Estrogen and progesterone regulate α, β, and γENaC subunit mRNA levels in female rat kidney

Gambling, Lorraine; Dunford, Susan; Wilson, Catherine; McArdle, Harry J; Baines, Deborah L.

doi:10.1111/j.1523-1755.2004.00593.x

Cited by 60 publications

(40 citation statements)

References 40 publications

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“…Substances present in the culture media may stimulate ␣ENaC expression or factors that normally suppress ␣ENaC expression in vivo are absent in culture. These results raise the possibility that ␣ENaC expression in VSMCs may be regulated by hormonal, paracrine, or autocrine substances, as other investigators have shown (3,16,19). It remains unclear whether ␣ENaC is expressed in VSMCs in vivo.…”

Section: Discussionmentioning

confidence: 62%

Vascular ENaC proteins are required for renal myogenic constriction

Jernigan

Drummond

2005

American Journal of Physiology-Renal Physiology

131

164

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(VSMCs) to contract in response to increases in intraluminal pressure. Although mechanosensitive ion channels are thought to initiate VSMC stretch-induced contraction, their molecular identity is unknown. Recent reports suggest degenerin/epithelial Na ϩ channels (DEG/ENaC) may form mechanotransducers in sensory neurons and VSMCs; however, the role of DEG/ENaC proteins in myogenic constriction of mouse renal arteries has not been established. To test the hypothesis that DEG/ ENaC proteins are required for myogenic constriction in renal vessels, we first determined expression of ENaC transcripts and proteins in mouse renal VSMCs. Then, we determined pressure-and agonistinduced constriction and changes in vascular smooth muscle cytosolic Ca 2ϩ and Na ϩ in isolated mouse renal interlobar arteries following DEG/ENaC inhibition with amiloride and benzamil. We detect ␣-, ␤-, and ␥ENaC transcript and protein expression in cultured mouse renal VSMC. In contrast, we detect only ␤-and ␥-but not ␣ENaC protein in freshly dispersed mrVMSC. Selective DEG/ENaC inhibition, with low doses of amiloride and benzamil, abolishes pressure-induced constriction and increases in cytosolic Ca 2ϩ and Na ϩ without diminishing agonist-induced responses in isolated mouse interlobar arteries. Our findings indicate that DEG/ENaC proteins are required for myogenic constriction in mouse interlobar arteries and are consistent with our hypothesis that DEG/ENaC proteins may be components of mechanosensitive ion channel complexes required for myogenic vasoconstriction. mechanotransduction; renal blood flow autoregulation; amiloride; benzamil; isolated renal vessel; stretch-activated cation channel; calcium; sodium MYOGENIC VASOCONSTRICTION is an intrinsic property of most resistance vessels characterized by a decrease in luminal diameter in response to an increase in intraluminal pressure. The response is important in establishing basal vascular tone and maintaining blood flow autoregulation. It is well established that vascular smooth muscle (VSM) membrane depolarization and subsequent Ca 2ϩ influx via voltage-gated Ca 2ϩ channels mediate myogenic constriction (23,32,36). However, the mechanism that transduces mechanical stimuli (pressure-induced stretch) into a cellular event (depolarization) is less understood. Although mechanosensitive nonselective cation channels are thought to initiate pressure-induced depolarization (9,29,38,46), the molecule(s) involved has not been identified.Members of the degenerin/epithelial Na ϩ channel (DEG/ ENaC) family have recently been identified as mechanosensors in a variety of species and cell types (2,17,20,28,33). In mammals, DEG/ENaC proteins are found at several important sites of mechanotransduction, including dorsal root ganglion, arterial baroreflex sensory neurons, osteoblasts, keratinocytes, and vascular smooth muscle cells (VSMCs) (5, 12-14, 18, 30, 34). Two subfamilies of proteins are expressed in mammals: ENaC and acid-sensing ion channel. Acid-sensing ion channel proteins are activated by protons ...

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Section: Discussionmentioning

confidence: 62%

Vascular ENaC proteins are required for renal myogenic constriction

Jernigan

Drummond

2005

American Journal of Physiology-Renal Physiology

131

164

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“…Apical Na ϩ channels have been sparsely investigated, yielding results consistent with the findings described in this work. ENaC subunit mRNA expression has been shown to be enhanced in rat kidney cells (24). Higher levels of ␣-ENaC were detected in female rat lungs compared with males, and combined administration of E2 and P to immature or ovarectomized rats increased pulmonary mRNA levels of ␣-and ␥-ENaC after 24 h (18).…”

Section: Discussionmentioning

confidence: 99%

Modulation of Sodium Transport in Alveolar Epithelial Cells by Estradiol and Progesterone

Laube¹,

Küppers

Thomé³

2011

Pediatr Res

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ABSTRACT:The effects of estradiol (E2) and progesterone (P) on alveolar epithelial Na ϩ transport were studied in isolated alveolar epithelial cells from 18-to 19-d GA rat fetuses, grown to confluence in serum-free media supplemented with E2 (0 -1 M) and P (0 -2.8 M). Short-circuit currents (I SC ) were measured, showing an increase by E2 and P in a dose-dependent manner. The Na,K-ATPase subunits -␣ 1 and -␤ 1 were detected by Western blotting, but total expression was not significantly altered. Furthermore, all three epithelial Na ϩ channel (ENaC) subunits -␣, -␤, and -␥ were detected, with trends toward a higher expression in the presence of E2 and P. Real-time PCR revealed an increase of ␣-and ␤-ENaC expression but no alteration of ␥-ENaC. In addition, the mRNA expression of cystic fibrosis transmembrane conductance regulator (CFTR) and Na,K-ATPase-␤ 1 subunit were elevated in the presence of E2 and P. Single-channel patch clamp analysis demonstrated putative highly selective and nonselective cation channels in the analyzed cells, with a higher percentage of responsive patches under the influence of E2 and P. We conclude that E2 and P increased Na ϩ transport in alveolar epithelial cells by enhancing the expression and activity of ENaC and Na,K-ATPase.

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“…For example, estrogen has been shown to increase ENaC functional activity in the airways [11,12]. In the kidneys, estrogen could induce acute upregulation of a-, b-, and g-ENaC mRNA expression [13].…”

Section: Introductionmentioning

confidence: 99%

Estrogen, progesterone, and genistein differentially regulate levels of expression of α-, β-, and γ-epithelial sodium channel (ENaC) and α-sodium potassium pump (Na+/K+-ATPase) in the uteri of sex steroid–deficient rats

2015

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Estrogen and progesterone regulate α, β, and γENaC subunit mRNA levels in female rat kidney

Abstract: Female gonadal steroids differentially modulate expression of ENaC subunit mRNA in the rat kidney.

Cited by 60 publications

References 40 publications

Vascular ENaC proteins are required for renal myogenic constriction

Vascular ENaC proteins are required for renal myogenic constriction

Modulation of Sodium Transport in Alveolar Epithelial Cells by Estradiol and Progesterone

Estrogen, progesterone, and genistein differentially regulate levels of expression of α-, β-, and γ-epithelial sodium channel (ENaC) and α-sodium potassium pump (Na+/K+-ATPase) in the uteri of sex steroid–deficient rats

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