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SUMMARY
Corticotrophin (ACTH) release induced by stressful stimuli has been studied in rats with completely deafferentated medial basal hypothalamus (MBH) pituitary islands or median eminence (ME)-stalk pituitary islands. The plasma corticosterone level was used as index of ACTH release.
In rats with MBH pituitary islands, capsaicin failed to raise the plasma corticosterone level, but the intraperitoneal administration of E. coli endotoxin, histamine, insulin or a large subcutaneous dose of formaldehyde caused ACTH release which could not be distinguished from that in the controls. Histamine and insulin induced ACTH release even in rats with a ME-stalk pituitary island.
It is suggested that E. coli endotoxin, histamine, insulin hypoglycaemia and large doses of formaldehyde may be classified as 'humoral' stimuli of ACTH release, since a neural afferent input to the MBH is not essential for their action. On the other hand, the integrity of some neural pathways to the MBH is essential for the ACTH-releasing effect of capsaicin.
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The activity of corticotrophin releasing factor (CRF) in extracts of the stalk median eminence (SME) complex proper (average protein content, 30·6 μg) of male rats was assayed by monolayer cultures of anterior pituitary cells using the release of immunoreactive ACTH. Extracts which were equivalent to 0·025 SME of control rats usually had detectable CRF activity, while there was no detectable activity in extracts of 0·4 SME equiv. taken 8 days after complete surgical isolation of the medial basal hypothalamus (MBH). The activity of CRF in extracts from rats with an anterolateral cut around the MBH was at least ten times less than that in the control rats. One day after placing an anterolateral cut around the MBH the ACTH releasing activity of the SME was not significantly different from that of the control animals but activity decreased significantly 3 days after the operation and was at least ten times less than in the control animals on day 7 after the operation.
It is suggested that most of the CRF activity of the SME is contained in nerve fibres entering the neurohaemal region from outside the MBH and that transection of these fibres produced the fall in CRF content of the SME in rats with partial or total surgical isolation of the MBH.
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SUMMARY
Corticotrophin (ACTH) release induced by various stressful stimuli has been studied in rats with antero-lateral deafferentation of the medial basal hypothalamus (MBH). The plasma corticosterone level was determined as an index of ACTH release.
In rats with antero-lateral deafferentation of the MBH, ACTH release was prevented after exposure to noise and vibration, sham adrenalectomy and s.c. injection of 1% formalin. ACTH release induced by the injection of histamine (1 mg./100 g., i.p.) and capsaicin (0·25 mg./100 g., s.c.) was significantly less than in the controls. Escherichia coli lipopolysaccharide (25 μg./100 g., i.p.) induced an ACTH release that could not be distinguished from that in the controls.
We suggest that (a) noise and vibration, sham adrenalectomy and injection of 1% formalin trigger ACTH release through neural pathways arriving at the MBH from anterior, lateral and dorsal directions, (b) histamine or capsaicin releases ACTH partly through antero-lateral neural afferents to the MBH. In contrast, the ACTH-releasing stimulus of bacterial endotoxin injection reaches the hypothalamo—hypophysial unit by humoral pathways and/or posterior nerve fibres.
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SUMMARY
Hypophysectomy abolishes the aldosterone secretory response to sodium deficiency in rats. Sodium deficiency causes a significant increase in plasma renin activity in chronically hypophysectomized rats which is of the same order as that found in intact animals.
Long-term treatment with either adrenal maintenance doses of corticotrophin (ACTH) or with growth hormone (STH) did not affect the low rate of aldosterone production of hypophysectomized rats on a sodium-deficient diet. However, ACTH and STH given simultaneously restored the aldosterone secretory response to sodium deficiency in chronically hypophysectomized rats.
The plasma renin activity of hypophysectomized rats on a sodium-deficient or a normal diet remained unaltered during treatment with either ACTH or STH or with the two hormones given simultaneously. This was also reflected in the systolic blood pressure of rats which, under the conditions used, did not change when the animals were sodium-deficient, or after hypophysectomy or hormone treatment.
These results indicate that the effect of STH, in restoring the aldosterone secretory response to sodium deficiency in the presence of adrenal maintenance doses of ACTH in chronically hypophysectomized rats, is independent of changes in the renin-angiotensin system.
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SUMMARY
Daily administration of growth hormone (STH) to hypophysectomized rats treated with adrenal maintenance doses of corticotrophin restored the aldosterone secretory response (as measured by the synthetic capacity of the adrenal in vitro) to sodium restriction. Treatment with STH for the first 2 days after hypophysectomy or on the 7th day after hypophysectomy failed, but treatment during the 6th and 7th day after hypophysectomy with 100, 200 or 400 μg STH/day restored the aldosterone secretory response to sodium deprivation in a dose-dependent manner.
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SUMMARY
The rate of aldosterone production in vitro by adrenal glands from rats hypophysectomized 7 days previously, treated with corticotrophin (ACTH) and subjected to dietary sodium restriction for 2 weeks, was decreased 6 h after nephrectomy. However, 18 h and 48 h after nephrectomy there was a marked increase in the rate of aldosterone production in vitro. In addition there was a rise in the plasma potassium concentration. These results indicated that in order to detect whether the influence of growth hormone on aldosterone secretory response to sodium restriction in hypophysectomized rats was mediated by the kidney, studies had to be performed within 6 h after removal of the kidneys.
Since the effect of growth hormone on aldosterone production requires 2 days to develop (Palkovits, de Jong, van der Wal & de Wied, 1971), rats hypophysectomized 54 h previously were used. The kidneys were removed 6 h before decapitation. In these animals, the administration of growth hormone in the presence of ACTH restored the aldosterone secretory response to sodium deficiency.
The results suggest that growth hormone maintains the aldosterone secretory response to sodium restriction in hypophysectomized rats in the absence of the kidneys.
