Key result
Hypertension with carotid stenosis is linked to carotid body cell remodeling and lost marker correlations.
Why the study?
The carotid body plays an important role in blood pressure regulation, but its structural changes in patients with comorbid arterial hypertension and hemodynamically significant carotid artery stenosis remain poorly understood.
Does comorbid arterial hypertension and hemodynamically significant common carotid artery stenosis alter the histoarchitecture and cellular regulation of the carotid body compared to healthy controls?
Case-Control (n=20)
Does comorbid arterial hypertension and hemodynamically significant common carotid artery stenosis alter the histoarchitecture and cellular regulation of the carotid body compared to healthy controls?
Identifies structural disconnection between chief and supporting cells in the carotid body as a potential pathophysiological mechanism driving chemoreceptor hyperactivation and hypertension progression in patients with carotid stenosis.
Answers are grounded in this paper and cite their sources.
Carotid body remodeling may link stenosis to hypertension progression; leaves open causal role and therapeutic relevance pending larger studies.
The comorbidity of arterial hypertension and hemodynamically significant carotid artery stenosis presents a serious clinical challenge. The carotid body is a peripheral chemoreceptor that plays an important role in blood pressure regulation, but its structural changes in this comorbid condition remain poorly understood. The aim of this study was to evaluate changes in the histoarchitecture of the carotid body in patients with the combined pathology of arterial hypertension and hemodynamically significant common carotid artery stenosis using the morphometric and immunohistochemical markers PGR9.5 and S-100. Research methodology: Ten carotid body preparations from healthy controls and ten preparations from patients with verified hypertension and hemodynamically significant common carotid artery stenosis were studied. Immunohistochemical staining with PGR9.5 and S-100 markers was used, followed by morphometric analysis in ImageJ. Statistical analysis included descriptive statistics, Shapiro-Wilk, Mann-Whitney, and Student's t-tests, as well as Spearman's correlation analysis. The results of the research: In the group with hypertension and hemodynamically significant stenosis, a significant reduction in the number of supporting cells was observed. Against this background, compensatory hypertrophy of chief cells was observed, manifested by an increase in their overall area, nucleus, and nuclear-cytoplasmic ratio. Correlation analysis in the comorbid group demonstrated the disappearance of significant correlations for PGR9.5 and S-100 previously observed in the control group, as well as the emergence of new pathological associations, indicating a profound disruption of tissue regulation. Conclusions: The obtained data suggest a new pathophysiological mechanism for carotid body dysfunction in hypertension and common carotid artery stenosis, based on the disconnection of functional elements within the organ's parenchyma. Disruption of cooperation between cell populations creates the basis for persistent chemoreceptor hyperactivation, which contributes to elevated blood pressure and the progression of hypertension.
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Ganina et al. (2026) conducted a case-control in Arterial hypertension and hemodynamically significant common carotid artery stenosis (n=20). Arterial hypertension and hemodynamically significant common carotid artery stenosis vs. Healthy controls was evaluated on Histoarchitectural changes of the carotid body assessed by morphometry and immunohistochemical markers (PGR9.5 and S-100). Comorbid hypertension and carotid stenosis showed reduced supporting cells, chief cell hypertrophy, and lost PGR9.5/S-100 correlations in 10 preparations vs 10 controls.
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