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1 Division of Cardiovascular Diseases and Internal Medicine, Mayo Clinic, Rochester, Minnesota 55905; and 2 University of Rochester Medical Center School of Medicine, Rochester, New York 14642
-Adrenergic hyporesponsiveness
in congestive heart failure (CHF) is mediated, in part, by nitric oxide
(NO). NO and brain natriuretic peptide (BNP) share cGMP as a second
messenger. Left ventricular (LV) function and inotropic response to
intravenous dobutamine (Dob) were assessed during sequential
intracoronary infusion of saline, HS-142-1 (a BNP receptor antagonist),
and HS-142-1 + NG-monomethyl-L-arginine
(L-NMMA) in anesthetized dogs with CHF due to rapid
pacing and in normal dogs during intracoronary infusion of saline,
exogenous BNP, and sodium nitroprusside (SNP). In CHF dogs,
intracoronary HS-142-1 did not alter the inotropic response to Dob
[percent change in first derivative of LV pressure
(%
dP/dt) 47 ± 4% saline vs. 54 ± 7%
HS-142-1, P = not significant]. Addition of
intracoronary L-NMMA to HS-142-1 enhanced the response to
Dob (%dP/dt 73 ± 8% L-NMMA + HS-142-1, P < 0.05 vs. H142-1). In normal dogs,
intracoronary SNP blunted the inotropic response to Dob (%dP/dt 93 ± 6% saline vs. 71 ± 5% SNP,
P < 0.05), whereas intracoronary BNP had no effect. In
CHF dogs, the time constant of LV pressure decay during isovolumic
relaxation increased with intracoronary HS-142-1 (48 ± 4 ms
saline vs. 58 ± 5 ms HS-142-1, P < 0.05) and further increased with intracoronary L-NMMA (56 ± 6 ms HS-142-1 vs. 66 ± 7 ms L-NMMA + HS-142-1,
P < 0.05). Endogenous BNP and NO preserve diastolic
function in CHF, whereas NO but not BNP inhibits -adrenergic responsiveness.
inotropy; cGMP; lusitropy
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