1. The mechanism by which the blood pressure remains elevated after temporary administration of deoxycorticosterone (DOCA) and saline has been studied by comparing vascular reactivity in the resistance bed of the isolated perfused rat tail in animals with post-DOCA hypertension and normotensive controls.
2. Animals with post-DOCA hypertension showed increased arteriolar responses to noradrenaline and 5-hydroxytryptamine, increased maximum contractile responses to noradrenaline, and increased resistance to flow under conditions of maximum vasodilation.
3. These abnormalities may be explained largely on the basis of arteriolar wall thickening resulting from hypertension and they will lead to a high peripheral resistance.
4. Evidence from experiments on chronic renal hypertension indicates that hypertension only becomes irreversible when the ability of the kidneys to regulate blood pressure is impaired. When this has occurred the high resistance offered by abnormal systemic arterioles will be a significant factor in maintaining a high arterial pressure and the high pressure will in turn continue to exert deleterious effects on resistance vessels, including those of the kidney.
5. It is suggested that persistence of hypertension in patients in whom the initial cause of the hypertension has apparently been removed is due to changes in morphology and reactivity of renal and systemic resistance vessels similar to those described in arterioles of animals with post-DOCA hypertension.