The mammalian adrenal circulation and the relationship between adrenal blood flow and steroidogenesis

Vinson, G. P.; Pudney, Jeffrey; Whitehouse, B. J.

doi:10.1677/joe.0.1050285

Cited by 105 publications

(73 citation statements)

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“…This factor has been named endothelium-derived steroidogenic factor (EDSF) and is a peptide discrete from endothelin-1 (ET-1), bradykinin (BK), angiotensin II (AII), and ACTH (2). The adrenal cortex is highly vascularized, with steroidogenic cells surrounding arterioles, capillaries, and sinusoids (3,4). As a result, there is a close anatomical association of steroidogenic cells such as ZG cells with ECs (3,4).…”

Section: E Ndothelial Cells (Ecs) Release a Factor That Stim-mentioning

confidence: 99%

“…The adrenal cortex is highly vascularized, with steroidogenic cells surrounding arterioles, capillaries, and sinusoids (3,4). As a result, there is a close anatomical association of steroidogenic cells such as ZG cells with ECs (3,4). This close relationship suggests a role for EDSF in the paracrine regulation of aldosterone release.…”

Section: E Ndothelial Cells (Ecs) Release a Factor That Stim-mentioning

confidence: 99%

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Endothelium-Derived Steroidogenic Factor Enhances Angiotensin II-Stimulated Aldosterone Release by Bovine Zona Glomerulosa Cells

Hanke¹,

Holmes²,

Xu³

et al. 2007

Endocrinology

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Section: E Ndothelial Cells (Ecs) Release a Factor That Stim-mentioning

confidence: 99%

Section: E Ndothelial Cells (Ecs) Release a Factor That Stim-mentioning

confidence: 99%

Endothelium-Derived Steroidogenic Factor Enhances Angiotensin II-Stimulated Aldosterone Release by Bovine Zona Glomerulosa Cells

Hanke¹,

Holmes²,

Xu³

et al. 2007

Endocrinology

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“…Regardless of the specific expression of NOS within the ZG cell, the close association of microvascular and capillary endothelial cells and other potential NO-producing cell types suggests that NO may be produced in close proximity to ZG cells and may affect ZG steroidogenesis. 18 Measurements of nitrate/nitrite as stable metabolites of NO 22 were used to confirm eNOS enzymatic activity after AdeNOS gene transfer. DAF-2 was recently described as a selective fluorescent probe for the detection of NO.…”

Section: Discussionmentioning

confidence: 99%

“…The close association of these cells with ZG cells in the intact adrenal gland suggests that they may be a prominent source of ZG cell NO. 18 The results of recent studies have indicated the presence of eNOS in ZG cells of the rat and humans and a currently unidentified form of NOS in rat zona fasciculata cells. 2,17 However, workers at our laboratory have not been able to detect eNOS in bovine ZG cells through the use of Western immunoblotting or enzymatic activity assays.…”

mentioning

confidence: 99%

Inhibition of Adrenal Cell Aldosterone Synthesis by Endogenous Nitric Oxide Release

et al. 2000

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Abstract-Adrenal zona glomerulosa (ZG) cells do not contain nitric oxide (NO) synthase (NOS).Key Words: nitric oxide Ⅲ aldosterone Ⅲ adrenal glands Ⅲ adenovirus Ⅲ nitric oxide synthase Ⅲ zona glomerulosa N itric oxide (NO) derived from NO donors inhibits aldosterone synthesis in adrenal zona glomerulosa (ZG) cells from bovine, rat, and human adrenal glands. 1-3 NOmediated inhibition occurs in ZG cells stimulated with angiotensin II (Ang II), adrenocorticotropic hormone, and potassium ion, as well as with the steroidogenic substrates 25-hydroxycholesterol and progesterone. 2,3 NO stimulates the accumulation of cGMP in adrenal ZG cells; however, this appears to be unrelated to NO-mediated inhibition of aldosterone release. 3 The mechanism of inhibition appears to occur primarily via direct interaction of NO with cytochrome P450 enzymes of the steroidogenic pathway. 3 The results of studies of the effects of NO on other steroidogenic cell types indicate that the inhibitory effects are not limited to aldosterone. NO inhibits the synthesis of testosterone in rat Leydig cells and the synthesis of corticosterone in rat adrenal zona fasciculata cells. 4 -8 Thus, it appears likely that the inhibitory effects of NO may be seen in a variety of cells containing steroidogenic cytochrome P450 enzymes. Studies of the biochemical interactions between NO and various cytochrome P450 enzymes have clearly demonstrated the ability of NO to rapidly bind the heme portion of the cytochrome P450 enzyme. 9,10 This binding process inactivates the enzyme by preventing binding to oxygen. 11 Raman spectrophotometric analysis of the cytochrome P450/NO interaction suggests that there may be 2 phases to the inhibition by NO. The first phase involves a rapid occupation of the heme group by NO and results in a reversible inhibition of enzymatic activity. After a 2-hour exposure to NO, a second phase of inhibition appears, which likely involves the nitrosylation of a tyrosine of the cytochrome P450 enzyme. 9,10 This second phase results in irreversible inhibition of enzymatic activity.Determination of the physiological role of NO in aldosterone synthesis is complicated by the interactions of vasodilatory effects of NO with the regulatory pathways that stimulate aldosterone synthesis. The administration of NO donors such as sodium nitroprusside and nitroglycerin has long been recognized to dramatically lower blood pressure. Conversely, the inhibition of endogenous NO production through the use of NO synthase (NOS) inhibitors increases blood pressure. 12 The effects of these manipulations on plasma aldosterone concentrations have produced conflicting results. Usui et al 13 demonstrated an increase in plasma aldosterone concentrations and ZG cell angiotensin II type 1 (AT 1 ) receptor expression in rats after NOS inhibition

