Sympathetic nerve activity, including that in the kidney, is increased in
heart failure with increased plasma concentrations of
norepinephrine and the
vasoconstrictor cotransmitter
neuropeptide Y (NPY). We examined the contribution of NPY to sympathetically mediated alterations in kidney function in normal and
heart failure rats.
Heart failure rats were created by left coronary
ligation and
myocardial infarction. In anesthetized normal rats, the NPY Y(1) receptor antagonist,
H 409/22, at two doses, had no effect on heart rate, arterial pressure, or renal hemodynamic and excretory function. In conscious severe
heart failure rats, high-dose
H 409/22 decreased mean arterial pressure by 8 +/- 2 mm Hg but had no effect in normal and mild
heart failure rats. During graded frequency renal sympathetic nerve stimulation (0 to 10 Hz), high-dose
H 409/22 attenuated the decreases in renal blood flow only
at 10 Hz (-36% +/- 5%, P <.05) in normal rats but did so at both 4 (-29% +/- 4%, P <.05) and 10 Hz (-33% +/- 5%, P <.05) in
heart failure rats. The glomerular filtration rate, urinary flow rate, and
sodium excretion responses to renal sympathetic nerve stimulation were not affected by high-dose
H 409/22 in either normal or
heart failure rats. NPY does not participate in the regulation of kidney function and arterial pressure in normal conscious or anesthetized rats. When sympathetic nervous system activity is increased, as in
heart failure and intense renal sympathetic nerve stimulation, respectively, a small contribution of NPY to maintenance of arterial pressure and to sympathetic renal
vasoconstrictor responses may be identified.