Limits...
Sub-chronic testosterone treatment increases the levels of epithelial sodium channel (ENaC)-α, β and γ in the kidney of orchidectomized adult male Sprague-Dawley rats.

Loh SY, Giribabu N, Salleh N - PeerJ (2016)

Bottom Line: Methods.Co-treatment with flutamide or finasteride resulted in the levels of α, β and γ-ENaC proteins and mRNAs in kidneys to decrease.In conclusions, increases in α, β and γ-ENaC protein and mRNA levels in kidneys mainly in the distal tubules and collecting ducts under testosterone influence might lead to enhance Na(+) reabsorption which subsequently might cause an increase in blood pressure.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Physiology, University of Malaya , Kuala Lumpur , Malaysia.

ABSTRACT
Testosterone has been reported to cause blood pressure to increase. However mechanisms that underlie the effect of this hormone on this physiological parameter are currently not well understood. The aims of this study were to investigate effects of testosterone on expression of α, β and γ-epithelial sodium channel (ENaC) proteins and messenger RNAs (mRNAs) in kidneys, the channel known to be involved in Na(+) reabsorption, which subsequently can affect the blood pressure. Methods. Adult male Sprague-Dawley (SD) rats were orchidectomized fourteen days prior to receiving seven days treatment with testosterone propionate (125 µg/kg/day or 250 µg/kg/day) with or without flutamide (androgen receptor blocker) or finasteride (5α-reductase inhibitor). Following sacrifice, the kidneys were removed and were subjected for α, β and γ-ENaC protein and mRNA expression analyses by Western blotting and Real-time PCR (qPCR) respectively. The distribution of α, β and γ-ENaC proteins in kidneys were observed by immunofluorescence. Results. The α, β and γ-ENaC proteins and mRNA levels in kidneys were enhanced in rats which received testosterone-only treatment. In these rats, α, β and γ-ENaC proteins were distributed in the distal tubules and collecting ducts of the nephrons. Co-treatment with flutamide or finasteride resulted in the levels of α, β and γ-ENaC proteins and mRNAs in kidneys to decrease. In conclusions, increases in α, β and γ-ENaC protein and mRNA levels in kidneys mainly in the distal tubules and collecting ducts under testosterone influence might lead to enhance Na(+) reabsorption which subsequently might cause an increase in blood pressure.

No MeSH data available.


(A) α-Enac mRNA level (B) whole membrane image of α-ENaC protein band and (C) ratio of α-ENaC/GAPDH protein band intensity in kidneys.Values represent mean ± S.E.M of four rats. ∗p < 0.05 compared to sham-operated rats, #p < 0.05 compared to orcidectomized control rats, &p < 0.05 compared to T125. $p < 0.05 compared to T250. S, sham operated; O, orchiectomized non-treated; T125, 125 µg/kg/day testosterone-treated; T250, 250 µg/kg/day testosterone-treated rats; FU, flutamide; FN, finasteride. Molecular weight of α-ENaC protein = 78 kDa (cleaved).
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4933084&req=5

fig-1: (A) α-Enac mRNA level (B) whole membrane image of α-ENaC protein band and (C) ratio of α-ENaC/GAPDH protein band intensity in kidneys.Values represent mean ± S.E.M of four rats. ∗p < 0.05 compared to sham-operated rats, #p < 0.05 compared to orcidectomized control rats, &p < 0.05 compared to T125. $p < 0.05 compared to T250. S, sham operated; O, orchiectomized non-treated; T125, 125 µg/kg/day testosterone-treated; T250, 250 µg/kg/day testosterone-treated rats; FU, flutamide; FN, finasteride. Molecular weight of α-ENaC protein = 78 kDa (cleaved).

Mentions: In Fig. 1A, the levels of α-Enac mRNA were highest following testosterone-only treatment. Co-treatment with flutamide or finasteride caused α-Enac mRNA levels to decrease (p < 0.05). The effect of flutamide was greater in rats which received 125 µg/kg/day testosterone when compared to 250 µg/kg/day testosterone. However, the effect of finasteride in rats treated with 125 µg/kg/day testosterone- was not significantly different when compared to its effect in rats treated with 250 µg/kg/day testosterone.


