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Vol. 286, Issue 1, 70-76, July 1998
Department of Pharmacology, Shinshu University School of Medicine,
Matsumoto 390-8621, Japan
There are no available data on the direct effect of C-type natriuretic
peptide (CNP) and brain natriuretic peptide (BNP) on the myocardial
contractility in mammalian hearts. Thus we studied the inotropic and
chronotropic effects of CNP-22 and BNP-32 compared with those of atrial
natriuretic peptide (ANP)-28 using the isolated, blood-perfused canine
right atrial or left ventricular preparations. CNP increased the atrial
contractile force in a dose-dependent manner with a small increase in
sinus rate in isolated atria, whereas neither ANP nor BNP changed
atrial force and rate. CNP but not BNP also increased the ventricular
contractile force in isolated ventricles. Pretreatment with a high dose
(3 nmol) of CNP attenuated the positive inotropic response to CNP at a
low dose (1 nmol) but not to norepinephrine. A guanylyl cyclase-linked natriuretic peptide receptor antagonist, HS-142-1, inhibited the increases in atrial contractile force and sinus rate in response to
CNP, but it did not affect the positive cardiac responses to norepinephrine. Propranolol did not block the positive cardiac responses to CNP. 3-Isobutyl-1-methylxanthine in rates of 0.6 to 1.3 µmol/min attenuated the CNP-induced positive inotropic responses,
when it potentiated the positive inotropic response to norepinephrine.
On the other hand, parasympathetic nerve stimulation attenuated the
positive cardiac responses to CNP and norepinephrine. These results
demonstrate that CNP increases myocardial contractile force with a
small increase in sinus rate mediated by guanylyl cyclase-linked
natriuretic peptide receptors, probably type B receptors in the dog
heart, and suggest that the positive inotropic response to CNP is
influenced by the cyclic adenosine 3',5'-monophosphate-dependent signal
transduction.
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