Vascularization of the adrenal cortex: its possible involvement in the regulation of steroid hormone release

Bassett, J.R.; West, Sandra

doi:10.1002/(sici)1097-0029(19970315)36:6<546::aid-jemt11>3.0.co;2-o

Cited by 59 publications

(37 citation statements)

References 104 publications

(169 reference statements)

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“…There is a direct relationship between adrenal gland activity and increased gland weight (20). Hypertrophy and macroscopic hyperemia have been described in response to administration of ACTH, or following prolonged exposure to stress (20).…”

Section: Resultsmentioning

confidence: 99%

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Prolactin induces adrenal hypertrophy

Silva

Felício

Nasello

et al. 2004

Braz J Med Biol Res

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Although adrenocorticotropic hormone is generally considered to play a major role in the regulation of adrenal glucocorticoid secretion, several reports have suggested that other pituitary hormones (e.g., prolactin) also play a significant role in the regulation of adrenal function. The aim of the present study was to measure the adrenocortical cell area and to determine the effects of the transition from the prepubertal to the postpubertal period on the hyperprolactinemic state induced by domperidone (4.0 mg kg -1 day -1 , sc). In hyperprolactinemic adult and young rats, the adrenals were heavier, as determined at necropsy, than in the respective controls: adults (30 days: 0.16 ± 0.008 and 0.11 ± 0.007; 46 days: 0.17 ± 0.006 and 0.12 ± 0.008, and 61 days: 0.17 ± 0.008 and 0.10 ± 0.004 mg for treated and control animals, respectively; P < 0.05), and young rats (30 days: 0.19 ± 0.003 and 0.16 ± 0.007, and 60 days: 0.16 ± 0.006 and 0.13 ± 0.009 mg; P < 0.05). We selected randomly a circular area in which we counted the nuclei of adrenocortical cells. The area of zona fasciculata cells was increased in hyperprolactinemic adult and young rats compared to controls: adults: (61 days: 524.90 ± 47.85 and 244.84 ± 9.03 µm 2 for treated and control animals, respectively; P < 0.05), and young rats: (15 days: 462.30 ± 16.24 and 414.28 ± 18.19; 60 days: 640.51 ± 12.91 and 480.24 ± 22.79 µm 2 ; P < 0.05). Based on these data we conclude that the increase in adrenal weight observed in the hyperprolactinemic animals may be due to prolactin-induced adrenocortical cell hypertrophy.

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Section: Resultsmentioning

confidence: 99%

“…Hypertrophy and macroscopic hyperemia have been described in response to administration of ACTH, or following prolonged exposure to stress (20).…”

Section: Resultsmentioning

confidence: 99%

Prolactin induces adrenal hypertrophy

Silva

Felício

Nasello

et al. 2004

Braz J Med Biol Res

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“…PRL-R mRNA has been detected in both the adrenal cortex and medulla of many species [7,[11][12][13]. Adrenal sensitivity to ACTH is regulated by adrenal innervation (for example, splanchnic nerve stimulation) with the subsequent release of catecholamines and vasoactive neuropeptides that affect adrenal blood flow and hence, increase the presentation of ACTH to the steroidogenic cells of the adrenal cortex and result in an increase of corticosterone release [50][51][52][53][54][55][56][57][58]. Indeed, while accumulated evidence shows the effect of PRL on adrenal innervation remains controversial, the physiological role of PRL, whether circulating or intraadrenal, in this interplay requires further investigation.…”

Section: Discussionmentioning

confidence: 99%

Physiological Roles of Prolactin in the Adrenocortical Response to Acute Restraint Stress

