Adrenal 17-Hydroxycorticosteroid Secretion Research Articles

Effects of exogenous acetylcholine upon adrenal 17-hydroxycorticosteroid secretion of intact and head X-irradiated dogs.

Adrenocortical response to exogenous acetylcholine (Ach) was investigated, under anesthetized conditions, in intact, hypophysectomized and head X-irradiated dogs. Intravenous injection of Ach (1 mg/kg b.w.) to intact dogs resulted in marked increases in the secretion of 17-hydroxycorticosteroids (17-OHCS) by the adrenal gland. The maximum response was seen at 10 min after the injection and a return to preinjection levels tended to occur by 60 min. This effect was abolished completely by hypophysectomy. In dogs whose heads had been irradiated with 200 and 1,000 R of X-rays 1 day previously, a considerably lower response to Ach was found; 17-OHCS output at the time when the secretion had been maximum was 44--53% less than that in non-irradiated dogs.

Effect of ingestion of food on adrenal 17-hydroxy-corticosteroid secretion in the dog.

The present investigation was undertaken to know the effect of food ingestion on adrenal cortical secretion. In conscious dogs adrenal venous blood was collected before and after ingestion of food (boiled beef) and analyzed for 17-hydroxycorticosteroids (17-OHCS). The adrenal 17-OHCS secretion rate before the ingestion of food was 0.04-0.25μg/ kg/min. After the food ingestion it was increased only slightly and transitorily, the maximal secretion rate being 0.36-0.55μg/kg/min.

Effect of muscular exercise on adrenal 17-hydroxycorticosteroid secretion in the dog.

In conscious dogs, whose dorsal spinal roots (T11-L3) had been previously sectioned, adrenal venous blood was collected and analyzed for 17-hydroxycorticosteroids (17- OHCS) by the method of Nelson and Samuels. The animals, paced by an attendant on a bicycle, were run 1.2–13.1 km at speeds of 106–181 meters /min. Dogs, in which no signs of fatigue were observed during and after running, showed no definite changes in 17-OHCS secretion rate. In dogs which seemed to be somewhat tired but were notcompletely exhausted, adrenal 17-OHCS secretion rate increased only transitorily. In completely exhausted dogs adrenal 17-OHCS secretion rate increased markedly and attained 1.1– 2.1 μg/kg/min after running, while it had been less than 0.3 μg/kg/min before running. Generally speaking, increased adrenal 17-OHCS secretion is related to exhaustion but not to exercise, its duration or intensity. {Endocrinology 80: 1148, 1967)

On the Mechanism of Stimulatory Action of Histamine upon the Adrenal 17-Hydroxycorticosteroid Secretion in the Dog

Under sodium pentobarbital anesthesia adrenal venous blood was collected from intact, bilaterally splanchnicotomized and hypophysectomized dogs and was analyzed for 17-hydroxycorticosteroids (17-OHCS). Adrenal 17-OHCS secre-tion in response to histamine in intact dogs anesthetized with pentobarbital was not different from that in conscious ones. Section of the splanchnic nerves did not alter the adrenocortical secretion response to histamine, whereas hypo-physectomy abolished or markedly depressed the 17-OHCS secretion response. These results suggest that the adrenal 17-OHCS secretion in response to histamine in the dog is mainly mediated through pituitary adrenocorticotrophin release and it is due neither to psychic excitement producible by histamine administration nor to adrenomedullary hormone release.

Effects of atropine, eserine and tetramethylammonium on the adrenal 17-hydroxycorticosteroid secretion in anesthetized dogs.

Effects of atropine, eserine and tetramethylammonium (TMA) on the adrenal 17-hydroxycorticosteroid (17-OHCS) secretion in dogs anesthetized with sodium pentobarbital were directly evaluated. Atropine, eserine or TMA was administered intravenously. Eserine (0.3mg/kg of body-wt.) produced a marked increase in 17-OHCS secretion and the maximal secretion rate was mostly observed at 10min after injection. TMA (1.0mg/kg) induced also a definite increase in adrenal 17-OHCS secretion, the maximal secretion rate being observed at 5 or 10min after administration. Atropine (1.0mg/kg) which had been proved to produce a marked increase in 17-OHCS secretion in conscious dogs had no effects on the secretion of 17-OHCS in dogs anesthetized with sodium pentobarbital.

