Impact of Bradykinin B1 Receptor Blockade on Angiotensin II‐Induced Cardiac and Aortic Remodeling
Bibliographic record
Abstract
Angiotensin II (AngII) is a growth factor known to induce vascular and cardiac hypertrophy and fibrosis. AngII has been shown to regulate bradykinin B1 receptor (B1R) expression in the heart and aorta and we have recently shown that concomitant B1R antagonism could prevent AngII‐induced cardiac fibrosis. The present study investigated the impact of AngII and bradykinin B1R antagonism on blood pressure and left ventricular (LV) and aortic hypertrophy. Male Sprague‐Dawley rats were treated for 4 weeks with vehicle or AngII (200 ng/kg per min) in the presence or absence of the B1R antagonist R‐954 (400 μg/kg per day). In addition, bromodeoxyuridine (BrdU) was infused to assess cellular proliferation. At sacrifice, mean arterial pressure (MAP) was assessed via carotid artery cannulation in anesthetized rats. The LV and aorta were weighed, and the aortic and cardiomyocyte cross sectional area (CSA) were measured. Additionally, LV DNA content was determined and aortic cellular proliferation was assessed via immunohistochemistry to measure BrdU incorporation. Relative to vehicle, AngII increased MAP (59%), aortic cell proliferation (144%), and aortic CSA (34%), ‐ effects that were not offset by B1R antagonism. However, B1R antagonism did attenuate the AngII‐induced increase in aortic mass. Similarly, AngII increased LV hypertrophy (35%) and total DNA content (44%) relative to control, both of which were prevented by concomitant B1R antagonism. Cardiomyocyte CSA was not different across treatment groups. This study reveals tissue‐specific effects of bradykinin B1R antagonism. Although AngII induced significant remodeling in both the heart and aorta, concomitant B1R blockade only prevented cell accumulation and remodeling in the LV. Future studies will investigate the mechanism underlying this effect to further elucidate the role of the bradykinin B1R and its interaction with AngII in remodeling heart and aorta. Support or Funding Information Canadian Male Sexual Health Council
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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 | 0.000 |
| 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 | 0.000 |
| Scholarly communication | 0.000 | 0.000 |
| Open science | 0.000 | 0.000 |
| Research integrity | 0.000 | 0.001 |
| Insufficient payload (model declined to judge) | 0.002 | 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 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".