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

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

Dissociation between plasma, urine, and renal papillary cyclic AMP content following vasopressin and DDAVP

1979 ◽  
Vol 237 (3) ◽  
pp. F218-F225 ◽  
Author(s):  
M. J. Bia ◽  
S. Dewitt ◽  
J. N. Forrest
Keyword(s):  
Cyclic Amp ◽  
Urine Osmolality ◽  
Brattleboro Rats ◽  
Renal Papilla ◽  
Brattleboro Rat ◽  
Clearance Studies ◽  
Urinary Cyclic Amp ◽  
Stimulation Of

The effects of in vivo physiologic doses of vasopressin and 1-deamino-8-D-arginine vasopressin (DDAVP) on the cyclic AMP content of plasma, urine, and renal papillary tissue were determined in the ADH-deficient Brattleboro rat. During clearance studies, plasma cyclic AMP concentrations and both total and nephrogenous urinary cyclic AMP excretion in vasopressin- and DDAVP-treated rats were similar to the values in time-matched controls. In contrast, in situ renal papillary cyclic AMP content was higher (P less than 0.001) in both vasopressin- (35.7 +/- 3.6 pmol/mg protein) and DDAVP- (29.7 +/- 2.2 pmol/mg protein) treated rats compared to controls (15.1 +/- 1.3 pmol/mg protein). Endogenous stimulation of vasopressin by dehydration in normal rats increased both papillary cyclic AMP content (27.1 +/- 2.7 pmol/mg protein) and urine osmolality, whereas no change in papillary cyclic AMP was observed following dehydration in Brattleboro rats (13.6 +/- 0.8 pmol/mg protein) despite an increase in urine osmolality. The results demonstrate that changes in cyclic AMP following in vivo vasopressin are best demonstrated by measurement of in situ cyclic AMP content of the renal papilla, whereas total urinary cyclic AMP and nephrogenous cyclic AMP are not useful indices of tubular sensitivity to this hormone.

Immunoreactive vasopressin and oxytocin in hypothalamo-hypophysial portal blood of the Brattleboro and Long–Evans rat: effect of adrenalectomy and dexamethasone

1988 ◽  
Vol 117 (1) ◽  
pp. 27-34 ◽  
Author(s):  
D. J. A. Eckland ◽  
K. Todd ◽  
S. L. Lightman
Keyword(s):  
High Pressure ◽  
Liquid Chromatography ◽  
High Pressure Liquid Chromatography ◽  
Portal Blood ◽  
Brattleboro Rats ◽  
Brattleboro Rat ◽  
Long Evans ◽  
High Concentrations ◽  
Very High ◽  
Hypophysial Portal

ABSTRACT Immunoreactive vasopressin and oxytocin were measured in the hypothalamo-hypophysial portal blood of both Long–Evans and homozygous Brattleboro rats. Adrenalectomy caused an increase in vasopressin immunoreactivity in portal blood in the Long–Evans strain, whilst administration of dexamethasone to these adrenalectomized animals resulted in a reduction in portal vasopressin immunoreactivity to levels below those seen in sham-operated animals. This vasopressin immunoreactivity co-eluted with synthetic vasopressin on high-pressure liquid chromatography (HPLC), and diluted in parallel in radioimmunoassay. In Brattleboro rats, however, although vasopressin-like immunoreactivity was detected, the portal concentration did not vary with the adrenal status of the animal, nor did it show the characteristics of standard vasopressin on HPLC or in immunoassay. Oxytocin was present in the portal blood of both Long–Evans and Brattleboro rats at similar very high concentrations, but did not vary in response to adrenalectomy. These results are consistent with a role for vasopressin, but not oxytocin, in the hypothalamic response to adrenalectomy and glucocorticoid feedback. Neither vasopressin immunoreactivity nor oxytocin appear to subserve this role in the homozygous Brattleboro rat. J. Endocr. (1988) 117, 27–34

