Nicole M Rummery1, T Hilton Grayson, Caryl E Hill. 1. Division of Neuroscience, John Curtin School of Medical Research, Australian National University, Canberra, ACT, 2601, Australia. nicole.rummery@nottingham.ac.uk
Abstract
OBJECTIVE AND DESIGN: Remodelling in the media and decreases in connexin (Cx) expression and size of endothelial cells occur in the caudal artery of spontaneously hypertensive rats (SHR). The objective of this study was to determine whether similar changes are found in the aorta and whether effects in both aorta and caudal artery are present in the pre-hypertensive period or can be reversed by antihypertensive treatment. METHODS AND RESULTS: In the aorta of SHR, there was no difference in endothelial cell size although Cxs 37 and 40 were decreased, compared with normotensive Wistar-Kyoto rats. Cxs 37 and 43 were also reduced in the media. These differences were not apparent in pre-hypertensive SHR. Inhibition of angiotensin-converting enzyme (ACE) in SHR decreased blood pressure and restored Cx expression in the endothelium of both aorta and caudal artery. The decreased endothelial cell size in the caudal artery or the reduced Cxs in the media of the aorta of SHR were unaffected by ACE inhibition. CONCLUSION: We conclude that cellular coupling is reduced in the endothelium of arteries of SHR, but this can be restored by inhibition of the renin-angiotensin system. Decreased cellular coupling in the media or decreased endothelial size in SHR were not reversed by this antihypertensive treatment.
OBJECTIVE AND DESIGN: Remodelling in the media and decreases in connexin (Cx) expression and size of endothelial cells occur in the caudal artery of spontaneously hypertensiverats (SHR). The objective of this study was to determine whether similar changes are found in the aorta and whether effects in both aorta and caudal artery are present in the pre-hypertensive period or can be reversed by antihypertensive treatment. METHODS AND RESULTS: In the aorta of SHR, there was no difference in endothelial cell size although Cxs 37 and 40 were decreased, compared with normotensive Wistar-Kyoto rats. Cxs 37 and 43 were also reduced in the media. These differences were not apparent in pre-hypertensive SHR. Inhibition of angiotensin-converting enzyme (ACE) in SHR decreased blood pressure and restored Cx expression in the endothelium of both aorta and caudal artery. The decreased endothelial cell size in the caudal artery or the reduced Cxs in the media of the aorta of SHR were unaffected by ACE inhibition. CONCLUSION: We conclude that cellular coupling is reduced in the endothelium of arteries of SHR, but this can be restored by inhibition of the renin-angiotensin system. Decreased cellular coupling in the media or decreased endothelial size in SHR were not reversed by this antihypertensive treatment.
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