Adrenal 17-hydroxycorticosteroid secretion in response to alloxan in unanaesthetized dogs.

Adrenal 17-hydroxycorticosteroid secretion in response to alloxan in unanaesthetized dogs.

Adrenal 17-hydroxycorticosteroid secretion in response to cyanide anoxia.

Adrenal venous blood samples were collected from conscious dogs and analysed for 17-hydroxycorticosteroids (17-OHCS) and catechol amines. Potassium cyanide was administered subcutaneously in doses of 1.0–4.0 mg/kg. The pre-injection secretion rates of 17-OHCS per gland were 0.02–0.26 μg/kg/min. In all the experiments, the 17-OHCS secretion rates increased after cyanide injection to maximal values of 0.60–1.55 μg/kg/min. After injection of 1.0–3.0 mg/kg cyanide, the adrenal medullary secretion rates remained unchanged. Dogs given 4.0 mg/kg cyanide had elevated adrenal medullary secretion rates when anoxic symptoms, such as convulsions, were manifested. The present findings suggest that adrenal cortical response is more sensitive than adrenal medullary response to cyanide anoxia.

Effect of spinal cord transection on adrenal 17-hydroxycorticosteroid secretion in response to insulin hypoglycaemia.

ADRENAL 17-hydroxycorticosteroid (17-OHCS) secretion in response to insulin hypoglycaemia has been evaluated directly in anaesthetized1 and unanaesthetized2 dogs. As to the mechanism of insulin-induced adrenocortical secretion, Dury3 suggested from his experimental results that insulin hypoglycaemia resulted in an increase in adrenal medullary secretion, which induced the release of adrenocortical hormones. On the other hand, it was claimed by some authors that insulin-induced adrenocortical secretion was not dependent on the sympathoadreno-medullary activity4–6. In the experiments of Egdahl7 the adrenal medullary response to E. coli endotoxin was found to be abolished by the transection of the spinal cord at C7 and the adrenal 17-OHCS secretion in response to endotoxin was not affected by the spinal cord transection. He suggested that the adrenal cortical response to endotoxin was not dependent on the activity of the sympatho-adrenomedullary system. Thus it seems of interest to evaluate directly the adrenal 17-OHCS secretion in response to insulin in cord-sectioned dogs.

Effect of tetramethylammonium and potassium chloride on adrenal 17-hydroxycorticosteroid secretion in unanesthetized dogs.

Adrenal 17-hydroxycorticosteroid (17-OHCS) secretion was followed after injection of tetramethylammonium or potassium chloride. In unanesthetized dogs the adrenal venous blood was collected by a modification of the method of Satake and his co-workers and was analyzed for 17-OHCS by the method of Nelson and Samuels. The 17-OHCS secretion rate before injection was 0.03-0.29μg/kg/min. After injection of tetramethylammonium it increased markedly in all of 3 dogs and attained to 1.10-1.43μg/kg/min. After injection of potassium chloride it increased definitely in 2 of 3 dogs and attained to 1.14-1.73μg/kg/min.

INHIBITORY EFFECT OF PRE-OPTIC STIMULATION ON ADRENAL 17-HYDROXYCORTICOSTEROID SECRETION RATE IN THE CAT.

IN diencephalic stimulation experiments of Suzuki et al.1 a definite decrease in 17-hydroxycorticosteroid (17-OHCS) secretion rate was observed in one dog after stimulation of the pre-optic area. Similar observation was made in one cat with encephale isole by Slusher and Hyde2. These observations suggested a possible inhibitory effect of preoptic stimulation on the pituitary-adrenocortical function. However, since they were made only on one dog and on one cat, many more experiments seem to be necessary before this problem can be settled. The present investigation was undertaken in order to settle this problem.

