Aldosterone In Dogs Research Articles

Evaluation of Aldosterone Concentrations in Dogs with Hypoadrenocorticism

BackgroundSome dogs with primary hypoadrenocorticism (HA) have normal sodium and potassium concentrations, a phenomenon called atypical Addison's disease. The assumption that the zona glomerulosa and aldosterone secretion in these dogs are normal seems widely accepted; however, aldosterone measurements are missing in most published cases.ObjectivesTo measure aldosterone in dogs with HA with and without electrolyte abnormalities and to determine the time point of aldosterone peak concentrations during ACTH stimulation.AnimalsSeventy dogs with HA, 22 dogs with diseases mimicking HA, and 19 healthy dogs.MethodsProspective study. Blood samples were taken before and 60 minutes after injection of 250 μg ACTH in all dogs. Additional blood samples were taken 15, 30, and 45 minutes after ACTH in 7 dogs with HA and in 22 with diseases mimicking HA.ResultsBaseline and ACTH‐stimulated aldosterone was significantly lower in dogs with HA than in the other groups. Aldosterone was low or undetectable in 67/70 dogs with HA independently of sodium and potassium levels. In 3 dogs, sodium/potassium concentrations were normal; in 1 dog, sodium was normal and potassium decreased. In all 4, ACTH‐stimulated aldosterone concentrations were below the detection limit of the assay. Aldosterone concentrations were not different at 30, 45, or 60 minutes after ACTH administration.Conclusion and Clinical ImportanceCortisol and aldosterone secretion is compromised in dogs with HA with and without electrolyte abnormalities. The term atypical Addison's disease, used for dogs with primary HA and normal electrolytes, must be reconsidered; other mechanisms allowing normal electrolyte balance without aldosterone should be evaluated in these dogs.

Influence of aging on adrenal responsiveness in a population of eleven healthy beagles

The present study aimed at investigating the effects of aging on the adrenal cortex response of cortisol and aldosterone in dogs. A population of healthy adult Beagles was evaluated twice at a five-year interval. At each evaluation, plasma basal cortisol and aldosterone, cortisol and aldosterone following ACTH-stimulation, sodium, and potassium concentrations and arterial blood pressure were measured. We observed significantly ( p < 0.05) greater sodium, urea and creatinine concentrations with aging. Nevertheless urea and creatinine remained within our laboratory reference ranges. This study showed a highly significant age-related elevation of basal cortisol ( p < 0.01). Inversely, both aldosterone following ACTH-stimulation levels and difference between aldosterone following ACTH-stimulation and basal aldosterone values plummeted significantly ( p < 0.01) with aging. In conclusion, the evaluation of the adrenal cortex function in dogs should take in consideration the age of the individuals.

Metabolism of Aldosterone in Dogs with Renovascular Hypertension

SummaryThe rate of metabolism of aldo-sterone was measured in seven normal dogs, 4 dogs with chronic renal hypertension and five dogs with malignant renal hypertension. Tritiated aldosterone was injected intravenously and the rate of disappearance of authentic aldosterone was determined. The disappearance curves were resolved into two exponential components and the plasma half-life was measured from the slow component which reflects the rate of metabolism of aldosterone. The half-life of aldosterone was essentially the same for the three groups of dogs. It is concluded, therefore, that the rate of aldosterone metabolism is normal in dogs with experimental renal hypertension.

Urinary excretion of aldosterone in dogs with elevated plasma titers of antirenin.

SummaryDaily injections of crude hog renin into 7 trained, normotensive dogs elicited formation of antirenin titers ranging from 4-80 AR units/ml plasma. Urinary aldosterone excretion levels determ...

Distribution of body sodium, potassium, and water and the excretion of aldosterone in dogs with spontaneous heart failure

A series of studies was made in the compensated and decompensated phases of spontaneously occurring canine congestive heart failure secondary to mitral insufficiency of undetermined etiology. In 12 dogs, results were obtained for body composition and distribution of water, sodium, and potassium, and for the excretion of aldosterone. The data show highly significant increases in plasma volume, red-cell mass, extracellular water and extracellular sodium content, and in the excretion of aldosterone. Extracellular concentration of sodium and potassium remains normal, although serum potassium is increased slightly (p = 0.05) over that of the compensated state. Intracellular water is increased 11 per cent, and intracellular potassium concentration is decreased 6 per cent. Although neither change reaches statistical significance, the latter is suggestively close (p = 0.08). Intracellular sodium concentration varies considerably, but, on the average, is negligibly increased. The results in the compensated animals approximate the results in normal man and dog. The pattern of response found in decompensation is virtually identical to the usual response to low-output right heart failure in man.

HYPERSECRETION OF ALDOSTERONE IN DOGS WITH A CHRONIC AORTIC-CAVAL FISTULA AND HIGH OUTPUT HEART FAILURE.

Hypersecretion of aldosterone occurred at the onset of signs of congestive heart failure in a large series of dogs with a large infrarenal aortic-caval fistula. There was evidence of right heart failure in all animals and in four of the dogs râles or frank pulmonary edema was present. Marked sodium retention and ascites or edema were consistent findings and in the majority of the animals central venous pressure was elevated. Hypophysectomy was followed by a striking fall in both aldosterone and corticosterone secretion but in several animals hypersecretion of aldosterone was evident in the absence of the anterior pituitary. Subsequent acute bilateral nephrectomy of these hypophysectomized dogs resulted in a marked drop of aldosterone secretion to a very low level, and a precipitous fall in arterial pressure frequently occurred. An intravenous infusion of a saline extract of each animal's kidneys produced a striking elevation in aldosterone output; corticosterone secretion and arterial pressure increased consistently. The kidneys of these dogs with heart failure secondary to an A-V fistula frequently showed hypergranulation and hyperplasia of the juxtaglomerular cells. The present findings suggest that the increased rate of aldosterone secretion was mediated by the renin-angiotensin system. Measurements of arterial pressure and renal hemodynamic function demonstrated a fall of mean renal arterial pressure, glomerular filtration rate, and renal plasma flow, whereas arterial pulse pressure above the fistula and presumably in the kidneys was increased. The data suggest that decreased pulse pressure is unnecessary for activation of the renal mechanism leading to hyperaldosteronism.

On the hemodynamic regulation of the secretion of aldosterone.

Evidence is presented that the secretion of aldosterone in dogs may be considerably influeneed by hemodynamic factors. The experiments indicate that secretion of aldosterone may be decreased by expanding the "low pressure" system, and may be increased by reducing the amplitude of the pulse pressure in the carotid arteries. The decrease may be prevented by prior section of the vagi, the increase by prior denervation of the thyro-carotid arterial junctions.