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“…Endothelial cells have a close anatomical proximity to steroidogenic cells in the adrenal cortex (24). As endothelial cells release NO, and NO stimulates guanylyl cyclase, we tested the hypothesis that NO inhibits steroidogenesis through the activation of guanylyl cyclase.…”

Section: Discussionmentioning

confidence: 99%

Nitric Oxide Inhibits Aldosterone Synthesis by a Guanylyl Cyclase-Independent Effect**This work was supported by grants from the NHLBI (HL-52159 and HL-54717).

et al. 1998

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To investigate the mechanism of nitric oxide (NO) inhibition of aldosterone release, this study compared the effects of type A natriuretic peptide and heat-stable enterotoxin to a nitric oxide donor, deta nonoate, on cGMP production and angiotensin II-stimulated aldosterone synthesis in primary cultures of bovine adrenal zona glomerulosa cells. Type A natriuretic peptide (10 Ϫ10 -10 Ϫ6 M) and deta nonoate (10 Ϫ6-10 Ϫ3 M) stimulated concentration-related increases in cGMP production. Heat-stable enterotoxin (10 Ϫ6 M) failed to stimulate cGMP synthesis in zona glomerulosa cells. Type A natriuretic peptide and deta nonoate attenuated angiotensin II-stimulated aldosterone production over the same concentration range that stimulated cGMP production. Heat-stable enterotoxin (10 Ϫ6 M) was without effect on aldosterone release. To further test the hypothesis that cGMP mediated the inhibition of aldosterone synthesis, the selective inhibitor of soluble guanylyl cyclase, 1H-(1,2,4)oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) was used. ODQ pretreatment (10 Ϫ5 M) completely prevented deta nonoate-stimulated cGMP production without altering the inhibitory effect of deta nonoate on angiotensin II-stimulated steroidogenesis. Consistent with its selectivity for inhibiting soluble guanylyl cyclase, ODQ did not block type A natriuretic peptide-stimulated cGMP synthesis or type A natriuretic peptide inhibition of steroidogenesis. Deta nonoate completely blocked 25-hydroxycholesterol-and progesterone-stimulated aldosterone synthesis in zona glomerulosa cells and inhibited the conversion of 25-hydroxycholesterol to pregnenolone in mitochondrial fractions from bovine adrenal cortex. Deta nonoate-derived NO gave an absorbance maximum of the mitochondrial cytochrome P450 of 453 nm and inhibited the absorbance at 450 nm caused by carbon monoxide binding to the enzyme. These results suggest that deta nonoate reduces steroidogenesis independent of guanylyl cyclase activation and that NO has a direct effect to inhibit the activity of cytochrome P450, probably by binding to the heme groups of the cytochrome. (Endocrinology 139: [4053][4054][4055][4056][4057][4058][4059][4060] 1998) S INCE the discovery (1, 2) of type A natriuretic peptide and the realization that endothelium-derived relaxing factor is nitric oxide (NO) (3, 4), several studies have focused on determining the mechanisms by which these agents mediate similar activities in various biological systems. The receptors for both type A natriuretic peptide and NO are related forms of the guanylyl cyclase enzyme (5, 6). NO activates the soluble or cytosolic forms of the enzyme (7, 8). Type A natriuretic peptide, type B natriuretic peptide, and type C natriuretic peptide bind to the particulate forms of this enzyme family, referred to as guanylyl cyclase A and guanylyl cyclase B. The guanylyl cyclase C enzyme is found in the intestine and is a receptor for heat-stable enterotoxin (9) and a family of endogenous peptides called guanylins (10).It is well established that the natriure...

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The mammalian adrenal circulation and the relationship between adrenal blood flow and steroidogenesis

Cited by 105 publications

References 0 publications

Endothelium-Derived Steroidogenic Factor Enhances Angiotensin II-Stimulated Aldosterone Release by Bovine Zona Glomerulosa Cells

Endothelium-Derived Steroidogenic Factor Enhances Angiotensin II-Stimulated Aldosterone Release by Bovine Zona Glomerulosa Cells

Inhibition of Adrenal Cell Aldosterone Synthesis by Endogenous Nitric Oxide Release

Nitric Oxide Inhibits Aldosterone Synthesis by a Guanylyl Cyclase-Independent Effect**This work was supported by grants from the NHLBI (HL-52159 and HL-54717).

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