probes (RBFprobe, 433 +/- 27 ml/min). The discrepancy could not be explained by flow probe calibration, because in vivo comparison of flow probe values with renal venous outflow showed only a slight underestimation of renal blood flow (slope 0.93, 95% confidence interval 0.89-0.97). Redistribution of hippurate from erythrocytes into renal venous plasma during or shortly after blood sampling led to an underestimation of Ehip by 4 +/- 1% and thus could only explain a small part of the difference. Extrarenal hippurate clearance was excluded, because the amount of 131I-hippurate cleared from plasma equaled that appearing in the urine (303 +/- 17 and 307 +/- 17 ml/min). Applying these corrections, we found that RBFhip still exceeded RBFprobe by 37 +/- 3%. These data indicate that renal blood flow measured by the hippurate clearance technique markedly overestimates true renal blood flow. Because other errors were excluded, a combination of sampling of nonrenal blood and intrarenal hippurate extraction from erythrocytes might play a role.

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Effect of adrenomedullin infusion on basal and stimulated aldosterone secretion in conscious sheep with cervical adrenal autotransplants

Journal of Endocrinology ◽

10.1677/joe.0.1660389 ◽

2000 ◽

Vol 166 (2) ◽

pp. 389-399 ◽

Cited By ~ 10

Author(s):

R Salemi ◽

JG McDougall ◽

KJ Hardy ◽

EM Wintour

Keyword(s):

Adrenal Gland ◽

Zona Glomerulosa ◽

Cortisol Secretion ◽

Aldosterone Secretion ◽

Stimulation Experiments ◽

Gland Function ◽

Conscious Sheep ◽

Stimulation Of

In vivo and in vitro studies have shown conflicting effects of adrenomedullin (ADM) on the secretion of steroid hormones from the adrenal gland. While some investigators report no effect of this peptide on the output of various hormones, others have reported both stimulatory and inhibitory roles for ADM. We have shown that basal aldosterone secretion rate (ASR), in conscious sheep with cervical adrenal autotransplants, did not change when ADM was infused directly into the adrenal arterial supply. While not affecting basal ASR, ADM did produce pronounced increases in adrenal blood flow (BF). This elevation of BF in association with ADM infusion was seen in all subsequent experiments. When aldosterone output was acutely stimulated by angiotensin II (AngII), potassium chloride (KCl) and adrenocorticotrophic hormone (ACTH), ADM was seen to drastically reduce the secretion of aldosterone with all agonists studied. After pre-exposure to ADM, all three agonists increased ASR but the magnitude of the responses were somewhat blunted. ADM did not have the same effect on cortisol secretion stimulated by ACTH, suggesting that the ability of this peptide to influence adrenal gland function is limited to the zona glomerulosa. In conditions of chronic elevation of aldosterone levels, such as in Na deficiency, ADM did not display the same inhibitory abilities seen in the acute stimulation experiments. Hence, ADM has been shown to have a direct, inhibitory role on the acute stimulation of aldosterone by AngII, KCl and ACTH while not affecting basal or chronic aldosterone secretion or cortisol secretion stimulated by ACTH.

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In vivo and in vitro evidence for the production of inhibin-like immunoreactivity in human adrenocortical adenomas and normal adrenal glands: relatively high secretion from adenomas manifesting Cushing's syndrome

Acta Endocrinologica ◽

10.1530/eje.0.1320292 ◽

1995 ◽

Vol 132 (3) ◽

pp. 292-299 ◽

Cited By ~ 23

Author(s):

Yoshihiro Nishi ◽

Masafumi Haji ◽

Ryoichi Takayanagi ◽

Toshihiko Yanase ◽

Shoichiro Ikuyama ◽

...