Ammonia detoxification by the rat kidney in vivo

1978 ◽  
Vol 56 (5) ◽  
pp. 305-314 ◽  
Author(s):  
Patrick Vinay ◽  
Guy Lemieux ◽  
André Gougoux
Keyword(s):  
Glutamate Dehydrogenase ◽  
Time Course ◽  
Tissue Concentration ◽  
Rat Kidney ◽  
Venous Blood ◽  
Ammonia Concentration ◽  
Constant Infusion ◽  
Glutamine Concentration

The time course of changes in the concentration of metabolites in response to a nontoxic load of ammonia was measured in freeze-clamped kidneys of fasted rats. Following a single NH4HCO3 load, a decrease in tissue concentration of 2-oxoglutarate occurs but this change is small and delayed in relation to the peak of blood ammonia concentration. An immediate but transient increment in tissue glutamine also occurs. No close relationship between the mitochondrial free NAD:NADH ratio calculated from the glutamate dehydrogenase and the 3-hydroxybutyrate dehydrogenase systems is seen during alteration of ammonia concentration. In contrast with previously reported observations in the liver under similar circumstances, no increase in tissue or renal venous blood aspartate or alanine concentration occurs. A constant infusion of NH4HCO3 doubles the tissue glutamine concentration and changes net renal extraction of glutamine to net production. The infusion of NH4+ together with a carbon source (malate, lactate) results in similar increase in tissue and renal vein glutamine concentration. No accumulation of aspartate or alanine are seen. In vitro studies on isolated kidney tubules indicate that the net flux through both aspartate aminotransferase and glutamate dehydrogenase is dependent on the concentration of the reactants as expected for systems in near-equilibrium situation. It is concluded that the rat kidney response to an ammonia load differs from that of the liver despite the apparent existence of a similar network of near-equilibrium systems. Such a difference is best explained by renal glutamine synthesis and sequestration of glutamate as glutamine in vivo.

THE SECRETION OF THE ADRENAL CORTEX IN THE SHEEP

1953 ◽  
Vol 10 (1) ◽  
pp. 1-8 ◽  
Author(s):  
I. E. BUSH ◽  
K. A. FERGUSON
Keyword(s):  
Adrenal Cortex ◽  
Paper Chromatography ◽  
Venous Blood ◽  
Adrenocortical Function ◽  
Secretory Product ◽  
Direct Knowledge ◽  
Direct Experiment ◽  
Isolated Tissues ◽  
Considerable Doubt

SUMMARY Adrenal venous blood was collected from six anaesthetized sheep, of which two had been previously hypophysectomized. The blood was extracted and analysed for adrenocortical steroids by paper chromatography. In each case the predominant secretory product found in the extracts was 17α-hydroxycorticosterone. Small amounts of corticosterone and a substance tentatively identified as 11β-hydroxyandrost-4-ene-3,17-dione were also found in all the extracts. Only traces of other reducing steroids or αβ-unsaturated ketosteroids were found: their irregular appearance makes it likely that they were artifacts. It seems unlikely that the secretion of the adrenal cortex in vivo is as complex as the mixture of products released by the perfused beef adrenals in the experiments of Hechter, Zaffaroni, Jacobsen, Levy, Jeanloz, Schenker & Pincus [1951]. The reported actions of cortical steroids, or whole adrenal extracts, when injected into mammals or added to isolated tissues have become so numerous that it has become essential to find out by direct experiment what the adrenal cortex actually secretes into the blood in various conditions. In the absence of direct knowledge of the nature of the cortical secretion, various theories of adrenocortical function have been proposed from time to time [e.g. Sayers, 1950], but recent work has cast considerable doubt upon them. All such theories postulate that the adrenal cortex secretes one or more steroid substances at particular rates in various physiological conditions, and it is necessary to find out whether this is the case or not. This paper describes experiments on six sheep in which adrenal venous blood was collected and analysed by paper chromatography [Bush, 1953] in order to determine the rate and type of secretion in this species.

scholarly journals Dynamic High-Resolution MR Imaging of Brain Deoxygenation during Transient Anoxia in the Anesthetized Rat

