Effects of Nitric Oxide on Aldosterone Synthesis and Nitric Oxide Synthase Activity in Glomerulosa Cells from Bovine Adrenal Gland

Sainz, Juan; Reche, Cecilia; Rábano, María A.; Mondillo, Carolina; Patrignani, Zoraida J.; Macarulla, J. M.; Pignataro, Omar Pedro; Trueba, Miguel

doi:10.1385/endo:24:1:061

Cited by 21 publications

(13 citation statements)

References 39 publications

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“…A similar trend was noted in adrenal cells from the control fetuses but was not significant. The effects of L-NAME on steroidogenesis in the present study are in agreement with the effects of NOS inhibition on aldosterone production in the adrenal 24, 44 and androgen in the testis 20. It has become clear that the extent of the effect of NO is probably dependent on species, tissue type, and physiological condition.…”

Section: Discussionsupporting

confidence: 89%

Nitric Oxide Inhibits ACTH-Induced Cortisol Production in Near-Term, Long-Term Hypoxic Ovine Fetal Adrenocortical Cells

et al. 2010

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We previously reported that in the sheep fetus, long term hypoxia (LTH) resulted in elevated basal plasma ACTH1–39 while cortisol levels were not different from normoxic controls. We also showed that LTH enhances endothelial nitric oxide synthase (eNOS) expression in the fetal adrenal. This study was designed to determine the effect of nitric oxide on cortisol production in adrenocortical cells from LTH fetal sheep. Ewes were maintained at high altitude (3,820 m) from ~40 days’ gestation (dG) to near term. Between 138–141 dG, fetal adrenal glands were collected from LTH and age-matched normoxic control fetuses. Adrenal cortical cells were pre-treated with sodium nitroprusside (SNP), L-NAME, L-arginine, or Diethyleneamine nitric oxide (DETA-NO) then challenged with 10nM ACTH. Cortisol responses were compared after 1 h. ACTH induced cortisol secretion was significantly higher in LTH vs. control (p<0.01). Enhancement of nitric oxide with L-arginine resulted in a significant reduction of ACTH-mediated cortisol production in the LTH group. DETA-NO also caused a significant decrease in ACTH-mediated cortisol production (p<0.05). Inhibition of NOS with L-NAME significantly increased cortisol production in the LTH group (p<0.05 compared to ACTH alone) while the effect on the control group was not significant. NOS activity was significantly higher in the LTH group compared to control but this difference was eliminated following ACTH treatment. These data indicate that LTH enhances adrenal cortical sensitivity to the inhibitory effects of NO on cortisol production. NO may therefore play an important role in regulating ACTH-induced cortisol production in the LTH fetal adrenal.

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Section: Discussionsupporting

confidence: 89%

Nitric Oxide Inhibits ACTH-Induced Cortisol Production in Near-Term, Long-Term Hypoxic Ovine Fetal Adrenocortical Cells

et al. 2010

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“…NOS activity is increased during stress and infection (Gadek-Michalska et al 2005, Monau et al 2009). Nitric oxide can regulate cortical and medullary adrenal gland functions such as the secretion of aldosterone (Sainz et al 2004) and corticosterone (Cymeryng et al 1998). In the present study, similar to cortisol concentration in group C, NO increased during 0.5 and 1 h but this increment was not statistically significant.…”

Section: Discussioncontrasting

confidence: 44%

Comparison of flunixin meglumine and meloxicam influence on postoperative and oxidative stress in ovariohysterectomized bitches

