Endothelium-dependent and -independent vasoreactivity of rat basilar artery in chronic heart failure

Citation
J. Widder et al., Endothelium-dependent and -independent vasoreactivity of rat basilar artery in chronic heart failure, J CARDIO PH, 35(4), 2000, pp. 515-522
Citations number
49
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY
ISSN journal
01602446 → ACNP
Volume
35
Issue
4
Year of publication
2000
Pages
515 - 522
Database
ISI
SICI code
0160-2446(200004)35:4<515:EA-VOR>2.0.ZU;2-1
Abstract
Alterations of vasoreactivity are a well-known phenomenon in chronic heart failure (CHF), and activation of the endogenous endothelin (ET) system is s uspected to contribute significantly. Regional differences in alterations o f vasoreactivity exist; however, nothing is known about cerebrovascular rea ctivity in CHF. This is of interest in view of increased stroke risk in CHF . Therefore, 12 weeks after coronary artery ligation to induce CHF in rats, studies of vasoreactivity of the isolated basilar artery (BA) were perform ed and compared with third-order branches (MA-A3) and the main trunk (MA) o f the superior mesenteric artery. Some of the animals received longterm ET- receptor antagonism by 11 weeks of treatment with the selective ETA-recepto r antagonist LU 135252 or the mixed ETA/ETB-receptor antagonist bosentan. I n rats with CHF, endothelium-dependent relaxation by acetylcholine and A231 87 as well as endothelium-independent relaxation by sodium nitroprusside (S NP) was largely unaffected in BA or MA. However, in MA-A3, potency of SNP w as diminished without change of maximal effect. ET-1-induced contraction di d not differ in arteries from CHF and control rats, either in placebo- or E T-receptor antagonist-treated animals. In summary, there was essentially no change of vascular reactivity in similar sized arteries obtained from brai n and mesentery. This is in contrast to results on arteries from a variety of vascular regions published previously, thus supporting the concept of or gan- and probably time-related changes of vascular function in the developm ent of CHF. The absence of significant alteration of cerebral vasoreactivit y may be taken to indicate that changes in cerebral blood flow and increase d incidence of ischemic stroke in patients with CHF are caused not by local alterations of vascular function.