Regulation of blood pressure, the epithelial sodium channel (ENaC), and other key renal sodium transporters by chronic insulin infusion in rats

Song, Jian; Hu, Xinqun; Riazi, Shahla; Tiwari, Swasti; Wade, James B.; Ecelbarger, Carolyn A.

doi:10.1152/ajprenal.00108.2005

Cited by 83 publications

(91 citation statements)

References 55 publications

(68 reference statements)

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“…This resulted in a significant reduction in excreted sodium due to an increase in ENaC activity. Biochemical isolation of the plasma membrane proteins from insulin-and vehicle-treated mouse kidneys demonstrated an increase in the abundance of ENaC subunits in those mice injected with insulin, suggesting that ENaC was trafficked to the apical membrane in response to acute insulin stimulation in agreement with the earlier in vitro studies (168).…”

Section: Insulin and Vasopressinsupporting

confidence: 86%

Regulation of the epithelial sodium channel by membrane trafficking

Butterworth¹,

Edinger²,

Frizzell³

et al. 2009

American Journal of Physiology-Renal Physiology

113

100

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Section: Insulin and Vasopressinsupporting

confidence: 86%

Regulation of the epithelial sodium channel by membrane trafficking

Butterworth¹,

Edinger²,

Frizzell³

et al. 2009

American Journal of Physiology-Renal Physiology

113

100

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“…Similarly, chronic metabolic acidosis also increases aldosterone and therefore NCC [26]. Why other hormones such as insulin [13,57,108,109], vasopressin [83,91,104], estrogen [125], and norepinephrine [82] regulate NCC is less clearly defined ( Table 1), but warrants further study given the role of these hormones in normal physiology and human diseases such as diabetes mellitus, obesity, and hypertension.…”

Section: Structure-function Relationshipmentioning

confidence: 99%

The sodium chloride cotransporter SLC12A3: new roles in sodium, potassium, and blood pressure regulation

Moes

Lubbe

Zietse

et al. 2013

Pflugers Arch - Eur J Physiol

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SLC12A3 encodes the thiazide-sensitive sodium chloride cotransporter (NCC), which is primarily expressed in the kidney, but also in intestine and bone. In the kidney, NCC is located in the apical plasma membrane of epithelial cells in the distal convoluted tubule. Although NCC reabsorbs only 5 to 10 % of filtered sodium, it is important for the fine-tuning of renal sodium excretion in response to various hormonal and non-hormonal stimuli. Several new roles for NCC in the regulation of sodium, potassium, and blood pressure have been unraveled recently. For example, the recent discoveries that NCC is activated by angiotensin II but inhibited by dietary potassium shed light on how the kidney handles sodium during hypovolemia (high angiotensin II) and hyperkalemia. The additive effect of angiotensin II and aldosterone maximizes sodium reabsorption during hypovolemia, whereas the inhibitory effect of potassium on NCC increases delivery of sodium to the potassium-secreting portion of the nephron. In addition, great steps have been made in unraveling the molecular machinery that controls NCC. This complex network consists of kinases and ubiquitinases, including WNKs, SGK1, SPAK, Nedd4-2, Cullin-3, and Kelch-like 3. The pathophysiological significance of this network is illustrated by the fact that modification of each individual protein in the network changes NCC activity and results in salt-dependent hypotension or hypertension. This review aims to summarize these new insights in an integrated manner while identifying unanswered questions.

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“…Diets and treatments have been detailed previously. 20 For studying the effect of hyperglycemia, in study 4, 12 SpragueDawley rats weighing approximately 210 g were obtained from Taconic Farms. For inducing type 1 diabetes, STZ (55 mg/kg body wt, dissolved in 0.2 ml of 0.1 M citric acid) was injected intraperitoneally into half of the rats (n ϭ 6).…”

Section: Animals and Study Designmentioning

confidence: 99%

Reduced Expression of Insulin Receptors in the Kidneys of Insulin-Resistant Rats

Tiwari¹,

Halagappa²,

Riazi³

et al. 2007

Journal of the American Society of Nephrology

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Insulin resistance is accompanied by hyperinsulinemia and activation of the renin-angiotensin system, both of which are associated with hypertension. Because the kidney plays a major role in the regulation of blood pressure, we studied the regulation of insulin receptor expression in the kidney during states of insulin resistance. Using two rat models of insulin resistance, Western blot analysis demonstrated a significant reduction in the expression of insulin receptor subunits in the kidney compared to lean control rats. Treatment of insulin resistance in Zucker rats with the insulin-sensitizing drug rosiglitazone partially restored renal insulin receptor levels. Conversely, treatment with the angiotensin II type 1 receptor (AT1) antagonist candesartan increased renal insulin receptor expression compared to untreated rats. Streptozotocin-induced hyperglycemia, which results from hypoinsulinemia, reduced expression of renal insulin receptors. Hyperinsulinemia induced by insulin infusion, however, did not produce a similar effect. In conclusion, insulin receptors are downregulated in the kidneys of insulin resistant rats, possibly mediated by hyperglycemia and angiotensin II.

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Regulation of blood pressure, the epithelial sodium channel (ENaC), and other key renal sodium transporters by chronic insulin infusion in rats

Abstract: . Regulation of blood pressure, the epithelial sodium channel (ENaC), and other key renal sodium transporters by chronic insulin infusion in rats.

Cited by 83 publications

References 55 publications

Regulation of the epithelial sodium channel by membrane trafficking

Regulation of the epithelial sodium channel by membrane trafficking

The sodium chloride cotransporter SLC12A3: new roles in sodium, potassium, and blood pressure regulation

Reduced Expression of Insulin Receptors in the Kidneys of Insulin-Resistant Rats

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