TY - JOUR
T1 - The effect of local angiotensin converting enzyme inhibition on the action of atrial natriuretic peptide in the human forearm
AU - Cockcroft, J. R.
AU - Allen, M. J.
AU - Benjamin, N.
AU - Webb, D. J.
PY - 1989
Y1 - 1989
N2 - It has been suggested that angiotensin converting enzyme (ACE) may play a role in the metabolism of atrial natriuretic peptide (ANP), and that ANP may interfere with angiotensin-induced vasoconstriction. This has been investigated within the forearm vascular bed during local ANP infusion and ACE inhibition. Six normotensive volunteers were studied, each on two occasions. On both occasions, after saline infusion, volunteers were given initially a 20 min infusion of ANP at 0.1 μg/min via the brachial artery. This was followed, after 20 min, by a second infusion of ANP at the same dose, co-infused with enalapril at (5 μg/min) on one occasion, and placebo (saline) on the other (in random order). Forearm blood flow was measured using venous occlusion plethysmography with mercury-in-silastic strain gauges. Blood flow in the cannulated arm increased significantly during the first ANP infusion; by 52 ± 15% before placebo (P < 0.05), and by 41 ± 8% before enalaprilat (p < 0.005). This increase was similar with the second ANP infusion during co-infusion of either placebo (40 ± 10%) or enalaprilat (45 ± 11%). Enalaprilat did not affect the half-life of vasodilatation produced by ANP (t( 1/2 ) = 5 min). These studies in healthy subjects demonstrate no effect of local ACE inhibition on resting blood flow, or on the vasodilatation produced by ANP in the human forearm, and provide no evidence of a role of ACE in the metabolism of ANP in this vascular bed.
AB - It has been suggested that angiotensin converting enzyme (ACE) may play a role in the metabolism of atrial natriuretic peptide (ANP), and that ANP may interfere with angiotensin-induced vasoconstriction. This has been investigated within the forearm vascular bed during local ANP infusion and ACE inhibition. Six normotensive volunteers were studied, each on two occasions. On both occasions, after saline infusion, volunteers were given initially a 20 min infusion of ANP at 0.1 μg/min via the brachial artery. This was followed, after 20 min, by a second infusion of ANP at the same dose, co-infused with enalapril at (5 μg/min) on one occasion, and placebo (saline) on the other (in random order). Forearm blood flow was measured using venous occlusion plethysmography with mercury-in-silastic strain gauges. Blood flow in the cannulated arm increased significantly during the first ANP infusion; by 52 ± 15% before placebo (P < 0.05), and by 41 ± 8% before enalaprilat (p < 0.005). This increase was similar with the second ANP infusion during co-infusion of either placebo (40 ± 10%) or enalaprilat (45 ± 11%). Enalaprilat did not affect the half-life of vasodilatation produced by ANP (t( 1/2 ) = 5 min). These studies in healthy subjects demonstrate no effect of local ACE inhibition on resting blood flow, or on the vasodilatation produced by ANP in the human forearm, and provide no evidence of a role of ACE in the metabolism of ANP in this vascular bed.
UR - http://www.scopus.com/inward/record.url?scp=0024539408&partnerID=8YFLogxK
M3 - Article
C2 - 2542549
AN - SCOPUS:0024539408
SN - 0950-9246
VL - 3
SP - 49
EP - 52
JO - Journal of Human Hypertension
JF - Journal of Human Hypertension
IS - 1
ER -