1993 ◽  
Vol 13 (5) ◽  
pp. 889-894 ◽  
Author(s):  
Franz Prielmeier ◽  
Klaus-Dietmar Merboldt ◽  
Wolfgang Hänicke ◽  
Jens Frahm
Keyword(s):  
Time Course ◽  
High Spatial Resolution ◽  
Venous Blood ◽  
Blood Pool ◽  
Magnetic Resonance Images ◽  
Brain Oxygenation ◽  
Voxel Size ◽  
Difference Images ◽  
The Brain

Transient alterations in brain oxygenation during 60-s periods of anoxia were visualized at high spatial resolution (voxel size ≤ 0.15 μl) with the use of serial long echo time FLASH (fast low-angle shot) magnetic resonance images (measuring time ≥ 6 s) of halothaneanesthetized rats in vivo. Difference images from normoxia and anoxia exploit the signal decrease associated with increased levels of paramagnetic deoxyhemoglobin in the arterial and venous blood pool. Insights into the spatial heterogeneity of oxygen deprivation are complemented by physiologic information from the time course of pertinent signal changes in different regions of the brain.

Regional hemodynamic effects of endothelin-2 and sarafotoxin-S6b in conscious rats

1990 ◽  
Vol 258 (4) ◽  
pp. R912-R917 ◽  
Author(s):  
S. M. Gardiner ◽  
A. M. Compton ◽  
T. Bennett
Keyword(s):  
Blood Pressure ◽  
High Dose ◽  
Brattleboro Rats ◽  
Pulsed Doppler ◽  
Hemodynamic Effects ◽  
Doppler Flow ◽  
Conscious Rats ◽  
Long Evans ◽  
Dose Dependent

Regional hemodynamic responses to bolus doses (4 and 40 pmol) and 60-min infusions (12 and 120 pmol/h) of endothelin-2 (ET-2) and sarafotoxin-S6b (S6b) were measured in conscious Long-Evans and Brattleboro rats chronically instrumented with pulsed Doppler flow probes. In both strains of rat the two bolus doses of ET-2 and S6b peptides caused an initial fall in mean blood pressure (MBP). At the higher dose S6b caused a greater fall in MBP than ET-2. In Long-Evans rats the fall in MBP after S6b was associated with renal, mesenteric, and hindquarters vasodilatations; in Brattleboro rats there was no renal or mesenteric vasodilatation with S6b. The high dose of ET-2 caused early mesenteric vasoconstriction in both strains. After the initial fall in MBP there were dose-dependent increases in MBP together with renal and mesenteric vasoconstrictions. These effects were generally greater after S6b than after ET-2 and no less marked in Brattleboro than in Long-Evans rats, indicating that release of endogenous vasopressin was not an indispensable component of the response. Infusions of the higher dose of ET-2 or S6b caused increases in MBP only, associated with renal, mesenteric, and hindquarters vasoconstrictions. The results indicate that S6b is a more potent stimulus than ET-2 of vasodilator mechanisms in vivo; despite this, S6b also exerts more marked vasoconstrictor effects than ET-2.

scholarly journals Mechanisms for the formation of alanine and aspartate on rat liver in vivo after administration of ammonium chloride

1974 ◽  
Vol 138 (3) ◽  
pp. 453-462 ◽  
Author(s):  
John T. Brosnan ◽  
Dermot H. Williamson
Keyword(s):  
Ammonium Chloride ◽  
Alanine Aminotransferase ◽  
Time Course ◽  
Urea Cycle ◽  
Absolute Increase ◽  
The Absolute ◽  
Prior Administration ◽  
Toxic Load ◽  
Stimulation Of

