# Altered Expression Levels of Angiogenic Peptides in the Carotid Body of Spontaneously Hypertensive Rats

## TL;DR

This study shows that high blood pressure in rats causes changes in blood vessel-related proteins in the carotid body, which may affect how it senses blood chemistry.

## Contribution

The paper reveals new insights into how hypertension alters angiogenic peptide expression in the carotid body.

## Key findings

- VEGF-A, VEGF-B, and VEGFR-2 levels are increased in the carotid body of hypertensive rats.
- VEGFR-1 expression is reduced in hypertensive carotid body cell clusters.
- ETB receptor expression is enhanced in endothelial cells of hypertensive carotid body blood vessels.

## Abstract

The carotid body (CB), the main peripheral arterial chemoreceptor, exhibits considerable structural and neurochemical plasticity in response to pathological conditions such as high blood pressure. Previous studies have shown that morphological alterations in the hypertensive CB are characterized by enlarged parenchyma due to cellular hypertrophy and hyperplasia, and vasodilation. To test whether hypertension can also induce neoangiogenesis and modulate its chemosensory function, we examined the immunohistochemical expression of two angiogenic factors, vascular endothelial growth factor (VEGF) and endothelin-1 (ET), and their corresponding receptors in the CB of adult spontaneously hypertensive rats (SHRs), and compared their expression patterns to that of age-matched normotensive Wistar rats (NWR). We found an increased VEGF-A and B, and VEGFR-2 expression in glomus and endothelial cells in the enlarged CB glomeruli of SHRs compared with that in NWR. Conversely, weaker immunoreactivity to VEGFR-1 was detected in cell clusters of the hypertensive CB. The expression of endothelin-converting enzyme 1 and its receptor ETA was higher in a subset of glomus cells in the normotensive CB, while the immunoreactivity to the ETB receptor was enhanced in endothelial cells of CB blood vessels in SHRs. The elevated endothelial expression of VEGF and ET-1 suggests their role as local vascular remodeling factors in the adaptation to hypertension, though their involvement in the cellular rearrangement and modulation of chemosensory function could also be implied.