HYPERTENSION may be induced in several species by excessive dietary salt, and is accentuated by the removal of a kidney and deoxycorticosterone administration1–5. The blood pressure is raised because peripheral resistance is increased, but the exact mechanism leading to arteriolar narrowing is unknown. Vascular hyper-reactivity to pressor stimuli has been implicated6,7, but when assessing this it is difficult to determine the relative importance of true vascular smooth muscle hyper-reactivity, smooth muscle hypertrophy and minor changes in starting diameter of the resistance vessels8,9. These problems can be largely circumvented by studying vascular reactivity in isolated perfused organs devoid of their normal nervous and humoral stimuli, and for this purpose we developed the vascular bed of the isolated perfused rat tail10. This preparation has a relatively simple structure; it includes terminal resistance vessels, and when perfused at constant flow rates with an artificial electrolyte medium containing dialysed bovine serum albumen, baseline resistance is stable for several hours. The tail responds with reproducible dose response curves to a variety of pressor agents.
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BEILIN, L., WADE, D. Vascular Hyper-reactivity with Sodium Loading and with Deoxycorticosterone Induced Hypertension in the Rat. Nature 227, 1141–1142 (1970) doi:10.1038/2271141a0
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