Aldosterone secretion and adrenal angiotensin II receptors in the Brattleboro rat

1988 ◽  
Vol 117 (2) ◽  
pp. 215-221 ◽  
Author(s):  
J. P. Laulin ◽  
G. Simonnet ◽  
R. Brudieux ◽  
A. Carayon ◽  
J. D. Vincent
Keyword(s):  
Angiotensin Ii ◽  
Time Course ◽  
Low Dose ◽  
Binding Capacity ◽  
Venous Blood ◽  
Zona Glomerulosa ◽  
High Dose ◽  
Brattleboro Rats ◽  
Angiotensin Ii Receptor ◽  
Long Evans

ABSTRACT The basal secretion of aldosterone, measured in adrenal venous blood, was three- to fourfold lower in Brattleboro than in Long–Evans rats used as controls. Infusion of a low dose of angiotensin II (1 ng/min per 100 g body/wt) to Long–Evans rats caused a fourfold increase in aldosterone release but neither the low dose nor a tenfold higher dose changed the rate of release in Brattleboro rats. Only a very high dose (300 ng/min per 100 g body wt) succeeded in increasing the secretion of aldosterone in Brattleboro rats but throughout the time-course of the infusion, secretion remained about fivefold lower than in Long-Evans rats and the incremental response was reduced by 74·9%. Adrenal zona glomerulosa angiotensin II receptor sites had similar affinity and maximum binding capacity in the two groups of rats. It is suggested that the reduced corticosteroidogenic capacity of the adrenal cortex of Brattleboro rats results from an impairment of the post-receptor mechanisms involved in the biosynthesis of aldosterone. J. Endocr. (1988) 117, 215–221

Release of aldosterone and corticosterone from the adrenal cortex of the Brattleboro rat in response to administration of ACTH

1986 ◽  
Vol 111 (3) ◽  
pp. 375-381 ◽  
Author(s):  
R. Brudieux ◽  
M. N. Krifi ◽  
J. P. Laulin
Keyword(s):  
Adrenal Cortex ◽  
Time Course ◽  
Venous Blood ◽  
Mechanisms Of Action ◽  
Brattleboro Rats ◽  
Brattleboro Rat ◽  
Absolute Increase ◽  
Long Evans ◽  
Secretion Rates

ABSTRACT The time-course and dose–response of the in-vivo secretion of aldosterone and corticosterone after administration of ACTH(1–24) were measured in adrenal venous blood from female Brattleboro rats, homozygous for hypothalamic diabetes insipidus and lacking arginine vasopressin (AVP). Female Long–Evans rats were used as controls. All animals were pretreated with dexamethasone and anaesthetized with pentobarbital. Basal secretions of aldosterone and corticosterone were four- to sixfold lower in Brattleboro than in Long–Evans rats. Administration of ACTH consistently increased the secretion of aldosterone and corticosterone similarly in the two groups of rats; maximum values were observed 20–30 min after ACTH injection. However, for all the doses of ACTH (0·05, 0·5 and 5·0 mi.u./100 g body wt) and at every stage of response the secretion rates of aldosterone and corticosterone were twofold lower in Brattleboro than in Long–Evans rats. Furthermore the absolute increase in steroid secretion induced by ACTH was reduced by half in Brattleboro rats. These results show that the impairment of adrenal activity is largely due to a reduced capacity for corticosteroidogenesis in the adrenal cortex of Brattleboro rats. The mechanisms of action of AVP are discussed. J. Endocr. (1986) 111, 375–381

A study of the effect of X-rays on the electrical properties of mammalian nerve and muscle

1963 ◽  
Vol 157 (969) ◽  
pp. 536-561 ◽  
Keyword(s):  
Dose Rate ◽  
Action Potentials ◽  
Time Course ◽  
Low Dose ◽  
High Dose ◽  
X Rays ◽  
Low Dose Rate ◽  
End Plate ◽  
Small Doses ◽  
Motor End Plate

Resting potentials, action potentials, and miniature end-plate potentials have been re­corded from isolated phrenic-diaphragm preparations of the rat during and after irradiation with X-rays. Relatively small doses of a few thousand roentgens have no obvious effect on the preparation for many hours but larger doses, of the order of 70 to 150 kr irreversibly block neuromuscular transmission. The block is not accompanied by any change in the size of action potentials, resting potentials, membrane constants or miniature potentials recorded in the muscle with intracellular electrodes, or in the size of action potentials recorded in the nerve. Records made at the motor end-plate show that the cause of the block is a ‘pre-synaptic ’ failure of impulse propagation in the intramuscular part of the nerve. The time course of the failure depends largely on the rate at which X-rays are delivered to the pre­paration: at a high dose-rate (70kr/min) the block develops rapidly and is accompanied by an increase in the frequency of miniature potentials; at a low dose-rate (7 kr/min) larger doses are required, the latency is longer and the miniature potentials continue at a normal frequency. The sequence in which different parts of the muscle become blocked, the abrupt nature of the failure at an individual motor end-plate, and the increase in frequency of the miniature potentials together suggest that the action of X-rays is to block conduction in the nerve near its terminals, possibly by depolarizing points where the axons branch and the safety factor for the propagation of impulses is low. The results reported in this paper do not support the hypotheses that small doses of X-rays at a high or a low dose-rate lead to an initial 'enhancement' of function or that they produce immediate and reversible changes in the permeability of excitable membranes to ions.

