A Critical Review of the Role of Endothelial Factors in the Pathogenesis of Hypertension
Bibliographic record
Abstract
The endothelium produces a variety of substances that play important roles in regulation of the circulation and vascular wall homeostasis. The control of blood vessel wall homeostasis is achieved via production of vasorelaxants and vasoconstrictors. Among the vasorelaxants are nitric oxide (NO), prostacyclin, various endothelium-derived hyperpolarizing factors (EDHFs, such as cytochrome P-450 monooxygenase metabolites of arachidonic acid like epoxyeicosatrienoic acids, and endocannabinoids), and C-type natriuretic peptide. Among the vasoconstrictors we find endothelin-1 (ET-1) and endothelium-derived contracting factors (EDCF) that are cyclooxygenase products such as endoperoxides and thromboxanes. The endothelium, via these and other agents, also exerts a critical influence on the blood stream, particularly formed elements such as leucocytes and platelets, and on substances involved in blood coagulation. All these effects contribute to modulating the growth of the vascular wall in hypertension, and participate in the development of atherothrombotic complications associated with hypertension. Inhibition of NO production may induce elevation of blood pressure in experimental animals. However, even today, we do not have incontrovertible evidence of participation of NO, EDHFs or EDCFs, or other endothelial products, in the pathogenesis of hypertension, although there is evidence of abnormal endothelium-dependent relaxation in hypertension in many but not all hypertensives. It is unclear, however, to what extent this may precede hypertension or be a consequence of elevated blood pressure, possibly contributing to its complications. Also, it is often difficult to dissociate abnormal endothelium-dependent relaxation from confounding factors such as the presence of associated conditions like dyslipidaemia, diabetes, smoking, obesity, hyperhomocysteinaemia, and others, that are accompanied themselves by abnormal endothelium-dependent relaxation. There is some evidence for a role of ET-1 in blood pressure elevation in some experimental forms of hypertension, particularly severe, sodium-sensitive hypertension, in which it may play a role in accentuating rather than initiating blood pressure elevation. Endothelin-1 may play a similar role in human hypertension.
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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 | 0.002 | 0.001 |
| Meta-epidemiology (narrow) | 0.000 | 0.000 |
| Meta-epidemiology (broad) | 0.003 | 0.005 |
| Bibliometrics | 0.000 | 0.000 |
| Science and technology studies | 0.000 | 0.000 |
| Scholarly communication | 0.000 | 0.000 |
| Open science | 0.001 | 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".