Keyword(s):

Adrenal Gland ◽

Cushing’S Syndrome ◽

General Circulation ◽

Adrenal Glands ◽

Cushing's Syndrome ◽

Secretion Rate ◽

Pathological Conditions ◽

Adrenocortical Adenomas

Nishi Y, Haji M, Takayanagi R, Yanase T, Ikuyama S, Nawata H. In vivo and in vitro evidence for the production of inhibin-like immunoreactivity in human adrenocortical adenomas and normal adrenal glands: relatively high secretion from adenomas manifesting Cushing's syndrome. Eur J Endocrinol 1995;132:292–9. ISSN 0804–4643 To clarify whether adrenal gland secretes inhibin in vivo in physiological or pathological conditions, we measured the levels of inhibin-like immunoreactivity (inhibin-LI) in adrenal veins (A-vein) and compared them with those in inferior vena cava (IVC) using blood samples obtained at catheterization of adrenal vein in the patients with adrenal adenoma manifesting Cushing's syndrome (Cs), aldosterone-producing adenoma, clinically non-functioning adenoma and normal adrenal gland. The tumor sides of A-veins in the patients with adenomas and also both sides of A-veins in subjects with normal adrenal glands showed significantly higher contents of inhibin-LI than their IVC. When the inhibin-LI secretion rate from adrenal gland was estimated by the difference between the levels of A-vein (tumor side) and IVC, Cs adenomas showed the highest secretion rate. Similarly, the tissue inhibin-LI content and the basal secretion rate of inhibit-LI from primary cultured cells were the highest in Cs adenomas. These findings indicated that normal adrenal glands and adrenocortical adenomas produced and secreted inhibin-LI into the general circulation in vivo and Cs adenomas have relatively high capacity for secreting inhibin-LI, and the present study provided the first in vivo evidence for adrenal inhibin-LI production in pathological conditions Yoshihiro Nishi, Third Department of Internal Medicine, Faculty of Medicine, Kyushu University, Maidashi 3-1-1, Higashi-Ku, Fukuoka 812, Japan

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Comparison of corticotropin-releasing factor and acetylcholine on catecholamine secretion in dogs

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1987.253.2.r209 ◽

1987 ◽

Vol 253 (2) ◽

pp. R209-R215 ◽

Cited By ~ 1

Author(s):

W. C. Engeland ◽

M. P. Lilly ◽

T. O. Bruhn ◽

D. S. Gann

Keyword(s):

Blood Flow ◽

Adrenal Gland ◽

Synergistic Effect ◽

Corticotropin Releasing Factor ◽

High Dose ◽

Response Relationship ◽

Dose Response Relationship ◽

Similar Dose ◽

Adrenal Secretion

To test whether corticotropin-releasing factor (CRF) is a secretagogue for adrenal secretion of catecholamines, a preparation was developed that permits measurement of adrenal venous output in response to in vivo arterial injection into the dog adrenal gland. Dogs were prepared with catheters in the lumboadrenal vein for monitoring adrenal blood flow and secretion rate of epinephrine and norepinephrine and in the lumboadrenal and inferior phrenic arteries for adrenal injection. Under pentobarbital anesthesia 48 h after surgery, dogs received a series of intra-adrenal injections that included acetylcholine (0.2-200 nmol), CRF (2.0-20.0 nmol), and diluent. There was a log dose-response relationship before epinephrine secretion and norepinephrine secretion to acetylcholine. Adrenal injection of CRF stimulated epinephrine and norepinephrine secretion at the highest dose tested (20 nmol). The response observed was equivalent to the response to 0.2 nmol acetylcholine. A similar dose of CRF given systemically produced hypotension without stimulating catecholamine responses. Adrenal catecholamine responses to acetylcholine were not augmented by addition of CRF. These findings show that arterial injection of CRF into the intact dog adrenal stimulates secretion of epinephrine and norepinephrine. However, the low potency of CRF relative to that of acetylcholine, the lack of a synergistic effect of CRF on catecholamine responses to acetylcholine, and the high dose of CRF required to achieve a response suggest that CRF does not function in the adrenal medulla as a physiologically important secretagogue for catecholamines.

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