Effect of sodium pentobarbital and sodium hexobarbital anesthesia on the adrenal 17-hydroxycorticosteroid secretion rate in the dog.

Pre-injection samples of adrenal venous blood were taken in unanesthetized dogs. Intravenous injection of sodium hexobarbital or sodium pentobarbital was then made. The animals were deeply anesthetized. After injection of barbiturate blood samples were also taken with intervals. The adrenal venous plasma was analyzed for 17-hydroxycorticosteroids. The secretion rate of 17-hydroxycorticosteroids was found to decrease definitely after barbiturate injection when simultaneous abdominal surgery was avoided.

Effect of morphine upon the adrenal 17-hydroxycorticosteroid secretion in the dog.

IT has been reported that morphine is a potent stimulus to the anterior pituitary–adrenal cortical system, as judged by indirect index such as depletion of adrenal ascorbic acid in rats1–3. However, little is known quantitatively of adrenal corticosteroid secretion in response to morphine. In the present investigation, experiments were carried out to evaluate directly the effect of morphine upon the secretion-rate of 17-hydroxycorticosteroids in dogs.

Muscular Exercise and Adrenal 17-Hydroxycorticosteroid Secretion in Dogs

EVIDENCE of increased adrenocortical secretory activity elicited by muscular exercise has been provided by indirect evaluations such as fall in ascorbic acid or cholesterol content of the adrenal gland1–3. However, no direct measurements of corticosteroid secretion in response to muscular exercise have been reported. The present studies were undertaken to evaluate quantitatively the effect of muscular exercise on adrenocortical activity by estimating directly the rate of secretion of adrenal 17-hydroxycorticosteroid in unanaesthetized dogs.

Effect of CO2 exposure and respiratory acidosis on adrenal 17-hydroxycorticosteroid secretion in anesthetized dogs.

Effect of CO2 exposure on adrenocortical function has been studied by measuring 17-hydroxycorticosteroids in adrenal venous blood of anesthetized dogs. In dogs exposed to 2.5%, 5% and 10% CO2 successively for 1 hour each, and 10%, 20% and 30% CO2 successively for 1 hour each, adrenocortical stimulation occurred in 10% of the total number of dogs exposed to 2.5% CO2, 40% of the animals exposed to 5% CO2, 75% of dogs exposed to 10% CO2 and in all dogs subjected to 20% and 30% CO2. Exposure to increasing concentrations of CO2 was accompanied by a progressively severe respiratory acidosis. Dogs exposed to 20% CO2 for 4 hours displayed a maximal adrenocortical stimulation within the first 15–30 minutes, and this marked response persisted for the remainder of the exposure period. The adrenocortical stimulatory response to 20% CO2 exposure is abolished by hypophysectomy. It is concluded that the pituitary adrenal stimulation occurring in anesthetized dogs exposed to CO2 is induced by one or more of the physiologic alterations attendant respiratory acidosis.

Effect of acute hyperthermia on adrenal 17-hydroxycorticosteroid secretion in dogs.

Effect of acute hyperthermia on adrenocortical function has been studied by measuring 17-hydroxycorticosteroids in adrenal venous blood of anesthetized dogs. Dogs immersed to the shoulders in 50°C water respond initially with a rapid increase in rectal temperature (42°C in 15–20 min.), a marked (two to sevenfold) increase in adrenal corticoid output, and a slight (10–20%) increase in adrenal venous blood flow. When a rectal temperature of 44–45°C was attained, circulatory failure occurred and a concomitant decrease in adrenal corticoid output and venous blood flow ensued. Dogs subjected to a gradual increase in body temperature had increased adrenal 17-hydroxycorticosteroid secretion in the rectal temperature range of 39– 40°C, but this stimulatory response subsided as body temperature was further increased. Hypophysectomy abolished the adrenocortical response to hyperthermia, thus showing that the increased secretory activity of the adrenal cortex in hyperthermia is mediated via the pituitary gland.