Pathophysiology of diastolic hypertension

Two different mechanisms for long-term vasoconstriction that sustain diastolic hypertension in the experimental and clinical forms of primary aldosteronism and renovascular hypertension can also be identified and quantified among patients with essential hypertension. The first is renin-independent, requires antecedent sodium retention, and appears related to abnormal membrane transport of calcium. This vasoconstriction is identified by low plasma renin and ionized calcium values and is correctable by sodium depletion or calcium channel or alpha-blockade. The second is renin-mediated but also involves an increase in cytosolic calcium. This mechanism is quantifiable by the plasma renin level and by the hypotensive response to an anti-renin-system drug (CEI inhibitor, saralasin, beta-blocker). At the very extremes of the range of plasma renin values encountered in hypertensive patients, one of the two mechanisms predominates, whereas in the medium range of renin values either or both mechanisms can be operative.