Clinical parameters of concern in the pathology and treatment of hypertension

To sum up, the endocrine analysis of human hypertension, tracing the renin system patterns, has provided a convincing body of data revealing and defining the biochemical heterogeneity of human hypertension. The heterogeneity, and the ability to differentiate it by the study of renin, embraces the major category that we call essential hypertension, which brackets at least 85% of all hypertension patients. This spectrum of biochemical heterogeneity is manifested physiologically by two different forms of vasoconstriction. One form is renin-mediated vasoconstriction, signified by the finding of a medium or high plasma renin activity and corrected by antirenin surgical or pharmacologic means. Toward the other end of the spectrum, revealed by the finding of low plasma renin, a sodium-volume-induced form of vasoconstriction operates. This appears to involve abnormal calcium metabolism and can also be characterized by measurable changes in serum ionized calcium values. With the development of newer and more specific antihypertensive agents with actions that appear to be rather specific against a particular vasoconstriction mechanism, new patterns of treatment are emerging that are preferable to the undiscriminating protocols of diuretic-oriented stepped care. The beta blockers or the CEIs can now be considered as the first pharmacological step against high- or medium-renin hypertensive states. The prescription of diuretics as the first step against the low-renin state can now be weighed against a more rational physiologic attack involving the probably safer, less troublesome, and more specific calcium-channel blocking drugs and also by the less potent alpha-adrenergic blockers. These latter two types of agents may exhibit finer marksmanship than do diuretics in opposing the etiology of low-renin hypertension, for there is growing reason to believe that sodium-volume-mediated vasoconstriction is related to abnormal calcium influx and possibly to abnormal alpha-adrenergic traffic.