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Some principles of hypotensive therapy considered in relationship to the pathogenesis of essential hypertension

The American Journal of Cardiology
Publication Date
DOI: 10.1016/0002-9149(62)90102-9
  • Medicine


Abstract The basal part of the casual blood pressure is closely related to subsequent mortality and morbidity; the supplemental pressure has exhibited no significant relationship to prognosis in our 8 year observation period of substantially untreated patients. Basal blood pressures measured by a defined technic help us to decide which hypertensive patients need treatment. Basal and supplemental pressures are almost independent variables in the sense that the elevation of basal blood pressure in a subject does not increase or substantially diminish the expectation of elevation of the supplemental blood pressure. It seems unlikely, therefore, that the elevations have the same cause. When large doses of hexamethonium are administered with the patient in the horizontal position, we note that in some hypertensive patients the hexamethonium floor blood pressure falls only a little below the basal blood pressure, whereas in others there are large decreases. We may describe the part of the basal blood pressure which is removed by hexamethonium as being the neurogenically maintained part of the basal blood pressure. The remainder —the hexamethonium floor blood pressure—may be described as non-neurogenically maintained. The proportions in which the neurogenically maintained and non-neurogenically maintained parts of the basal blood pressure are raised above the normal level vary from patient to patient. There is evidence of an increase in the reactivity of the blood vessels to norepinephrine in essential hypertension and in several types of experimental hypertension. It seems very likely that such enhanced reactivity, however produced, is concerned in the pathogenesis of hypertension. But it cannot be the only explanation if the two broad categories into which the basal blood pressure may be subdivided vary greatly in magnitude and are inversely related, and if the basal and supplemental parts of the casual blood pressure are independent variables. The evidence presented is favorable to the idea that the blood pressure elevation in essential hypertension is multifactorial, involving probably at least four broad categories. These may be further subdivisible. Effective blood pressure reduction relieves some of the more prominent manifestations of hypertension. It reduces mortality, even in grade II patients. Blood pressure reduction operates preventively in the sense that it reduces the incidence of such clinical manifestations as heart failure and stroke. This finding supports the view that hypertensive disease is due to blood pressure elevation as such, or to the associated vasoconstriction, but mainly to blood pressure elevation. If this hypothesis is a close approximation to the truth, then every condition inducing a lasting elevation of blood pressure, even a small one, has to be accepted as a contributive factor in hypertensive disease. Whether a particular factor will be acceptable as part of the pathogenesis of essential hypertension depends mainly upon the definition of essential hypertension. The evidence presented suggests that the proportions in which certain broad category components are present vary from one patient to another. Thus, it is not a matter of choosing between rival hypotheses: our task is quantitative. It is to estimate the extent to which certain factors known to influence the blood pressure are, in fact, concerned.

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