Effects of nitric oxide synthesis blockade and angiotensin II on blood flow and spontaneous vasomotion in the rat cerebral microcirculation

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Abstract
The effects ofNω‐nitro‐l‐arginine methyl ester (l‐NAME) an inhibitor of NO synthesis, or angiotensin II on the frequency and amplitude of rhythmic variations (vasomotion) in blood flow of the intact rat cerebral circulation were investigated using laser‐Doppler flowmetry (LDF). Experiments were performed on Sprague‐Dawley rats anaesthetized withα‐chloralose. The rat's head was fixed on a stereotaxic frame and the microvascular blood flow of the parietal cortex on the right or on both sides was measured via a small hole in the parietal bone, keeping the dura and a thin bone layer intact. Following the intravenous injection ofl‐NAME, the mean arterial blood pressure (MABP) increased to 123 ± 1 mmHg (1.25 mg kg‐1) or to 144 ± 3 mmHg (5.0 mg kg‐1) but no significant changes in cerebral blood flow (CBF) or vasomotion could be detected. The observed increase in MABP was sustained untill‐arginine was administered. In the presence ofl‐NAME, during stepwise reduction of MABP, CBF remained constant when MABP was kept between 60 and 130 mmHg, the vasomotion frequency was lower when MABP was above 80 mmHg but its amplitude was two times higher than in the control group. In another group of animals, angiotensin was infused to give comparable increments in blood pressure. In contrast tol‐NAME, angiotensin II had no effect on either frequency or amplitude of vasomotion, compared to the control group, within the whole range of MABP studied. Our study suggests that NO might be a significant modulator of the microvascular tonus in the brain and that it plays a significant role in controlling vasomotion frequency and amplitude.