Atrial natriuretic factor response to acute volume expansion in borderline hypertension. Role of ACE-inhibition and changes in peripheral venous tone.

Abnormalities in the response of atrial natriuretic factor (ANF) to volume expansion have been reported in hypertensive-prone animals and men as well as in hypertensive patients undergoing ACE-inhibition. To investigate some of the mechanisms affecting ANF release in borderline hypertensive patients (BHT) we have studied 16 subjects by assessing their neuro-humoral and hemodynamic response to a two-hour isotonic i.v. NaCl infusion carried out during short-term administration of either placebo or captopril. ACE-inhibition increased baseline venous distensibility (VV30:1.4 vs 1.6 ml/100 ml; p < .05) and reduced the prompt (45') ANF response to saline loading (10.3 +/- 13 vs 42.7 +/- 15%; p < .05)) without affecting the overall ANF release (120':92 +/- 25 vs 65.8 +/- 20%; NS)). A significant pressor increase in response to NaCl loading was observed exclusively after ACE-inhibition (SBP: 5.2 +/- 2 vs 2.4 +/- 1%; p < .05--DBP: 7.1 +/- 3 vs 2 +/- 3%; p < .025) and occurred along with a peripheral arterial and venous constriction and with an increase in plasma levels of an endogeneous Na+/K+ATPase inhibitor (8.8 +/- 4 vs -2 +/- 4%; p < .05). We conclude that the ANF response to saline infusion is delayed by ACE-inhibition in borderline hypertensives. The abnormalities observed in ANF response could follow the changes in peripheral venous distensibility and contribute to the pressor and neuro-humoral derangements described in borderline hypertensives during volume expansion.