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1 University Laboratory of
Physiology,
Administration of
nitric oxide (NO) donors in vivo is accompanied by a
baroreflex-mediated increase in heart rate (HR). In vitro, however, NO
donors can increase HR directly by stimulating a pathway that involves
NO, cGMP, and the hyperpolarization-activated current
(If). The aim
of this study was to assess the functional significance of this pathway
in vivo by testing whether NO donors can increase HR in the
anesthetized rabbit independent of the autonomic nervous system. New
Zealand White rabbits were vagotomized, cardiac sympathectomized, and
treated with propranolol (0.3 mg/kg iv). The NO donor molsidomine (0.2 mg/kg iv) caused a progressive increase (
) in HR (HR, 14 ± 3 beats/min; P < 0.01). This effect was significantly reduced by the
If blocker
ZD-7288 (0.2 mg/kg iv; HR, 2 ± 3 beats/min;
P = not significant).
Similar results were seen with sodium nitroprusside. The positive
chronotropic effect of sodium nitroprusside (50 µM) was confirmed in
the isolated working rabbit heart preparation (HR, 17 ± 3 beats/min; P < 0.01). In conclusion,
NO donors exert a small, but significant, positive chronotropic effect
in vivo that is independent of the autonomic nervous system. These
results are also consistent with data in sinoatrial node cells that
show that NO donors increase HR by stimulating
If.
sodium nitroprusside; molsidomine; baroreflex; rabbit
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