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M F Dallman

Publications and source records attributed to M F Dallman.

177 records · Page 10Linked to original sources
PubMed1976

Compensatory adrenal growth: a neurally mediated reflex.

The responses of young rats to left adrenalectomy or left adrenal manipulation were compared to surgical sham adrenalectomy in which adrenals were observed but not touched. At 12 h right adrenal wet weight, dry weight, DNA, RNA, and protein content were increased (P less than 0.05) after the first two operations. Left adrenal manipulation resulted in increased right adrenal weight at 12 h but no change in left adrenal weight. Sequential manipulation of the left adrenal at time 0 and the right adreanl at 12 h resulted in an enlarged right adrenal at 12h (P less than 0.01), and an enlarged left adrenal at 24 h (P less than 0.05), showing that the manipulated gland was capable of response. Bilateral adrenal manipulation of the adrenal glands resulted in bilateral enlargement at 12 h (P less than 0.01). Taken together with previous results, these findings strongly suggest that compensatory adrenal growth is a neurally mediated reflex.

Adrenal Glands↗
PubMed1976

Neural mediation of compensatory adrenal growth.

Spinal cord hemisection between T2 and T3 inhibits compensatory adrenal growth when the contralateral but not the ipsilateral adrenal is removed (p less than 0.01). Pretreatment of left adrenals with 1 or 2% lidocaine, but not with saline, before removal inhibits compensatory right adrenal growth that is normally observed at 12 h (p less than 0.01). These results provide further functional evidence that both afferent and efferent neural elements mediate adrenal growth after unilateral adrenalectomy.

Adrenal Glands↗
PubMed1975

Corticosteroids and ACTH are not required for compensatory adrenal growth.

We have tested the hypothesis that unilateral adrenalectomy results in decreased glucocorticoid secretion, reflexly elevated ACTH secretion, and consequently, compensatory adrenal growth. Plasma ACTH and corticosterone and right adrenal weight were measured during the first 10 days after left adrenalectomy or sham adrenalectomy in young male rats. There is a decrease in plasma corticosterone after unilateral adrenalectomy compared to sham adrenalectomy that persists for 1 h. ACTH is elevated only at 2 h after unilateral adrenalectomy compared to shamoperated rats. Treatment with dexamethasone, shown to abolish the ACTH and corticosterone responses to laparotomy with intestinal traction, resulted in significantly increased adrenal weight after unilateral adrenalectomy by 6 h (wet or dry weight), and at 24 h. Compensatory adrenal growth also occurs after unilateral adrenalectomy in hypophysectomized rats (wet or dry weight). We conclude the compensatory adrenal growth after unilateral adrenalectomy requires neither a virtual decrease in circulating corticosterone levels nor elevated ACTH levels, and speculate that the phenomenon is neurally mediated.

Adaptation, Physiological↗
PubMed1975

Compensatory adrenal growth is neurally mediated.

We have tested the possibility that compensatory adrenal growth is neurally mediated. Small unilateral electrolytic lesions were made in the ventral hypothalamus of young male rats. Subsequently, unilateral adrenalectomy was performed on the side ipsilateral or contralateral to the hypothalamic lesion. Four days later the animals were killed and the remaining adrenal was weighed; the location and extent of the hypothalamic lesions were determined. Lesions placed on the same side as adrenalectomy prevented compensatory growth of the remaining gland (p less than 0.005), while lesions on the side opposite to the removed adrenal did not interfere with compensatory adrenal growth. We conclude from these findings, and from a review of some anatomical studies, that compensatory adrenal growth is effected through a reflex that involves both afferent and efferent neural limbs.

Adrenal Glands↗
PubMed1975

Corticosterone-induced changes in hypothalamic corticotropin-releasing factor (CRF) content after stress.

Central and peripheral humoral responses of the adrenocortical system were measured for 2 h after the application of several stimuli. Two min after the onset of the stresses of sham-adrenalectomy or laparotomy with intestinal traction there was a 4-6 fold increase in hypothalamic CRF content as compared to control content, This is the usual CRF response to stress. In contrast, after adrenalectomy or manipulation of the pedicles of adrenal glands; CRF content at 2 min was only slightly increased above baseline values. This finding suggests that touching the adrenal vascular and nervous supply results in a direct neural input to the hypothalamus that is qualitatively different from most other stimuli. At times later than 2 min after stress, whem plasma corticosterone levels rise in the intact rat, the patterns of CRF and ACTH responses that were observed after adrenalectomy were determined by whether corticosterone replacement therapy was given. Without corticosterone replacement, the CRF and ACTH responses to adrenalectomy resembled those of laparotomy with intestinal traction. When corticosterone was administered 2 and 40 min after adrenalectomy, the CRF and ACTH responses resembled those of sham-adrenalectomy. At 20 min, CRF content was low after laparotomy with intestinal traction or adrenalectomy and high after shan-adrenalectomy or adrenalectomy with corticosterone replacement. Plasma ACTH peaked by 20 min, and remained high for 2 h after the first 2 stimuli, and was significantly decreased from the 20 min peak by 40 min after application of the latter stimuli. CRF content increased to a second peak 80 min after laparotomy with intestinal traction or adrenalectomy. This rise in CRF must represent increased formation of the releasing factor because ACTH levels were elevated and constant for the preceding 60 min. After sham-adrenalectomy or adrenalectomy with corticosterone replacement, CRF content and ACTH are low at 80 min. Measurement of circulating ACTH levels in conjunction with CRF content after these stimuli have yielded sufficient information to assign mechanisms of altered synthesis and secretion to explain the observed changes in CRF content. Corticosterone damps the adrenocortical system response to the stimuli of sham-adrenalectomy or adrenalectomy with corticosterone replacement by two mechanisms. Firstly, it acts to inhibit CRF secretion probably via rate-sensitive feedback. Secondly, it acts to inhibit the second wave of CRF formation that is observed 80 min after stress is applied, probably via the proportional feedback mechanism.

Adrenal Glands↗
PubMedDate not supplied

Control of adrenocortical growth in vivo.

Adrenocortical growth is discussed with respect to its relation to body weight, elevated ACTH (provoked by sustained stress, adrenal enzyme deficiency, and adrenal enucleation), and unilateral adrenalectomy. It seems likely that these three conditions under which adrenal growth occurs are each controlled and mediated by different agents. Least is known about the growth of adrenals with the growth of the organism; however, because treatment with growth hormone is known to stimulate adrenal mitogenesis, and because adrenals grow in proportion to body growth by increasing cell number, it is proposed that this growth may be mediated by growth hormone (via somatomedin). ACTH causes primarily adrenocortical cellular hypertrophy which is subsequently followed by hyperplasia. It has been shown that the application of a sustained stressor, induction of adrenal enzyme deficiency and adrenal enucleation all result in persistent elevation in circulating ACTH levels and adrenal growth. It appears that the stimulus to ACTH secretion is a virtual or real decrease in corticosteroid feedback signal, and that ACTH secretion is regulated by corticosteroid levels. An additional humoral factor may be triggered by adrenal enucleation, and the possibility that a fragment of the N-terminal peptide of the ACTH precursor molecule plays this role is entertained. Finally, the evidence that the proliferative adrenal growth after unilateral adrenalectomy is mediated by afferent and crossed efferent neural pathways, and is regulated by aldosterone, pineal peptides and exposure to constant light is discussed.

Adrenal Cortex↗