Zona glomerulosa of the adrenal gland in a transgenic strain of rat: a morphologic and functional study.
Transgenic rats for the murine Ren-2 gene display high blood pressure, low circulating levels of angiotensin II, and high renin content in the adrenal glands. Moreover, transgenic rats possess an increased aldosterone secretion (maximal from 6 to 18 weeks of age), paralleling the development of hypertension. To investigate further the cytophysiology of the adrenal glands of this strain of rats, we performed a combined morphometric and functional study of the zona glomerulosa of 10-week-old female transgenic rats. Morphometry did not reveal notable differences between zona glomerulosa cells of transgenic and age- and sex-matched Sprague-Dawley rats, with the exception of a marked accumulation of lipid droplets, in which cholesterol and cholesterol esters are stored. The volume of the lipid-droplet compartment underwent a significant decrease when transgenic rats were previously injected with angiotensin II or ACTH. Dispersed zona glomerulosa cells of transgenic rats showed a significantly higher basal aldosterone secretion, but their response to angiotensin II and ACTH was similar to that of Sprague-Dawley animals. Angiotensin II-receptor number and affinity were not dissimilar in zona glomerulosa cells of transgenic and Sprague-Dawley rats. These data suggest that the sustained stimulation of the adrenal renin-angiotensin system in transgenic animals causes an increase in the accumulation in zona glomerulosa cells of cholesterol available for steroidogenesis, as indicated by the expanded volume of the lipid-droplet compartment and the elevated basal steroidogenesis. However, the basal hyperfunction of the zona glomerulosa in transgenic animals does not appear to be coupled with an enhanced responsivity to its main secretagogues, at least in terms of aldosterone secretion.
Rocco
S
S
Department of Medical Semeiology, University of Padua, Italy.
Rebuffat
P
P
Cimolato
M
M
Opocher
G
G
Peters
J
J
Mazzocchi
G
G
Ganten
D
D
Mantero
F
F
Nussdorfer
G G
GG
D000324:Adrenocorticotropic Hormone / Q000494:pharmacology; D000450:Aldosterone / Q000378:metabolism; D000804:Angiotensin II / Q000172:deficiency / Q000494:pharmacology; D000818:Animals; D030801:Animals, Genetically Modified; D048429:Cell Size; D002784:Cholesterol / Q000032:analysis; D002788:Cholesterol Esters / Q000032:analysis; D005260:Female; D006929:Hyperaldosteronism / Q000150:complications / Q000235:genetics* / Q000473:pathology; D006973:Hypertension / Q000209:etiology*; D008297:Male; D051379:Mice / Q000235:genetics*; D051381:Rats / Q000033:anatomy & histology* / Q000502:physiology; D017207:Rats, Sprague-Dawley; D011945:Receptors, Angiotensin / Q000032:analysis; D012083:Renin / Q000378:metabolism*; D012084:Renin-Angiotensin System / Q000502:physiology*; D012636:Secretory Rate; D015384:Zona Glomerulosa / Q000737:chemistry / Q000378:metabolism / Q000473:pathology*
D002788:Cholesterol Esters; D011945:Receptors, Angiotensin; D000804:Angiotensin II; D000450:Aldosterone; D000324:Adrenocorticotropic Hormone; D002784:Cholesterol; D012083:Renin