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Department of Physiology and Biophysics, University of Nebraska College of Medicine, Omaha, Nebraska 68198-4575
An
enhanced peripheral chemoreflex has been documented in patients with
chronic heart failure (CHF). This study aimed to examine the
characteristics of carotid body (CB) chemoreceptors in response to
isocapnic hypoxia in a rabbit model of pacing-induced CHF and to
evaluate the possible role that nitric oxide (NO) plays in the altered
characteristics. The chemosensitive characteristics of the CB were
evaluated by recording single-unit activity from the carotid sinus
nerve in both an intact and a vascularly isolated preparation. It was
found that the baseline discharge under normoxia (intact preparation:
arterial PO2 90-95 Torr;
isolated preparation: PO2
100-110 Torr) and the chemosensitivity in response to graded
hypoxia (PO2 40-70 Torr) were
enhanced in CHF vs. sham rabbits. These alterations were independent of the CB preparations (intact vs. isolated). NO synthase inhibition by
N
-nitro-L-arginine
increased the baseline discharge and the chemosensitivity in the intact
preparation, whereas L-arginine
(10
5 M) inhibited the
baseline discharge and the chemosensitivity in the isolated preparation
in sham but not in CHF rabbits.
S-nitroso-N-acetylpenicillamine, an NO donor, inhibited the baseline discharge and the chemosensitivity in both CB preparations in CHF rabbits but only in the isolated preparation in sham rabbits. The amount of NO produced in vitro by the
CB under normoxia was less in CHF rabbits than in sham rabbits
(P < 0.05). NO synthase-positive
varicosities of nerve fibers within the CB were less in CHF rabbits
than in sham rabbits (P < 0.05).
These data indicate that an enhanced input from CB occurs in the rabbit
model of pacing-induced CHF and that an impairment of NO production may
contribute to this alteration.
single-unit activity; carotid sinus nerve; N-nitro-L-arginine; S-nitroso-N-acetyl-penicillamine; hypoxia
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