Cortical Hormones Research Articles

Role of adrenal cortex and medulla in hypertension.

SPONTANEOUSLY hypertensive rats (Okamoto-Aoki) (SHR) became normotensive following bilateral adrenalectomy1. In adrenalectomized SHR, hypertension was restored by the administration of adrenal cortical hormones2,3. Other reports confirmed that adrenal cortical hormones may play a principal role in the development and maintenance of hypertension4–9; increased catecholamine content10, tyrosine hydroxylase and dopamine-β-hydroxylase11 in adrenal medulla in the hypertension have also been demonstrated. The hypertension in rats was genetical and developed spontaneously. Blood pressures of all SHR rats increased and systolic blood pressure was approximately 150 mm Hg at 8 weeks and approximately 200 mm Hg at 15 weeks old.

A humoral component of the natriuretic mechanism in sustained blood volume expansion.

A natriuretic and diuretic response to whole blood infusion in the rat, exaggerated and sustained by intravenous reinfusion of excreted urine, was shown to be associated with increased glomerular filtration and reduced tubular reabsorption. Cross-circulation of animals so responding (donor rats) with isovolemic recipients led to a modest natriuretic and diuretic response in the latter, not accounted for by altered physical composition of the blood nor by observed changes in filtration rate or arterial blood pressure. The recipient natriuresis was unchanged when nephrectomized donors were used and it occurred in experiments in which donor urine was simultaneously replaced by intravenously infused Ringer-Locke solution; the natriuretic property of the cross-circulating blood could therefore not have been due to reinfusion of urinary constituents, nor to accumulation of metabolites, nor to a factor of renal origin. A recipient natriuresis was also observed when the expanded and urine reinfused donor had been acutely adrenalectomized, ruling out an altered secretion of adrenal cortical or medullary hormones as a principal cause of this natriuresis; the data, however, do not exclude participation of reduced aldosterone secretion in the normal effector mechanism. In control experiments in which whole blood was exchanged for donor blood, a small delayed natriuresis did occur in the recipient; this could be completely prevented by administration of aldosterone. In similar exchange experiments with adrenalectomized donors, a small natriuresis developed in the recipient before blood administration but declined afterwards. These minor natriuretic effects probably resulted from altered mineralocorticoid content of the cross-circulating blood due to factors other than blood volume change. The larger natriuretic response seen in all recipients when the donor was volume expanded must have been due largely to a humoral natriuretic factor of other than renal or adrenal origin.

Effect of Escherichia coli endotoxins on plasma para-phenylenediamine oxidase (caeruloplasmin) activity in the domestic fowl

The intravenous injection of pathogen-free fowls with endotoxin preparations obtained from 3 strains of Escherichia coli (02, 078 and 0111) produced a two- to five-fold increase in caeruloplasmin levels as measured by the activity of p-phenylenediamine oxidase in the plasma. This response was maximal 24 hours after the injection, was still detectable after 48 hours and was similar for the 2 doses used (1 and 3 mg./kg. body weight). One batch of the 0111 preparation produced a greater response than the other preparations which did not differ appreciably from each other in this respect. Different potency patterns were revealed by mouse toxicity experiments in which lethality and effect on body weight were measured. When preparations were injected into chicks at weekly intervals the effect of the first injection on caeruloplasmin levels was greater than the subsequent responses which did not vary significantly. It was concluded that the elevations in caeruloplasmin levels which accompany infections involving gram-negative bacteria must be at least partly due to the action of endotoxins. These may induce caeruloplasmin synthesis by promoting the release of adrenal cortical hormones. One of the functions of caeruloplasmin may be to regulate the plasma levels of catecholamines and serotonin and so minimise metabolic disturbances.

The anti-inflammatory effect of catecholamines in the peritoneal cavity and hind paw of the mouse.

1. Carrageenin or 5-hydroxytryptamine-induced oedema of the mouse hind paw was antagonized by catecholamines acting on both alpha- and beta-adrenoceptors.2. Increased permeability of the mouse peritoneum induced by the local injection of acetic acid or pro-inflammatory mediators was antagonized by catecholamines acting predominantly on beta-adrenoceptors.3. The anti-inflammatory effect of catecholamines was due neither to hyperglycaemia nor to the release of adrenal cortical hormones.

Thymolytic and adrenal cortical responses to the LDH-elevating virus.

