Pattern of peripheral venous response to volume expansion in borderline systemic hypertension

Abstract

An increased venous tone responsible for changes in systemic hemodynamics has been described in borderline hypertensive patients along with the release, in response to intravenous sodium chloride, of an endogenous sodium ion/potassium ion adenosine triphosphatase ( Na + K + ATPase) inhibitor with vasoconstrictive properties. The hemodynamic and humoral effects of a 2-hour intravenous saline infusion were studied in 25 borderline hypertensives characterized on the basis of their forearm venous distensibility (VV30) in normal (n = 15) and low (n = 10) VV30. VV30 was slightly reduced by saline in the entire hypertensive group (1.47 vs 1.36 ml/ 100 ml; p < 0.05), whereas blood pressure and plasma Na + K + ATPase inhibitor were unchanged. Normal VV30 showed a sudden increase in plasma Na + K + ATPase inhibitor in response to saline associated with an increase in blood pressure, a forearm arterial and venous constriction, and a sluggish suppression in plasma renin activity, whereas low VV30 exhibited a completely opposite pattern. The changes in plasma Na + K + ATPase inhibitor inversely correlated to VV30 decreases in borderline hypertensives with normal VV30 (r = −0.49; p < 0.05), whereas they did not in all hypertensive patients. Atrial natriuretic peptide response to saline infusion was delayed in normal VV30 and inversely related to the changes in Na + K + ATPase inhibitory activity (r = −42; p < 0.05) attained after 2 hours of infusion in the entire hypertensive population. Results of this study suggest the ability of acute volume expansion to reduce peripheral venous distensibility in borderline hypertensive patients. The extent of venoconstrictive response is related to the increase in plasma levels of an endogenous Na + K + ATPase inhibitor whose release is apparently promoted either by delayed atrial natriuretic peptide stimulation or sluggish suppression of plasma-renin activity.