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(Hypertension. 1995;26:397-400.)
© 1995 American Heart Association, Inc.

Articles

Vasodilator Response of Mesenteric Arterioles to Histamine in Spontaneously Hypertensive Rats

Hidekazu Suzuki; Benjamin W. Zweifach; Geert W. Schmid-Schönbein

From the Department of Bioengineering and Institute for Biomedical Engineering, University of California–San Diego, La Jolla.

Correspondence to Dr Geert W. Schmid-Schönbein, Department of Bioengineering and Institute for Biomedical Engineering, University of California–San Diego, 9500 Gilman Dr, La Jolla, CA 92093-0412.

Abstract Recent evidence suggests that spontaneously hypertensive rats (SHR) exhibit an impaired response to inflammatory mediators. We designed this study to analyze the response of arterioles of SHR after stimulation with a proinflammatory agent, histamine, compared with the response of arterioles of normotensive Wistar-Kyoto (WKY) controls. We observed mesenteric arterioles by intravital microscopy in rats under general anesthesia and measured their lumen diameters after histamine superfusion. To compare the concentration-response curve with histamine, we also studied the effect of an endothelium-dependent vasodilator, acetylcholine, and an independent vasodilator, sodium nitroprusside. At the end of each experiment we applied papaverine topically to determine the maximal diameter for each vessel, from which we computed arteriolar tone. Arteriolar tone in SHR is set at a higher steady state level than in WKY. The concentration required for a 50% dilator response (EC₅₀) of histamine in SHR was significantly higher than that in WKY. In SHR the arteriolar response showed the same refractory pattern to histamine as to acetylcholine. In contrast, the EC₅₀ of sodium nitroprusside in SHR was similar to that in WKY. Our results indicate that SHR exhibit an impaired dilator response to histamine that is due to a blunted endothelium-dependent vasodilation.

Key Words: microcirculation • histamine • sodium nitroprusside • endothelium • acetylcholine

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