SummaryFollowing infection of intact mice with the LDH-virus, a significant thymus involution was observed. Since there was no thymus involution in adrenalectomized mice infected with the virus, a virus-induced adrenal cortical hormone increase or activation is postulated. The observation of an increase in spleen and lymph node weight in both intact and adrenalectomized LDH-virus infected mice may result from a virus-induced proliferation of thymus-independent lymphatic tissue, which is unaffected by the adrenal cortical hormones.

Mode of action of adrenal cortical hormones. IV. Enhanced glucocorticoidal activity of steroids associated with decreased chemical reactivity of the 4 -3-ketone and the C-20, 21-ketol groups.

Mode of action of adrenal cortical hormones. IV. Enhanced glucocorticoidal activity of steroids associated with decreased chemical reactivity of the 4 -3-ketone and the C-20, 21-ketol groups.

A Block in Epinephrine-induced Glycogenolysis in Hearts from Adrenalectomized Rats

Abstract Perfused hearts from adrenal-deficient rats showed an impaired glycogenolytic response to suboptimal concentrations of epinephrine as judged by measurements of tissue glycogen and lactate production. The glycogenolytic response could be restored to normal by treatment of these animals with cortisol in vivo. Individual steps in the path of epinephrine-stimulated glycogenolysis were examined. Adrenalectomy did not impair adenosine 3',5'-monophosphate accumulation in response to several concentrations of epinephrine; a histone kinase, partially purified from hearts of adrenalectomized rats, was as sensitive to activation by adenosine 3',5'-monophosphate as the enzyme prepared from normal hearts; and the activation of phosphorylase b kinase by several concentrations of epinephrine was unaffected by the deficiency of adrenal cortical hormones. However, suboptimal concentrations of epinephrine did not activate phosphorylase in hearts from adrenalectomized rats to the normal extent. These findings suggest therefore that the defect following adrenalectomy lies in the activity of phosphorylase b kinase. The defect could be overcome by administration of adrenal glucocorticoid in vivo or by raising the perfusate calcium concentration.

Postural Hypotension and Steroids

To the Editor.— Earlier literature concerning the use of the adrenal cortical hormones emphasized the occasional development of adrenal crisis, secondary to the prolonged suppression of the pituitary adrenal axis many months after cessation of these steroids. The problem was resurrected in a case in connection with cyclic use of large doses of prednisone as an adjunct to chemotherapy. Report of a Case.— In a 64-year-old black American, lymphadenopathy developed in the left inguinal region in May 1970. Initial biopsies showed only reactive hyperplasia. The lymphadenopathy appeared subsequently in the axilla and supraclavicular areas, and biopsies in October showed lymphosarcoma. The blood pressure at that time was 110/70 mm Hg, but the patient was not specifically checked for postural hypotension. A general medical evaluation was otherwise unremarkable. The hemoglobin level ranged from 9.5 to 10.8 gm/100 ml. The white blood cell count was 3,200/cu mm, with a normal differential cell

Seasonal changes of pelage in the vole ( Microtus agrestis) : III. The role of the endocrine system

The action of hormones on different aspects of hair growth in the vole ( Microtus agrestis) results in a seasonal change of pelage which is correlated with the environmentally controlled activity of the endocrine system. Our evidence suggests that sex hormones act by inhibiting the activity of hair follicles without affecting the type of hair produced. Thyroxine stimulates the amount of hair secreted by the individual hair follicles and adrenal cortical hormones encourage loss of club hairs. Thus, increased secretion of these hormones in spring leads to the production of a sparse coat with coarse hairs. A lowered secretion of hormones in autumn results in a dense coat with fine hairs.

Cold Acclimation of Adrenalectomized Male Leghorn Chickens

IT HAS been established that catecholamines, especially norepinephrine, play an important role in cold acclimation in small mammals (Hsieh and Carlson, 1957; Depocas and Secours, 1960; Héroux, 1962; Anderson et al., 1964). Evidence of their involvement in a thermoregulatory mechanism in birds has been reported by El-Halawani et al. (1970).The contribution of the adrenal medulla to the nonshivering, thermoregulatory mechanism has been studied on curarized rats by Cottle and Carlson (1956). Their results indicate a partial involvement of the adrenal glands.Despite accumulated evidence that the cortical hormones are not required for maintenance of cold acclimation, they have been found in rats to be involved in the initial phase of acclimation (Sellers et al., 1951; Héroux and Hart, 1954b; Rossiter and Nicholls, 1957). Certain degrees of cold acclimation and resistance to cold can be obtained in adrenalectomized rats by administering minimal doses of cortisone or desoxycorticosterone (DesMarais, 1956), or…

