High and low renin subgroups of essential hypertension: Differences and similarities in their renin and sympathetic responses to neural and nonneural stimuli

Abstract

This study was designed to test the hypothesis that the abnormally high and abnormally low levels of renin observed in essential hypertension may reflect different levels of sympathetic nervous activity and to evaluate the alternative possibility that they are due to different levels of renin responsiveness to neurogenic stimuli. Thus, plasma norepinephrine, epinephrine and renin activity were measured at rest and during 30 minutes of head-up tilt in 43 patients with uncomplicated essential hypertension classified as having high, normal and low plasma renin activity during a constant sodium intake of 100 mEq/day. In addition, to investigate the renin responsiveness to nonneural stimuli, the same humoral variables were measured at rest in 18 patients after dietary sodium restriction. While patients were consuming the 100 mEq sodium diet, supine plasma norepinephrine and epinephrine concentrations were similar, whereas supine plasma renin activity was significantly different among the three subgroups. During tilt, 40 percent of patients in the high renin subgroup had vasovagal episodes whereas only 5 percent in the normal renin and none in the low renin subgroup experienced similar reactions. Excluding the data obtained from patients who fainted, the tilt-induced absolute increments in norepinephrine and epinephrine were again similar whereas the percent renin responses were significantly greater in the high than in the low renin subgroups. In contrast, sodium deprivation caused similar percent increases in supine plasma renin activity without inducing significant changes in plasma norepinephrine and epinephrine. To the extent that plasma catecholamine measurements reflect sympathetic nervous activity, the results indicate that the differences in plasma renin activity among patients with essential hypertension cannot be attributed to differences in neural activity or in ability to produce renin, but rather are due to discrepancies in renin responsiveness to neural stimuli. Because the renin response to tilt is mediated through the juxtaglomerular beta adrenoreceptors, it is possible that patients with high and low renin activity have different sensitivities of these receptors to similar adrenergic stimulation.