Blood Pressure Modulation Through Epithelial Sodium Channel (ENaC) Alteration Induced by Microbiome Exchange Between Milan Normotensive and Hypertensive Rat Strains
Bibliographic record
Abstract
Background: Hypertension is a global health problem associated with diabetes, obesity and cardiovascular diseases. Recent studies indicate substantial changes in gut microbiome in hypertensive individuals, therefore suggesting kidney-gut axis. In the present study, we aimed at investigating possible connections between gut microbiome and blood pressure phenotype utilizing a congenic strain of Milan hypertensive (NA) rats and its littermate normotensive strain (MN) rats. We evaluated whether exchange of faeces between two strains may transfer phenotypes via gut microbiome, and mechanisms underlying altered phenotypes. Methods: NA and MN rats were subjected to ‘homogenization (HOM)’ of the microbiome, consisted of exchanges of bedding with faeces and co-housing (MN-HOM and NA-HOM). For the baseline (BSL) condition, rats were homogenized within the same strain. Systolic blood pressure (SBP) was measured every month. Metataxonomic analysis of faecal samples were performed by next generation sequencing of 16S ribosome encoding DNA. Expressions of sodium transporters were evaluated by immunoblotting utilizing kidney samples from those rats. Results: At 5 months age, different gut microbiota compositions were observed in the two strains of rats at baseline, and HOM altered both. In addition, MN-HOM showed a significantly enhanced SBP compared to MN-BSL, suggesting that gut microbiome could have impact on SBP in MN rats. In contrast, there was no difference in the average SBP between NA-BSL and NA-HOM. Immunoblotting revealed the upregulation of ENaC in the cortex of MN-HOM with respect to MN-BSL. Finally, MN-HOM showed a reduction in SBP comparable to MN-BSL after amiloride treatment with significantly enhanced urinary sodium excretion. Conclusion: We have demonstrated that hypertensive phenotype in NA rats was transferred to MN rats through homogenization, indicating that gut microbiota or metabolites derived therefrom could modulate ENaC in the cortex and eventually modulate SBP. Further studies are ongoing to identify metabolites from gut microbiota which may modulate ENaC and eventually blood pressure.
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How this classification was reachedexpand
Full frame distilled prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. Learned from the 10,348 direct Codex labels and 10,348 direct Gemma labels. Candidate is the union of thresholded teacher heads; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels or direct frontier model labels.
Codex and Gemma teacher scores by category
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.000 | 0.000 |
| Meta-epidemiology (narrow) | 0.000 | 0.000 |
| Meta-epidemiology (broad) | 0.001 | 0.000 |
| Bibliometrics | 0.000 | 0.000 |
| Science and technology studies | 0.000 | 0.001 |
| Scholarly communication | 0.000 | 0.000 |
| Open science | 0.000 | 0.000 |
| Research integrity | 0.000 | 0.001 |
| Insufficient payload (model declined to judge) | 0.000 | 0.000 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one teacher head, not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".