Beyond blood pressure: the endothelium and atherosclerosis progression<sup>*</sup>
Bibliographic record
Abstract
Endothelial dysfunction and remodeling of the vessel wall of large and small arteries is associated with hypertension and other risk factors for cardiovascular disease. These changes alter vascular function and mechanics, aggravate high blood pressure (BP), and may accelerate the progression of atherosclerosis. Activation of oxidative stress by angiotensin II is a key component of this process. Angiotensin II stimulates nicotinamide adenine dinucleotide phosphate (NADPH)/nicotinamide adenine dinucleotide (NADH) oxidase in endothelium, smooth muscle cells, and the adventitia of blood vessels to generate reactive oxygen species, leading to endothelial dysfunction, growth, and inflammation. Upregulation of endothelin-1, adhesion molecules, nuclear factor-kappaB, and other inflammatory mediators, as well as increased breakdown of nitric oxide and uncoupling of nitric oxide synthase, contribute to the progression of vascular disease and atherogenesis. Clinical studies in which treatment with angiotensin converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs) was used demonstrated correction of some of the changes in large and small arteries in hypertensive subjects, whereas identical BP lowering with beta-blockers had no effect on endothelial function. In experimental models of atherosclerosis, ARBs, including losartan potassium, valsartan, and olmesartan medoxomil, have demonstrated the ability to prevent the progression of atherosclerosis. This was in part associated with decreased expression of inflammatory mediators and improved endothelial function. Blockade of the renin-angiotensin-aldosterone system with ACE inhibitors or ARBs appears to blunt both the development and progression of vascular disease in both small and large vessels in experimental models and in humans beyond the effect of these agents on BP. This may help to explain the positive results of recently completed trials such as Heart Outcomes Prevention Evaluation (HOPE) and Losartan Intervention for Endpoint Reduction in Hypertension (LIFE).
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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) | 0.001 | 0.000 |
| Bibliometrics | 0.000 | 0.001 |
| Science and technology studies | 0.000 | 0.001 |
| Scholarly communication | 0.002 | 0.001 |
| Open science | 0.001 | 0.000 |
| Research integrity | 0.002 | 0.002 |
| Insufficient payload (model declined to judge) | 0.015 | 0.006 |
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".