Effect of pressure overload and its recovery on the rat carotid artery: change of vascular reactivity and remodeling process.
Compared to chronic hypertension, little is known about the pathophysiology of acute hypertension and its recovery. To characterize this, we investigated the functional and structural properties of the common carotid arteries (CCA) from 35 rats. We established a unilateral and reversible carotid arterial hypertension model using the partial transverse aortic constriction (TAC) technique. By TAC, the right CCAs were made to endure a pressure-overload environment, while the left CCAs remained under normotension. The TACs were removed 2 weeks later, which unloaded the hypertensive effects. We compared the contractile, histological, and molecular responses of the CCA before TAC, during TAC (the hypertension period), and after removal of TAC (the recovery period). Vessel contractility was nearly abolished during 2 weeks of TAC. The recovery process from hypertension showed an initial hypercontractile period within a week. The relaxation response due to acetylcholine, as measured during the recovery period, showed a longer time course than the contractility for recovering its magnitude. During the hypertension period, the media thickness increased and this persisted throughout the recovery period. Apoptosis of the endothelial layer was significantly increased during the hypertension period and this disappeared 2 weeks after recovery. Expression of endothelial NO synthase was not detectable at the end of the hypertension period, but this gradually returned to the basal level after 2 weeks of recovery. Although increased contractility is usually expected in chronic hypertensive vessels, an abrupt pressure overload decreases contractility and the endothelium-dependent relaxation. It also increases endothelial apoptosis and the media thickness. These findings have clinical relevance, and they could be applied to human acute and severe hypertension and its recovery.
Kwon
Jin-Sook
JS
Department of Internal Medicine, Chungbuk National University Hospital, 62 Gaeshin-Dong, Heungduk-Gu, Cheongju, South Korea.
Lee
Sang-Jin
SJ
Kim
Young-Gyu
YG
Bae
Jang-Whan
JW
Hwang
Kyung-Kuk
KK
Cho
Myeong-Chan
MC
Kim
Dong-Woon
DW
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D017209:Apoptosis; D001794:Blood Pressure / Q000187:drug effects; D015153:Blotting, Western; D017536:Carotid Artery, Common / Q000201:enzymology / Q000473:pathology* / Q000503:physiopathology*; D004195:Disease Models, Animal; D004730:Endothelium, Vascular / Q000201:enzymology / Q000473:pathology / Q000503:physiopathology; D006973:Hypertension / Q000201:enzymology / Q000473:pathology* / Q000503:physiopathology*; D007150:Immunohistochemistry; D008297:Male; D052250:Nitric Oxide Synthase Type III / Q000096:biosynthesis; D011189:Potassium Chloride / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D020127:Recovery of Function / Q000187:drug effects; D018490:Serotonin Agents / Q000494:pharmacology; D013997:Time Factors; D017540:Tunica Media / Q000473:pathology / Q000503:physiopathology; D014655:Vascular Resistance / Q000187:drug effects; D014661:Vasoconstriction / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects; D014665:Vasodilator Agents / Q000494:pharmacology
D018490:Serotonin Agents; D014665:Vasodilator Agents; D011189:Potassium Chloride; D052250:Nitric Oxide Synthase Type III; D000109:Acetylcholine