Abstract
Background and PurposeChronic hypertension decreases internal diameter of cerebral arteries and arterioles. We recently showed that short-term treatment with the angiotensin II receptor blocker telmisartan restored baseline internal diameter of small cerebral arterioles in spontaneously hypertensive rats (SHR), via reversal of structural remodeling and inhibition of the angiotensin II vasoconstrictor response. As larger arteries also participate in the regulation of cerebral circulation, we evaluated whether similar short-term treatment affects middle cerebral arteries of SHR.MethodsBaseline internal diameters of pressurised middle cerebral arteries from SHR and their respective controls, Wistar Kyoto rats (WKY) and responses to angiotensin II were studied in a small vessel arteriograph. Pressure myogenic curves and passive internal diameters were measured following EDTA deactivation, and elastic modulus from stress-strain relationships.ResultsActive baseline internal diameter was 23% lower in SHR compared to WKY, passive internal diameter (EDTA) 28% lower and elastic modulus unchanged. Pressure myogenic curves were shifted to higher pressure values in SHR. Telmisartan lowered blood pressure but had no effect on baseline internal diameter nor on structural remodeling (passive internal diameter and elastic modulus remained unchanged compared to SHR). Telmisartan shifted the pressure myogenic curve to lower pressure values than SHR.ConclusionIn the middle cerebral arteries of SHR, short-term treatment with telmisartan had no effect on structural remodeling and did not restore baseline internal diameter, but allowed myogenic tone to adapt towards lower pressure values.
Highlights
Chronic hypertension decreases internal diameter (ID) of cerebral arterioles [1,2,3]
As we previously showed that 10 days treatment with telmisartan (TELMI) - but not candesartan - reverses the narrowing of pial arteriolar ID in spontaneously hypertensive rats (SHR), via reversal of structural remodeling and inhibition of the angiotensin II (AngII) vasoconstrictor response [10], we further investigated the early therapeutic impact of TELMI on cerebral circulation
Baseline active (Figure 1A) and passive (Figure 1C) ID were 23 and 28% lower in SHR than in Wistar Kyoto rats (WKY) respectively; TELMI had no effect, contrary to the results obtained in pial arterioles (Foulquier et al, 2012) (Figure 1B/1D)
Summary
Chronic hypertension decreases internal diameter (ID) of cerebral arterioles [1,2,3]. This decrease in ID is due to changes in structure and/or function of the arterioles This contributes to the increase in cerebrovascular resistance and to the rightward shift of the limits of cerebral blood flow autoregulation, protecting the brain against higher blood pressure during hypertension [4,5]. At the onset of an antihypertensive treatment, such rightward shift of the lower limit of cerebral blood flow autoregulation - if not early reversed - may be responsible for iatrogenic cerebral hypoperfusion and neuronal dysfunction during the onset decrease in blood pressure. We recently showed that short-term treatment with the angiotensin II receptor blocker telmisartan restored baseline internal diameter of small cerebral arterioles in spontaneously hypertensive rats (SHR), via reversal of structural remodeling and inhibition of the angiotensin II vasoconstrictor response. As larger arteries participate in the regulation of cerebral circulation, we evaluated whether similar short-term treatment affects middle cerebral arteries of SHR
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