et al. 2007

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Abstract. The present study characterized the different hormonal responses to stress in the endocrine milieu with different circulating levels of prolactin (PRL) and examined the direct effects of PRL on adrenal steroidogenic responses to adrenocorticotropic hormone (ACTH) using experimentally induced hyperprolactinemia and hypoprolactinemia male rat models. Hyperprolactinemia was induced by transplantation of two adult female rat anterior pituitary glands under the kidney capsule for 2 weeks, and hypoprolactinemia was induced by daily subcutaneous injection of 2-Bromo-alphaErgocryptine (CB-154) for 2 weeks. Under stress conditions, the peak levels of ACTH were significantly higher in hypoprolactinemia than normal rats. Meanwhile, the peak levels of corticosterone and progesterone were significantly higher in hyperprolactinemia than in normal and hypoprolactinemia stressed rats. Results of in vitro experiments showed that adrenocortical cells in hyperprolactinemia exhibited higher basal levels of corticosterone and progesterone rats than normal and hypoprolactinemia rats. The stimulatory effect of ACTH on corticosterone and progesterone release was higher in hyperprolactinemia than hypoprolactinemia rats. In addition, PRL increased the stimulatory effect of ACTHinduced corticosterone secretion in all rat models. These results suggest that hypoprolactinemia and hyperprolactinemia rats exhibit marked differences in the response of their hypothalamic-pituitary-adrenal (HPA) axis during acute restrain stress. Additionally, these studies emphasize that the adrenal cortex might be more sensitive to ACTH stimulation in endocrine milieu with high levels of PRL resulting in high corticosterone and progesterone release.

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“…29 An additional level of regulation results from the interchange and cross-talk between the adrenal vasculature and steroidogenic cells. Relaxing factor(s) released by the cortical steroidogenic cells influence cortical arterial tone.…”

Section: Perspectivesmentioning

confidence: 99%

Angiotensin II Relaxations of Bovine Adrenal Cortical Arteries

et al. 2008

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Abstract-Angiotensin (Ang) II regulates adrenal steroidogenesis and adrenal cortical arterial tone. Vascular metabolism could decrease Ang II concentrations and produce metabolites with vascular activity. Our goals were to study adrenal artery Ang II metabolism and to characterize metabolite vascular activity. Bovine adrenal cortical arteries were incubated with Ang II (100 nmol/L) for 10 and 30 minutes. Metabolites were analyzed by mass spectrometry. Ang (1-7), Ang III, and Ang IV concentrations were 146Ϯ21, 173Ϯ42 and 58Ϯ11 pg/mg at 10 minutes and 845Ϯ163, 70Ϯ14, and 31Ϯ3 pg/mg at 30 minutes, respectively. Concentration-related relaxations of U46619-preconstricted cortical arteries to Ang II (maximum relaxationϭ29Ϯ3%; EC 50 ϭ3.4 pmol/L) were eliminated by endothelium removal and inhibited by the NO synthase inhibitor, nitro-L-arginine (30 mol/L; maximum relaxationϭ14Ϯ7%). Ang II relaxations were enhanced by the angiotensin type-1 receptor antagonist losartan (1 mol/L; maximum relaxationϭ41Ϯ3%; EC 50 ϭ11 pmol/L). Losartan-enhanced Ang II relaxations were inhibited by nitro-L-arginine (maximum relaxationϭ18Ϯ5%) and the angiotensin type-2 receptor antagonist PD123319 (10 mol/L; maximum relaxationϭ27Ϯ5%). Ang (1-7) and Ang III caused concentration-related relaxations with less potency (EC 50 ϭ43 and 24 nmol/L, respectively) but similar efficacy (maximum relaxationsϭ39Ϯ3% and 48Ϯ5%, respectively) as losartan-enhanced Ang II relaxations. Ang (1-7) relaxations were inhibited by nitro-L-arginine (maximum relaxationϭ16Ϯ4%) and the Ang (1-7) receptor antagonist 7 D -Ala-Ang (1-7) (1 mol/L; maximum relaxationϭ10Ϯ3%) and eliminated by endothelium removal. Thus, Ang II metabolism by adrenal cortical arteries to metabolites with decreased vascular activity represents an inactivation pathway possibly decreasing Ang II presentation to adrenal steroidogenic cells and limits Ang II vascular effects.

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Vascularization of the adrenal cortex: its possible involvement in the regulation of steroid hormone release

Cited by 59 publications

References 104 publications

Prolactin induces adrenal hypertrophy

Prolactin induces adrenal hypertrophy

Physiological Roles of Prolactin in the Adrenocortical Response to Acute Restraint Stress

Angiotensin II Relaxations of Bovine Adrenal Cortical Arteries

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