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The aim of the study was to examine the hypothesis that flow-dependent dilatation is impaired in distal mesenteric arteries from adult spontaneously hypertensive rats (SHR) compared with normotensive Wistar-Kyoto rat (WKY) controls and to assess the role of nitric oxide (NO).
Arterial segments were cannulated, pressurized to 80 mmHg and allowed to develop spontaneous myogenic tone. Flow was increased incrementally in vessels from both strains and responses were also assessed before and after incubation with the NO synthase inhibitor N
-nitro-L-arginine methyl ester (L-NAME). Responses to flow in control vessels were also assessed before and after intraluminal perfusion with antibody-complement to disrupt the endothelium.
At a flow rate of 5 µl min-1, arteries from the WKY dilated significantly (22 ± 5 %, P < 0·01, n = 29) compared with the diameter at zero flow, whereas arteries from the SHR did not (4 ± 4 %, n.s., n = 16). Incubation with L-NAME had no inhibitory effect on the responses to flow in either rat strain. In control arteries, antibody-complement treatment abolished the dilatation in response to both flow and acetylcholine (ACh, 1 µM).
We conclude that flow-dependent dilatation is impaired in distal mesenteric arteries from adult SHR compared with WKY controls. Furthermore, flow-dependent dilatation is endothelium dependent, but L-NAME insensitive, thus excluding the NO pathway in this abnormality. Impaired flow-dependent dilatation may contribute to the increased peripheral resistance in hypertension.
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