Yilmaz¹,

Korkmaz²,

Jaroszewski³

et al. 2014

Polish Journal of Veterinary Sciences

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The aim of this study was to compare the effect of flunixin meglumine (FM) and meloxicam (M) on postoperative and oxidative stress in ovariohysterectomized bitches. Twenty four bitches were divided into three groups (n=8 in each) and treated during premedication as follows: FM (2.2 mg/kg, iv, Fluvil, Vilsan, Turkey), M (0.2 mg/kg, sc, Maxicam, Sanovel, Turkey) or 0.9% saline (1 ml, iv, IE, Turkey) -control (C) group. The concentrations of serum cortisol, nitric oxide (NO), malondialdehyde (MDA), antioxidant potential (AOP) and glutation (GSH) were measured in blood samples collected during incision (0 h), closure of incision line (0.5 h) and 1, 2.5, 12 and 24 hours after incision. It was observed that cortisol level was higher at 0.5, 1 and 2.5 h in group C (p < 0.05), 0.5 h in group FM (p < 0.001), and 1 and 2.5 h in group M (p < 0.01), as compared to that determine at 0 h. Group C showed higher cortisol level during 0.5 h (p < 0.05) than that found in the other groups. Group FM displayed lower levels during 1 h (p < 0.01) and 2.5 h (p < 0.05) as compared to those observed in other groups. Concentrations of MDA, AOP and GSH between all the groups did not show any significant differences. MDA level was higher at 0.5 and 1 h in group M (p < 0.05) than that found in group C and it was the lowest at 2.5 h in group C (p < 0.05). AOP was higher at 2.5 h in group FM and M (p < 0.05) than that observed in group C, and at 12 and 24 h in group M than that found in group C and FM. GSH did not show any significant differences between the groups. NO level in group FM after 12 h was higher (p < 0.05) than that at 0.5, 1 and 24 h. Moreover, NO level was lower at 0.5 (p < 0.01), 1 (p < 0.05) and 24 h (p < 0.05) in group FM than that observed in group C and M. In conclusion, flunixin meglumine decreases cortisol and NO levels more efficiently than meloxicam. Therefore, it is suggested that postoperative stress following ovariohysterectomy may be prevented by flunixin meglumine in bitches.

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“…Conversely, nitric oxide inhibits the synthesis of aldo sterone in glomerulosa cells from bovine adrenal gland. 115 Thus, endothelial dysfunction could have a key role in inducing aldosterone breakthrough.…”

Section: Therapeutic Effects Of Ras Inhibitionmentioning

confidence: 99%

Endothelial dysfunction as a potential contributor in diabetic nephropathy

et al. 2010

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The mechanisms that drive the development of diabetic nephropathy remain undetermined. Only 30–40% of patients with diabetes mellitus develop overt nephropathy, which suggests that other contributing factors besides the diabetic state are required for the progression of diabetic nephropathy. Endothelial dysfunction is associated with human diabetic nephropathy and retinopathy, and advanced diabetic glomerulopathy often exhibits thrombotic microangiopathy, including glomerular capillary microaneurysms and mesangiolysis, which are typical manifestations of endothelial dysfunction in the glomerulus. Likewise, diabetic mice with severe endothelial dysfunction owing to deficiency of endothelial nitric oxide synthase develop progressive nephropathy and retinopathy similar to the advanced lesions observed in humans with diabetes mellitus. Additionally, inhibitors of the renin–angiotensin system fail to be renoprotective in some individuals with diabetic nephropathy (due in part to aldosterone breakthrough) and in some mouse models of the disease. In this Review, we discuss the clinical and experimental evidence that supports a role for endothelial nitric oxide deficiency and subsequent endothelial dysfunction in the progression of diabetic nephropathy and retinopathy. If endothelial dysfunction is the key factor required for diabetic nephropathy, then agents that improve endothelial function or raise intraglomerular nitric oxide level could be beneficial in the treatment of diabetic nephropathy.

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Effects of Nitric Oxide on Aldosterone Synthesis and Nitric Oxide Synthase Activity in Glomerulosa Cells from Bovine Adrenal Gland

Cited by 21 publications

References 39 publications

Nitric Oxide Inhibits ACTH-Induced Cortisol Production in Near-Term, Long-Term Hypoxic Ovine Fetal Adrenocortical Cells

Nitric Oxide Inhibits ACTH-Induced Cortisol Production in Near-Term, Long-Term Hypoxic Ovine Fetal Adrenocortical Cells

Comparison of flunixin meglumine and meloxicam influence on postoperative and oxidative stress in ovariohysterectomized bitches

Endothelial dysfunction as a potential contributor in diabetic nephropathy

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