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
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.