Effects of Cacna1d D307G Mutation on Blood Pressure and Kidney Function in Rats with Salt Loading

Introduction: Our recent findings revealed that CACNA1D D307G mutation participates in the early-onset hypertension. Methods: We used the CRISPR/Cas9 technique to generate the Cacna1d D307G mutation rat model and investigated the effects of Cacna1d D307G mutation on blood pressure (BP) an...

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Main Authors: Lan Cheng, Hui Chen, R. Nfornah Maboh, Huan Wang
Format: Article
Language:English
Published: Karger Publishers 2025-01-01
Series:Kidney & Blood Pressure Research
Online Access:https://karger.com/article/doi/10.1159/000542828
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author Lan Cheng
Hui Chen
R. Nfornah Maboh
Huan Wang
author_facet Lan Cheng
Hui Chen
R. Nfornah Maboh
Huan Wang
author_sort Lan Cheng
collection DOAJ
description Introduction: Our recent findings revealed that CACNA1D D307G mutation participates in the early-onset hypertension. Methods: We used the CRISPR/Cas9 technique to generate the Cacna1d D307G mutation rat model and investigated the effects of Cacna1d D307G mutation on blood pressure (BP) and renal function. Rats fed normal-salt diet had normal plasma aldosterone levels but higher plasma ET-1 and mildly elevated systolic BP (SBP) in D307G and G307G rats compared with the wild type (WT) until 24 weeks. Renal function and renal histopathology did not significantly differ among the three groups. Results: When fed high-salt diet (HSD), D307G and G307G rats showed more sensitivity to HSD. The results showed a further increase in SBP than in WT rats. Plasma and vascular endothelin-1 (ET-1) level and cortex and renal artery endothelin type A (ETA) receptor protein expression were significantly increased. Enhanced renal injury was also noted as indicated by an increased ratio of kidney weight/body weight, elevated urinary protein and albumin/creatinine ratio, higher kidney injury molecule-1 (KIM-1) levels, advanced fibrosis and apoptosis, and inflammation. Further experiments revealed a reduction in urinary sodium excretion and creatinine clearance. Higher protein expression of renal cortex epithelial sodium channel α subunit (αENaC) was confirmed in D307G and G307G rats fed HSD. However, a selective ETA receptor blockade (ABT-627) could partially reverse the increased SBP, increased serum KIM-1 level, upregulated renal cortex protein expression of αENaC, and reduced urinary sodium excretion with reduced creatinine clearance in D307G rats fed HSD. Conclusion: Activation of the ET-1/ETA system in D307G mutation rats might have contributed to increased sensitivity to salt loading, augmented hypertension, and exacerbated the renal injury.
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spelling doaj-art-df4e2e1afdd04398871dfe7aad7196ad2025-08-20T03:09:47ZengKarger PublishersKidney & Blood Pressure Research1423-01432025-01-01501466010.1159/000542828Effects of Cacna1d D307G Mutation on Blood Pressure and Kidney Function in Rats with Salt LoadingLan ChengHui ChenR. Nfornah MabohHuan Wang Introduction: Our recent findings revealed that CACNA1D D307G mutation participates in the early-onset hypertension. Methods: We used the CRISPR/Cas9 technique to generate the Cacna1d D307G mutation rat model and investigated the effects of Cacna1d D307G mutation on blood pressure (BP) and renal function. Rats fed normal-salt diet had normal plasma aldosterone levels but higher plasma ET-1 and mildly elevated systolic BP (SBP) in D307G and G307G rats compared with the wild type (WT) until 24 weeks. Renal function and renal histopathology did not significantly differ among the three groups. Results: When fed high-salt diet (HSD), D307G and G307G rats showed more sensitivity to HSD. The results showed a further increase in SBP than in WT rats. Plasma and vascular endothelin-1 (ET-1) level and cortex and renal artery endothelin type A (ETA) receptor protein expression were significantly increased. Enhanced renal injury was also noted as indicated by an increased ratio of kidney weight/body weight, elevated urinary protein and albumin/creatinine ratio, higher kidney injury molecule-1 (KIM-1) levels, advanced fibrosis and apoptosis, and inflammation. Further experiments revealed a reduction in urinary sodium excretion and creatinine clearance. Higher protein expression of renal cortex epithelial sodium channel α subunit (αENaC) was confirmed in D307G and G307G rats fed HSD. However, a selective ETA receptor blockade (ABT-627) could partially reverse the increased SBP, increased serum KIM-1 level, upregulated renal cortex protein expression of αENaC, and reduced urinary sodium excretion with reduced creatinine clearance in D307G rats fed HSD. Conclusion: Activation of the ET-1/ETA system in D307G mutation rats might have contributed to increased sensitivity to salt loading, augmented hypertension, and exacerbated the renal injury. https://karger.com/article/doi/10.1159/000542828
spellingShingle Lan Cheng
Hui Chen
R. Nfornah Maboh
Huan Wang
Effects of Cacna1d D307G Mutation on Blood Pressure and Kidney Function in Rats with Salt Loading
Kidney & Blood Pressure Research
title Effects of Cacna1d D307G Mutation on Blood Pressure and Kidney Function in Rats with Salt Loading
title_full Effects of Cacna1d D307G Mutation on Blood Pressure and Kidney Function in Rats with Salt Loading
title_fullStr Effects of Cacna1d D307G Mutation on Blood Pressure and Kidney Function in Rats with Salt Loading
title_full_unstemmed Effects of Cacna1d D307G Mutation on Blood Pressure and Kidney Function in Rats with Salt Loading
title_short Effects of Cacna1d D307G Mutation on Blood Pressure and Kidney Function in Rats with Salt Loading
title_sort effects of cacna1d d307g mutation on blood pressure and kidney function in rats with salt loading
url https://karger.com/article/doi/10.1159/000542828
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