Abstract 080: Dietary Fructose Enhances Protein Kinase C Activation by Angiotensin II in Proximal Tubules via Changes in Intracellular Calcium
Autor: | Nancy J. Hong, Jeffrey L. Garvin, Nianxin Yang |
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Rok vydání: | 2019 |
Předmět: | |
Zdroj: | Hypertension. 74 |
ISSN: | 1524-4563 0194-911X |
Popis: | Dietary fructose causes salt-sensitive hypertension. This is in part due to increasing the sensitivity of proximal nephron Na reabsorption to angiotensin II (Ang II) such that lower concentrations stimulate transport to a greater extent. Ang II stimulates Na transport in this segment by increasing protein kinase C (PKC) α, a calcium- and lipid-dependent kinase. We hypothesized that dietary fructose increases the ability of Ang II to elevate intracellular calcium (Cai) and, thereby, activate PKC α in proximal tubules. This, in turn, stimulates Na/H exchange activity, the primary transporter involved in Na reabsorption. To test our hypothesis rats were maintained on a diet of normal chow plus tap water or normal chow plus 20% fructose. The effect of Ang II on Cai was measured using Fura2 in perfused S2 segments. Na/H exchange (NHE) was measured in perfused tubules using the pH-sensitive dye BCECF. PKC α activity was measured by separating particulate and soluble fractions, performing Western blots and recording the particulate to soluble ratio. Basal Cai was 143±29 nM in proximal tubules from control rats while it was 160±30 nM in those given fructose, not significantly different. Ang II (1 nM) increased Cai by 43±10 nM in control tubules and by 148±53 nM in tubules from rats fed fructose (p < 0.03). A higher concentration of Ang II (100 nM) had a similar effect in tubules from both groups (Fructose: 237±100 nM vs. Control: 190±34 nM). Ang II increased the particulate to soluble ratio of PKC α, a measure of activation, by 0.134±0.026 in tubules from rats fed fructose (p |
Databáze: | OpenAIRE |
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