Abstract
Age-related changes in the contribution of BKCa-channels and NO to acetylcholine-induced dilation of pial arteries were studied in normotensive (Wistar-Kyoto) and spontaneously hypertensive rats (SHRs). Using intravital microphotography (×470), responses of pial arteries to acetylcholine chloride (ACh, 10−7 M, 5 min) with and without blockade of BKCa-channels by tetraethylammonium chloride (TEA, 2 mМ) and nitric oxide (NO) synthesis by L-NAME (10−3 M) were comparatively evaluated in WKY rats and SHRs aged 4 and 20 months. The evaluation criteria were the number and degree of arterial dilations arising in response to ACh after the application of inhibitors, with the latter criterion being evaluated, in turn, by measuring the erythrocyte flow width separately in three groups of arteries: small ( 40 µm). It was established that in WKY rats aging leads to diminish the role of BKCa-channels in ACh-induced dilation of all pial arteries, no matter the caliber. Similar processes were observed in the pial vascular bed of young SHRs. It appears that changes in the role of BKCa-channels in vascular dilatatory responses in aging WKY rats and young SHRs are largely associated with the impairment of NO synthesis and changes in the role of NO-mediated mechanisms of vasodilation. Aging in SHRs is accompanied by increasing the contribution of the NO-dependent mechanism to the regulation of ACh-induced dilatatory responses of small-caliber arteries.
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