TY - JOUR
T1 - Maintenance of forearm vasodilator action of atrial natriuretic factor in congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy
AU - Kubo, Spencer H.
AU - Atlas, Steven A.
AU - Laragh, John H.
AU - Cody, Robert J.
N1 - Funding Information:
From the Cardiology Division and Hypertension Center, Department of Medicine, Cornell Medical Center, New York Hospital, New York, New York. This study was supported by a Grant-in-Aid from the New York Heart Association; SCOR Grant HL-18323-12 from the National Heart, Lung, and Blood Institute, Bethesda, Maryland; General Clinical Research Center Grant RR-047, Bethesda,M aryland; and a grant from the Mathers Foundation,N ew York, New York, in memory of Ralph Menapace. Manuscript received October 16, 1991; revised manuscript received and acceptedJ anuary 9.1992.
PY - 1992/5/15
Y1 - 1992/5/15
N2 - Infusions of atrial natriuretic factor (ANF) are frequently associated with attenuated natriuretic and diuretic responses in patients with congestive heart failure. However, ANF infusions result in systemic vasodilation, suggesting that end organ responsiveness to ANF may not be uniformly decreased. To determine if the vasodilator effects of ANF were altered in heart failure, strain-gauge plethysmography was utilized to measure forearm blood flow responses to the intraarterial infusion of ANF using a dose range that was low enough to avoid systemic effects. In 9 control subjects, ANF infusions of 0.5, 1.0, 2.0 and 4.0 μg/min/100 ml forearm volume significantly increased forearm blood flow from 3.21 ± 1.71 to 5.69 ± 3.14, 6.20 ± 2.57, 6.64 ± 2.53 and 6.97 ± 2.49 ml/min/100 ml forearm volume, respectively (all p < 0.01). In 7 patients with heart failure, ANF infusion significantly increased forearm blood flow from 2.19 ± 0.98 to 3.18 ± 1.70, 3.76 ± 2.0 and 4.42 ± 2.80 ml/min/100 ml forearm volume for the 0.5, 1.0 and 2.0 μg doses, respectively (all p < 0.05). By analysis of variance, the forearm blood flow responses pooled over all doses were not significantly different between the 2 groups. At the 2.0 μg dose, the peak increase in forearm blood flow in normal subjects represented a 107% increase over baseline compared with a 102% increase in patients with heart failure. In summary, these data demonstrate that intraarterial administration of ANF in patients with heart failure resulted in dose-related increases in forearm blood flow. The responses were not significantly different from normal subjects expressed both as an absolute response and as a percent increase. These data therefore confirm that rat ANF in pharmacologic doses has a direct vasodilator action in humans and further suggest that ANF-mediated vasodilation in the peripheral circulation is relatively intact in heart failure.
AB - Infusions of atrial natriuretic factor (ANF) are frequently associated with attenuated natriuretic and diuretic responses in patients with congestive heart failure. However, ANF infusions result in systemic vasodilation, suggesting that end organ responsiveness to ANF may not be uniformly decreased. To determine if the vasodilator effects of ANF were altered in heart failure, strain-gauge plethysmography was utilized to measure forearm blood flow responses to the intraarterial infusion of ANF using a dose range that was low enough to avoid systemic effects. In 9 control subjects, ANF infusions of 0.5, 1.0, 2.0 and 4.0 μg/min/100 ml forearm volume significantly increased forearm blood flow from 3.21 ± 1.71 to 5.69 ± 3.14, 6.20 ± 2.57, 6.64 ± 2.53 and 6.97 ± 2.49 ml/min/100 ml forearm volume, respectively (all p < 0.01). In 7 patients with heart failure, ANF infusion significantly increased forearm blood flow from 2.19 ± 0.98 to 3.18 ± 1.70, 3.76 ± 2.0 and 4.42 ± 2.80 ml/min/100 ml forearm volume for the 0.5, 1.0 and 2.0 μg doses, respectively (all p < 0.05). By analysis of variance, the forearm blood flow responses pooled over all doses were not significantly different between the 2 groups. At the 2.0 μg dose, the peak increase in forearm blood flow in normal subjects represented a 107% increase over baseline compared with a 102% increase in patients with heart failure. In summary, these data demonstrate that intraarterial administration of ANF in patients with heart failure resulted in dose-related increases in forearm blood flow. The responses were not significantly different from normal subjects expressed both as an absolute response and as a percent increase. These data therefore confirm that rat ANF in pharmacologic doses has a direct vasodilator action in humans and further suggest that ANF-mediated vasodilation in the peripheral circulation is relatively intact in heart failure.
UR - https://www.scopus.com/pages/publications/0026763971
U2 - 10.1016/0002-9149(92)91226-T
DO - 10.1016/0002-9149(92)91226-T
M3 - Article
C2 - 1533988
AN - SCOPUS:0026763971
SN - 0002-9149
VL - 69
SP - 1306
EP - 1309
JO - American Journal of Cardiology
JF - American Journal of Cardiology
IS - 16
ER -