Effect of insulin on renal potassium metabolism

Rossetti, Luciano; Klein-Robbenhaar, G.; Giebisch, Gerhard; Smith, Douglas J.; DeFronzo, Ralph A.

doi:10.1152/ajprenal.1987.252.1.f60

Cited by 20 publications

(18 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Acute experiments have suggested that insulin may cause hypokalemia by increasing potassium uptake in extrarenal tissues. 30 In the present study, plasma potassium concentration was slightly reduced during long-term insulin infusion. Another possible cause of the decrease in potassium excretion is an increase in sodium reabsorption before the distal nephron, which would tend to reduce distal nephron flow rate and potassium secretion.…”

Section: Hyperinsulinemia and Renal Excretionsupporting

confidence: 49%

Chronic hyperinsulinemia and blood pressure. Interaction with catecholamines?

et al. 1990

View full text Add to dashboard Cite

Although hyperinsulinemia and increased adrenergic activity have been postulated to be important factors in obesity-associated hypertension, a cause and effect relation between insulin, catecholamines, and hypertension has not been established. The aim of this study was to determine whether chronic hyperinsulinemia, comparable with that found in obese hypertensive patients, causes hypertension in normal dogs, increases plasma catecholamines, or potentiates the blood pressure effects of norepinephrine. In six normal dogs, insulin infusion (1.0 milliunits/ kg/min) for 7 days, with euglycemia maintained, increased fasting insulin fourfold to sixfold. However, mean arterial pressure did not increase, averaging 99 ±2 mm Hg during the control period and 91 ±3 mm Hg during the 7 days of insulin infusion. Insulin did not alter plasma norepinephrine or epinephrine, which averaged 171±27 and 71±14 pg/ml, respectively, during the control period and 188 ±29 and 45 ±12 pg/ml during the 7 days of insulin infusion. In six dogs, norepinephrine was infused (0.2 /tig/kg/min) for 7 days to raise plasma norepinephrine to 2,940±103 pg/ml. Insulin infusion (1.0 milliunits/kg/min) for 7 days during simultaneous infusion of norepinephrine did not further increase mean arterial pressure, which averaged 101 ±3 during norepinephrine and 98 ±2 mm Hg during insulin plus norepinephrine infusion. Thus, chronic hyperinsulinemia did not increase mean arterial pressure or plasma catecholamines and did not potentiate the blood pressure actions of norepinephrine. These observations provide no evidence that chronic hyperinsulinemia or interactions between insulin and plasma catecholamines cause hypertension in normal dogs. (Hypertension 1990;15:519-527) A association between obesity and hypertension has been noted by numerous investigators, and reductions in caloric intake and body weight often lower blood pressure in obese hypertensive patients.1 -3 Several lines of indirect evidence suggest that insulin could be an important link between changes in caloric intake, activity of the sympathetic nervous system, and hypertension associated with obesity. 4 -5 Increased caloric intake because of carbohydrate ingestion elevates insulin levels and appears to activate the sympathetic nervous system, whereas caloric restriction suppresses insulin and sympathetic activity as assessed by variFrom the

show abstract

Section: Hyperinsulinemia and Renal Excretionsupporting

confidence: 49%

Chronic hyperinsulinemia and blood pressure. Interaction with catecholamines?

et al. 1990

View full text Add to dashboard Cite

show abstract

“…8 d after catheter insertion, rats in groups I-IV received a two-step euglycemic insulin-clamp study (20,21). Four rats in group III received a repeat two-step insulin-clamp study 14 was initiated and continued throughout the study (20).…”

Section: Methodsmentioning

confidence: 99%

Correction of hyperglycemia with phlorizin normalizes tissue sensitivity to insulin in diabetic rats.

