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The pituitary-adrenal and gonadal responses following stress were evaluated in the squirrel monkey. Plasma levels of cortisol (CS), ACTH and testosterone (T) were determined during a 4-h period following the combined stress of capture and ether anesthesia. The results indicated that the squirrel monkey manifests higher basal levels of steroids than typically found in other mammals. The endocrine response following stress was biphasic, involving an initial elevation and subsequent decline in hormone levels. Males manifested significantly higher plasma levels of CS and T and lower plasma levels of ACTH than did females.

Slow infusions (7.5 μl/min) of hypertonic NaCl into the 3rd brain ventricle of goats maintained on a NaCl‐supplemented diet provoked natriuresis reaching maximum about 70 min after onset of the infusions. The natriuresis was less pronounced in animals receiving no dietary NaCl‐supplementation. The magnitude of the natriuretic response was dependent on the molarity of the NaCl infused and on infusion duration. A much smaller relative increase in K excretion, reaching peak values 20 min before maximum natriuresis, also occurred. Aldosterone treatment did not prevent the natriuretic response and it could be elicited in diabetes insipidus animals, showing that release of posterior pituitary hormones was not essential. Determinations of inulin clearance (CIn) indicated that glomerular filtration rat (GFR) increased and that relative reabsorption of Na+ decreased during the natriuresis. Similar intraventricular infusions of hypertonic NH4Cl resulted in greatly diminished renal Na+ excretion lasting for about 2 hrs. Such infusions also delayed by 90 min the normal natriuretic response to an intravenous NaCl load. CIn determinations indicated that a diminished GFR may have contributed to this reduction in renal Na+ excretion. The results indicate that renal Na+ excretion is under hypothalamic control in the goat. Possible mechanisms for this control are discussed.

Intravenous angiotensin II and ether stress were found to produce a rapid, transient increase in the corticotropin-releasing hormone (CRH) content of the median eminence as measured by a radioimmunoassay employing an antibody against rat CRH(1–41). This confirms previous reports of transient increases in CRH measured by bioassay. The increase did not occur in the paraventricular region or in other parts of the brain. It occurred along with an increase in plasma adrenocorticotropic hormone (ACTH) when a second ether stress was administered 1 h after the first, and it also occurred when rats that had been adrenalectomized for 5 days were exposed to ether. The increases in CHR and the ACTH responses to ether were reduced or abolished by dexamethasone and pentobarbital. Four days after semicircular knife cuts in the posterior hypothalamus, resting CRH in the median eminence was increased but there was no further rise after ether stress. Plasma ACTH was normal at rest after the cuts, but the increase produced by ether was reduced. The ACTH responses to angiotensin II and immobilization were also reduced. Because the posterior knife cuts reduced hypothalamic catecholamine content, the effects of reducing hypothalamic norepinephrine and epinephrine by administration of the dopamine-β-hydroxylase inhibitor diethyldithiocarbamate (DDC) were tested. Five hours after DDC, plasma ACTH was elevated but there was no further increase with ether stress. The median eminence CRH content was normal but failed to increase after exposure to ether. The α₁-adrenergic-blocking drug, prazosin, did not affect the ACTH and median eminence CRH responses to ether, but the α₂-adrenergic-blocking drug, yohimbine, produced the same effects as DDC, i.e. elevated resting ACTH with no further increase following ether and a normal CRH content in the median eminence that failed to increase with ether. These results confirm the existence of a rapid, transient increase in the CRH content of the median eminence following stress and they show that stress fails to produce a similar change in other brain regions, that the increase is correleated with the occurrence of stress-induced increases in ACTH secretion, and that the increase does not occur when the ACTH response to stress is prevented. They also raise the possibility that neural pathways ascending in the brainstem are involved in the CRH and ACTH responses to ether and other stresses.

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