The central role of the brain in salt-sensitive hypertension
Bibliographic record
Abstract
PURPOSE OF REVIEW: To integrate recent studies showing that abnormal Na transport in the central nervous system plays a pivotal role in genetic models of salt-sensitive hypertension. RECENT FINDINGS: Na transport-regulating mechanisms classically considered to reflect renal control of the blood pressure, i.e. aldosterone-mineralocorticoid receptors-epithelial sodium channels-Na/K-ATPase, have now been demonstrated to be present in the central nervous system contributing to regulation of cerebrospinal fluid [Na] by the choroid plexus and to neuronal responsiveness to cerebrospinal fluid/brain [Na]. Dysfunction of either or both can activate central nervous system pathways involving 'ouabain' and angiotensin type 1 receptor stimulation. The latter causes sympathetic hyperactivity and adrenal release of marinobufagenin - a digitalis-like inhibitor of the alpha1 Na/K-ATPase isoform - both contributing to hypertension on high salt intake. Conversely, specific central nervous system blockade of mineralocorticoid receptors or epithelial sodium channels prevents the development of hypertension on high salt intake, irrespective of the presence of a 'salt-sensitive kidney'. Variants in the coding regions of some of the genes involved in Na transport have been identified, but sodium sensitivity may be mainly determined by abnormal regulation of expression, pointing to primary abnormalities in regulation of transcription. SUMMARY: Looking beyond the kidney is providing new insights into mechanisms contributing to salt-sensitive hypertension, which will help to dissect the genetic factors involved and to discover novel strategies to prevent and treat salt-sensitive hypertension.
Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.
How this classification was reachedexpand
Full frame machine prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.
Distilled classifier scores by category (both heads)
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.000 | 0.001 |
| Meta-epidemiology (narrow) | 0.001 | 0.000 |
| Meta-epidemiology (broad) | 0.002 | 0.000 |
| Bibliometrics | 0.001 | 0.001 |
| Science and technology studies | 0.000 | 0.001 |
| Scholarly communication | 0.001 | 0.001 |
| Open science | 0.001 | 0.001 |
| Research integrity | 0.001 | 0.001 |
| Insufficient payload (model declined to judge) | 0.005 | 0.003 |
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 source (direct Gemma or distilled Codex), 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".