Sub-chronic testosterone treatment increases the levels of epithelial sodium channel (ENaC)-α, β and γ in the kidney of orchidectomized adult male Sprague-Dawley rats.

Loh SY, Giribabu N, Salleh N - PeerJ (2016)

(A) α-Enac mRNA level (B) whole membrane image of α-ENaC protein band and (C) ratio of α-ENaC/GAPDH protein band intensity in kidneys.Values represent mean ± S.E.M of four rats. ∗p < 0.05 compared to sham-operated rats, #p < 0.05 compared to orcidectomized control rats, &p < 0.05 compared to T125. $p < 0.05 compared to T250. S, sham operated; O, orchiectomized non-treated; T125, 125 µg/kg/day testosterone-treated; T250, 250 µg/kg/day testosterone-treated rats; FU, flutamide; FN, finasteride. Molecular weight of α-ENaC protein = 78 kDa (cleaved).
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4933084&req=5

fig-1: (A) α-Enac mRNA level (B) whole membrane image of α-ENaC protein band and (C) ratio of α-ENaC/GAPDH protein band intensity in kidneys.Values represent mean ± S.E.M of four rats. ∗p < 0.05 compared to sham-operated rats, #p < 0.05 compared to orcidectomized control rats, &p < 0.05 compared to T125. $p < 0.05 compared to T250. S, sham operated; O, orchiectomized non-treated; T125, 125 µg/kg/day testosterone-treated; T250, 250 µg/kg/day testosterone-treated rats; FU, flutamide; FN, finasteride. Molecular weight of α-ENaC protein = 78 kDa (cleaved).
Mentions: In Fig. 1A, the levels of α-Enac mRNA were highest following testosterone-only treatment. Co-treatment with flutamide or finasteride caused α-Enac mRNA levels to decrease (p < 0.05). The effect of flutamide was greater in rats which received 125 µg/kg/day testosterone when compared to 250 µg/kg/day testosterone. However, the effect of finasteride in rats treated with 125 µg/kg/day testosterone- was not significantly different when compared to its effect in rats treated with 250 µg/kg/day testosterone.

Bottom Line: Methods.Co-treatment with flutamide or finasteride resulted in the levels of α, β and γ-ENaC proteins and mRNAs in kidneys to decrease.In conclusions, increases in α, β and γ-ENaC protein and mRNA levels in kidneys mainly in the distal tubules and collecting ducts under testosterone influence might lead to enhance Na(+) reabsorption which subsequently might cause an increase in blood pressure.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Physiology, University of Malaya , Kuala Lumpur , Malaysia.

ABSTRACT
Testosterone has been reported to cause blood pressure to increase. However mechanisms that underlie the effect of this hormone on this physiological parameter are currently not well understood. The aims of this study were to investigate effects of testosterone on expression of α, β and γ-epithelial sodium channel (ENaC) proteins and messenger RNAs (mRNAs) in kidneys, the channel known to be involved in Na(+) reabsorption, which subsequently can affect the blood pressure. Methods. Adult male Sprague-Dawley (SD) rats were orchidectomized fourteen days prior to receiving seven days treatment with testosterone propionate (125 µg/kg/day or 250 µg/kg/day) with or without flutamide (androgen receptor blocker) or finasteride (5α-reductase inhibitor). Following sacrifice, the kidneys were removed and were subjected for α, β and γ-ENaC protein and mRNA expression analyses by Western blotting and Real-time PCR (qPCR) respectively. The distribution of α, β and γ-ENaC proteins in kidneys were observed by immunofluorescence. Results. The α, β and γ-ENaC proteins and mRNA levels in kidneys were enhanced in rats which received testosterone-only treatment. In these rats, α, β and γ-ENaC proteins were distributed in the distal tubules and collecting ducts of the nephrons. Co-treatment with flutamide or finasteride resulted in the levels of α, β and γ-ENaC proteins and mRNAs in kidneys to decrease. In conclusions, increases in α, β and γ-ENaC protein and mRNA levels in kidneys mainly in the distal tubules and collecting ducts under testosterone influence might lead to enhance Na(+) reabsorption which subsequently might cause an increase in blood pressure.

No MeSH data available.