The effect of the administration of cortisol on the levels of cortisol and electrolytes in blood and cerebrospinal fluid in man

In some patients with brain tumor, neurosurgery involving ventricular drainage and ventriculography resulted in an increase in the sodium level in cerebrospinal fluid without any modification of its level in blood. In these patients, the effects of the administration of cortisol on the levels of corticosteroids, sodium, and potassium in blood and cerebrospinal fluid were studied. After the administration of cortisol, the corticosteroid levels in blood and cerebrospinal fluid were markedly increased. When patients had normal levels of sodium in cerebrospinal fluid, cortisol administration did not affect these sodium levels. However, when the sodium level in cerebrospinal fluid was high, the sodium level decreased 2 to 4 hr after the administration of cortisol. In all these patients, the sodium and potassium levels in blood were not influenced by cortisol administration. This finding may have bearing upon the apparent beneficial action of adrenal cortical hormones on cerebral edema following trauma or brain surgery.

Influence of surgical and steroidal bursectomy on the behavior of adrenal ascorbic acid during stress in juvenile pigeons

The experimental response of adrenal ascorbic acid (AAA) to stress in juvenile pigeons was studied after surgical removal of the bursa of Fabricius and chronic administration of cortical and male sex hormone. Surgical bursectomy facilitated the depletion of AAA during stress. Corticoid therapy caused an involution of the bursa while AAA was unaltered after exposure to stress. Androgen administration did not regress the bursa, but stress evoked major depletions in AAA concentration. The probable mediation of androgen in precipitating these stress responses has been briefly discussed.

Adrenal cortical and medullary hormones in recovery of tissues from local injury.

Adrenal cortical and medullary hormones in recovery of tissues from local injury.

On the role of antidiuretic hormone in the inhibition of acute water diuresis in adrenal insufficiency and the effects of gluco- and mineralocorticoids in reversing the inhibition.

In order to determine whether or not antidiuretic hormone (ADH) is essential to the inhibition of an acute water diuresis in adrenal insufficiency, the response to oral water loads was tested in rats with hereditary hypothalamic diabetes insipidus (DI) which lack ADH. It was found that 60 min after water loads of 3 or 5% of body weight urine flow was significantly lower and urine osmolality significantly higher in adrenalectomized DI rats than in the same DI rats before removal of their adrenal glands. The efficacy of gluco- and mineralocorticoids in reversing the inhibition was then determined in the same adrenalectomized DI rats. Prednisolone alone, administered either acutely or chronically, restored the response in urine flow to that seen in the same rats before adrenalectomy, but failed to correct the defect in urinary dilution. Aldosterone when given alone tended to correct the diluting ability but not the response in urine flow. When these two adrenal cortical hormones were given simultaneously, both the urine flow and urine osmolality were nearly identical to what they had been in the same DI rats before adrenalectomy. These studies strongly suggest (a) that ADH is not essential to the inhibition of an acute water diuresis in adrenal insufficiency, although it may abet the inhibition in individuals without diabetes insipidus, which can elaborate ADH; and (b) that both gluco- and mineralocorticoids are required in adrenal insufficiency in order to fully restore the water diuresis as judged by the dual criteria of urine flow and urine osmolality.

Effects of Host Fighting Behavior on the Course of Infection of Trypanosoma Duttoni in Mice

In one experiment, male albino mice were inoculated with Trypanosoma duttoni, and were allowed to begin fighting on the same day; the fighting animals developed significantly lower parasitemias than the isolated controls throughout the reproductive phase of the infection. In two other experiments, mice were allowed to fight for a period of 10 days prior to inoculation; the fighting animal exhibited higher parasitemias than the controls, with the subordinate mice developing slightly, but not significantly, higher parasitemias than the dominant animals. Since all differences noted among controls, dominants and subordinates were during the reproductive phase of the infection, and since no differences were observed in the length of infection among these groups, it was concluded that fighting altered the ablastic, but not the trypanocidal antibody response. This alteration is believed to have resulted from the action of adrenal cortical hormones on antibody—producing cells. Sustained elevation of plasma corticosterone levels during 10 days of fighting in the latter experiments may have been responsible for the different results obtained with the two experimental designs.

Escape from sodium-retaining effects of deoxycorticosterone in hypotensive and hypertensive dogs.

