Atrial Natriuretic Factor Response to Acute Volume Expansion in Borderline Hypertension. Role of Ace-Inhibition and Changes in Peripheral Venous Tone

Abstract

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.

Key Words:

• ANF
• Captopril
• Venodilatation
• NaCl
• Na⁺/K⁺ ATPase inhibitor