Internalisation of the type I angiotensin II receptor (ATI) and angiotensin II function in the rat adrenal zona glomerulosa cell.

1994 ◽  
Vol 141 (2) ◽  
pp. R5-R9 ◽  
Author(s):  
G. P. Vinson ◽  
M. M. Ho. ◽  
J.R. Puddefoot ◽  
R. Teja ◽  
S. Barker
Keyword(s):  
Monoclonal Antibody ◽  
Plasma Membrane ◽  
Angiotensin Ii ◽  
Zona Glomerulosa ◽  
Type I ◽  
Specific Monoclonal Antibody ◽  
Angiotensin Ii Receptor ◽  
Cellular Localisation ◽  
Glomerulosa Cells

ABSTRACT Little is known about the cellular localisation of the angiotensin II (AII) type 1 receptor (ATI) in the rat adrenal glomerulosa cell, but some studies have suggested that receptor internalisation and recycling may occur. Using a specific monoclonal antibody (6313/G2) to the first extracellular domain, we show here that most of the receptor is internalised in the unstimulated cell. When viable glomerulosa cells are incubated with 6313/G2, the receptor is transiently concentrated on the cell surface, and aldosterone output is stimulated. This stimulated output is enhanced by neither threshold nor maximal stimulatory concentrations of All amide, although the antibody does not inhibit All binding to the receptor. Conversely, the stimulatory actions of the antibody and those of ACTH are additive. The data suggest that recycling to the plasma membrane is constitutive, or regulated by unknown factors. Retention of the ATI receptor in the membrane is alone enough to allow sufficient G protein interaction to generate maximal stimulatory events.

scholarly journals Low Salt Intake and Changes in Serum Sodium Levels in the Combination Therapy of Low-Dose Hydrochlorothiazide and Angiotensin II Receptor Blocker

2013 ◽  
Vol 77 (10) ◽  
pp. 2567-2572 ◽  
Author(s):  
Masafumi Nakayama ◽  
Hirofumi Tomiyama ◽  
Iwao Kuwajima ◽  
Tetsushi Saito ◽  
Yohei Hokama ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Combination Therapy ◽  
Serum Sodium ◽  
Low Dose ◽  
Salt Intake ◽  
Receptor Blocker ◽  
Angiotensin Ii Receptor Blocker ◽  
Angiotensin Ii Receptor ◽  
Low Salt

Stimulation of aldosterone biosynthesis by sodium sequestration: role of angiotensin II

1982 ◽  
Vol 243 (6) ◽  
pp. E450-E457
Author(s):  
J. Muller ◽  
E. G. Lund ◽  
L. Hofstetter ◽  
D. B. Brunner ◽  
P. Haldy
Keyword(s):  
Angiotensin Ii ◽  
Enzyme Inhibitor ◽  
Zona Glomerulosa ◽  
High Dose ◽  
Converting Enzyme ◽  
Bilateral Nephrectomy ◽  
Stimulatory Action ◽  
Sodium Sequestration ◽  
Stimulation Of

The role of angiotensin II in the stimulation of aldosterone biosynthesis by sodium sequestration in potassium-deficient rats was assessed by experiments involving 1-day angiotensin II infusion, converting enzyme inhibition, and bilateral nephrectomy. In intact rats, only an extremely high dose of exogenous angiotensin II imitated the stimulatory effects of polyethylene glycol-induced edema on the conversions of deoxycorticosterone and corticosterone to 18-hydroxycorticosterone and aldosterone. Treatment with the converting enzyme inhibitor captopril as well as bilateral nephrectomy blocked the aldosterone-stimulating action of edema. This inhibition was prevented by the simultaneous infusion of angiotensin II in captopril-treated rats but not in nephrectomized animals. According to these results, angiotensin II is an essential mediator in the stimulation of aldosterone biosynthesis by sodium sequestration. However, the role of the kidneys appears to be twofold. First, they act through the secretion of renin. In addition, a second yet unknown kidney factor is necessary for a full response of the zona glomerulosa to the stimulatory action of angiotensin II.

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