SummaryThe ability of the mammalian kidney to escape from the sodium-retaining effects of mineralocorticoid hormones has not been thought to depend upon increases in blood pressure or renal perfusion. However, chronic exposure to excess endogenous or exogenous adrenal cortical hormones results in hypertension, and it seemed possible that early small increments in blood pressure might play a role in escape. To evaluate this, hypotension was produced with drugs in dogs, and their ability to escape was studied. A combination of hydralazine and guanethidine effectively lowered blood pressure but did not prevent or delay renal escape from deoxycorticosterone. Production of hypotension after escape resulted in sodium retention for 1 day, but then sodium balance resumed despite continued hypotension and lowered renal blood flow and filtration. Mean arterial blood pressure in dogs with thoracic inferior vena caval constriction was not significantly below normal, and elevation of blood pressure with ephedrine fail...

Lutenizing hormone bioassay based on uptake of radioactive phosphorus by the chick tests

1. 1. Neuraminidase, a bacterial enzyme, was used to selectively destroy follicle-stimulating hormone (FSH) activity of chicken anterior pituitary glands. 2. 2. The enzyme-treated pituitary material and various other pituitary hormones were tested to determine their effect on 32P uptake by chick testes. Adrenal cortical stimulating hormone (ACTH), growth hormone (GH) and prolactin did not increase 32P uptake. 3. 3. Treatment with 1 mg of the enzyme-treated pituitary material resulted in a 150 per cent increase in 32P uptake. This response was attributed solely to LH. 4. 4. An assay based on bovine LH standards (NIH-LH-B5) demonstrated that the LH activity of chicken anterior pituitary glands could be measured within the limits of 1·0 to 8·0 gmg.

Mode of action of adrenal cortical hormones. 3. Stimulation of 14C incorporation from 14CO2 and 14C-pyruvate into glucose by triamcinolone in the presence of ethanol in rat liver slices.

1. The effect of triamcinolone on the incorporation of 14C from 14CO2 and 14C-pyruvate into glucose and on the incorporation of pyruvate carbon into fatty acids and CO2 in rat liver slices was studied in the presence of sufficient amount of ethanol which inhibits gluconeogensis. 2. Ethanol is known to inhibit gluconeogenesis and the oxidation of pyruvate, glucose, and various amino acids in the liver by increasing the generation of NADH2. In fact, ethanol inhibition to the 14C incorporation from 14CO2 and 14C-pyruvate into glucose in rat liver slices was observed in the present investigation. The incorporation of 14C from 14C-pyruvate into fatty acids and CO2was also inhibited by ethanol. 3. Triamcinolone stimulated the 14C incorporation from 14CO2and 14C-pyruvate into glucose, but not the 14C incorporation into CO2and fatty acids. 4. Methylene blue, which is a redox dye capable of oxidizing NADH2, restored all these ethanol inhibitions. Triamcinolone counteracted the ethanol inhibition of 14C incorporation from 14CO2and 14C-pyruvate into glucose, but triamcinolone did not affect the ethanol inhibition of 14C incorporation from 14C-pyruvate into CO2 and fatty acids. Therefore, it is unlikely that the effect of adrenal cortical hormones to stimulate gluconeogenesis is primarily on the NADH2/NAD system.

Dependence of pancreatic integrity on adrenal and ovarian secretions.

Removal of the adrenal glands from male rats causes a significant decrease in protein content of the pancreas. In addition, microscopic examination of pancreatic tissue from these adrenalectomized animals indicated considerable depletion of zymogen granules. Treatment of such animals with the synthetic glucocorticoid triamcinolone acetonide reverts the biochemical and histological parameters to those observed in the intact animal within 12 hr. The female rat does not demonstrate thesechanges following adrenalectomy. However, if the ovaries are removed in addition to the adrenal glands, alterations similar to those observed in the adrenalectonized male pancreas become apparent. Treatment of the adrenalectomized - ovarectomized rat with triamcinolone acetonide reverts the pancreas to normal. In contrast to the male, the female rat apparently has dual control of the pancreas through estrogenic as well as adrenal cortical hormones. (Endocrinology85: 956, 1969)

Effect of adrenal cortical hormones and insulin on the alkaline phosphatase activity of alveolar bone in scorbutic guinea pigs

Effect of adrenal cortical hormones and insulin on the alkaline phosphatase activity of alveolar bone in scorbutic guinea pigs