Rossetti¹,

Smith²,

Shulman³

et al. 1987

J. Clin. Invest.

769

526

View full text Add to dashboard Cite

Insulin resistance is characteristic of the diabetic state. To define the role of hyperglycemia in generation of the insulin resistance, we examined the effect of phlorizin treatment on tissue sensitivity to insulin in partially pancreatectomized rats. Five groups were studied: group I, sham-operated controls; group II, partially pancreatectomized diabetic rats with moderate glucose intolerance; group III, diabetic rats treated with phlorizin to normalize glucose tolerance; group IV, phlorizin-treated controls; and group V, phlorizin-treated diabetic rats restudied after discontinuation of phlorizin. Insulin sensitivity was assessed with the euglyemic hyperinsulinemic clamp technique in awake, unstressed rats. Insulin-mediated glucose metabolism was reduced by approximately 30% (P < 0.001) in diabetic rats. Phlorizin treatment of diabetic rats completely normalized insulin sensitivity but had no effect on insulin action in controls. Discontinuation of phlorizin in phlorizin-treated diabetic rats resulted in the reemergence of insulin resistance. These data demonstrate that (a) a reduction of f-cell mass leads to the development of insulin resistance, and (b) correction of hyperglycemia with phlorizin, without change in insulin levels, normalizes insulin sensitivity. These results provide the first in vivo evidence that hyperglycemia per se can lead to the development of insulin resistance.

show abstract

“…In contrast, the effects of insulin are very dependent on plasma glucose and K ϩ levels and often do not lead to salt retention and elevation in blood pressure (5,20). Furthermore, IGF-1 reduces renal potassium excretion (6), whereas insulin can promote kaliuresis (5), particularly when plasma K ϩ levels are exogenously clamped (9,36). The molecular details of the distinct effects of insulin and IGF-1 on urinary excretion patterns are not clear.…”

mentioning

confidence: 99%

IGF-1 and insulin exert opposite actions on ClC-K2 activity in the cortical collecting ducts

Zaika

Mamenko

Boukelmoune

et al. 2015

American Journal of Physiology-Renal Physiology

View full text Add to dashboard Cite

Despite similar stimulatory actions on the epithelial sodium channel (ENaC)-mediated sodium reabsorption in the distal tubule, insulin promotes kaliuresis, whereas insulin-like growth factor-1 (IGF-1) causes a reduction in urinary potassium levels. The factors contributing to this phenomenon remain elusive. Electrogenic distal nephron ENaC-mediated Na+ transport establishes driving force for Cl− reabsorption and K+ secretion. Using patch-clamp electrophysiology, we document that a Cl− channel is highly abundant on the basolateral plasma membrane of intercalated cells in freshly isolated mouse cortical collecting duct (CCD) cells. The channel has characteristics attributable to the ClC-K2: slow gating kinetics, conductance ∼10 pS, voltage independence, Cl−>NO3− anion selectivity, and inhibition/activation by low/high pH, respectively. IGF-1 (100 and 500 nM) acutely stimulates ClC-K2 activity in a reversible manner. Inhibition of PI3-kinase (PI3-K) with LY294002 (20 μM) abrogates activation of ClC-K2 by IGF-1. Interestingly, insulin (100 nM) reversibly decreases ClC-K2 activity in CCD cells. This inhibitory action is independent of PI3-K and is mediated by stimulation of a mitogen-activated protein kinase-dependent cascade. We propose that IGF-1, by stimulating ClC-K2 channels, promotes net Na+ and Cl− reabsorption, thus reducing driving force for potassium secretion by the CCD. In contrast, inhibition of ClC-K2 by insulin favors coupling of Na+ reabsorption with K+ secretion at the apical membrane contributing to kaliuresis.

show abstract

Effect of insulin on renal potassium metabolism

Cited by 20 publications

References 0 publications

Chronic hyperinsulinemia and blood pressure. Interaction with catecholamines?

Chronic hyperinsulinemia and blood pressure. Interaction with catecholamines?

Correction of hyperglycemia with phlorizin normalizes tissue sensitivity to insulin in diabetic rats.

IGF-1 and insulin exert opposite actions on ClC-K2 activity in the cortical collecting ducts

Contact Info

Product

Resources

About