1. The time-course of the changes in the concentrations of hepatic metabolites in response to a non-toxic load of NH4Cl were measured in fed and starved rats. 2. There was a rapid increase (after 2min) in [alanine] and [aspartate] which remained high for 10–15min; the absolute increase in [alanine] was smaller in starved rats. 3. These changes were accompanied by a decrease in [oxoglutarate] and in the [3-hydroxybutyrate]/[acetoacetate] ratio. 4. Prior administration of l-arginine to fed rats resulted in smaller increases in [alanine] and [aspartate] after the ammonia load. This is presumably due to stimulation of the urea cycle. 5. Increased formation of alanine in starved rats occurred after prior administration of dihydroxyacetone to increase the availability of pyruvate. 6. Administration of l-cycloserine, an inhibitor of glutamate–alanine aminotransferase, completely prevented the increase in [alanine] after the ammonia load; in this case the absolute increase in [aspartate] was higher. 7. [Oxoglutarate], [citrate] and [isocitrate] at 25min after the ammonia load were higher than the initial concentrations, but returned to normal by 50min. It is suggested that this `overshoot' may be due to temporary compartmentation of oxoglutarate. 8. The mechanisms and physiological significance of alanine and aspartate formation in these experiments are discussed.

Progressive hypoxia until brain electrical silence: a useful model for studying protective interventions

1988 ◽  
Vol 66 (11) ◽  
pp. 1398-1406 ◽  
Author(s):  
Carl F. Cartheuser
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Time Course ◽  
Venous Blood ◽  
Hypoxia Tolerance ◽  
Sagittal Sinus ◽  
Progressive Hypoxia ◽  
Time Courses ◽  
Blood Data

Anesthetized spontaneously breathing rats, fitted with epicortical electrodes and catheters for sampling arterial, venous, and cerebral venous blood, were exposed to standardized progressive hypoxia. Three minutes of hypoxia sequentially caused hyperpnea, hypopnea, apnea, and cessation of electrocorticogram "spiking," of synchronization, and of background in electroencephalogram (EEG). Blood data and cerebral blood flow and metabolism were measured throughout and at "insults," i.e., at apnea and cessation events, to clarify their interdependence. Arterial and brain venous Po2 fell linearly with inspired oxygen (final value of 2% at 280 s). Hyperpnea induced arterial alkalosis; subsequent hypopnea led to near-normal Pco2 and pH when EEG ceased. Hypercapnia was more pronounced in cerebral than in systemic venous blood; time courses of pH changes were similar. Sagittal sinus blood pressure and outflow were linearly related and resembled the time course of local cerebral blood flow. Blood flow increased by 25% at apnea and only 60% at EEG silence. Cerebral metabolic rate of O2 rose during the hyperpnea phase and fell exponentially thereafter. Cerebral glucose uptake and lactate release increased within the first 3 min but fell abruptly when cortico-electric spiking ceased. Time courses of cerebral O2 consumption and spike rate were linearly related; both showed inverse linear relations to cerebral perfusion. The hypoxic insults were well defined by blood data; critical Po2 values were lower than previously assumed. This model is proving to be a useful, controlled method by which mechanisms of cerebral hypoxia tolerance may be studied in vivo.

Influence of oxytocin on sodium excretion in the anaesthetized Brattleboro rat

1991 ◽  
Vol 129 (1) ◽  
pp. 49-54 ◽  
Author(s):  
M. J. Brimble ◽  
R. J. Balment ◽  
C. P. Smith ◽  
R. J. Windle ◽  
M. L. Forsling
Keyword(s):  
Plasma Levels ◽  
Sodium Excretion ◽  
Plasma Concentrations ◽  
Saline Infusion ◽  
Brattleboro Rats ◽  
Posterior Pituitary ◽  
Brattleboro Rat ◽  
Long Evans ◽  
Hypotonic Saline

ABSTRACT The contribution of oxytocin to the maintenance of renal Na+ excretion in the Brattleboro rat has been examined in animals infused with hypotonic saline. Brattleboro rats exhibited hypernatraemia and hyperosmolality associated with greatly increased plasma concentrations of oxytocin by comparison with Long–Evans control rats. Neurohypophysectomy to remove the secretion of the remaining posterior pituitary peptide, oxytocin, led to greatly diminished rates of Na+ excretion in the Brattleboro rat. Oxytocin replacement to achieve plasma levels equivalent to those in intact Brattleboro rats produced a substantial and sustained natriuresis in the neurohypophysectomized animal. Oxytocin secretion evoked in response to saline infusion would thus appear to be effective in promoting renal Na+ excretion in the absence of vasopressin in the Brattleboro rat. Journal of Endocrinology (1991) 129, 49–54

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