Why the study?
Does intravenous valsartan improve the lower limit of cerebral blood flow autoregulation in spontaneously hypertensive rats?
Does intravenous valsartan improve the lower limit of cerebral blood flow autoregulation in spontaneously hypertensive rats?
Acute intravenous administration of valsartan shifts the lower limit of cerebral blood flow autoregulation to lower blood pressure levels in spontaneously hypertensive rats, likely via inhibition of AT1 receptors on cerebral endothelial cells.
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Should not change clinical practice; leaves open translation of AT1 effects on CBF autoregulation to humans.
The effects of angiotensin II type 1 receptor blockers (ARBs) on cerebral blood flow (CBF) autoregulation have not been fully clarified. Thus, we examined the acute effect of valsartan, the most selective ARB, on CBF autoregulation in spontaneously hypertensive rats. Intravenous administration of valsartan (0.3 mg/kg) reduced the mean arterial pressure (MAP) from 184±5 (mean±SEM) to 174±5 mmHg (p<0.001) without affecting CBF as measured by laser-Doppler flowmetry. The lower limit of CBF autoregulation (the MAP at which the CBF was 80% of the baseline value) in the valsartan-treated group (122±3 mmHg) was significantly lower than that in the control group (135±4 mmHg, p<0.05). Reverse transcribed–polymerase chain reaction and immunohistochemical staining demonstrated that both angiotensin II type 2 receptors and angiotensin II type 1 receptors (AT1Rs) were expressed in endothelial and smooth muscle cells of the rat cerebral arteries. These results suggest that specific inhibition of AT1Rs in the cerebral circulation causes the leftward shift of the lower limit of autoregulation.
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Takada et al. (2006) studied this question.
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