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PubMedDate not supplied

Neuropeptide Y (NPY) and the pig heart: release and coronary vasoconstrictor effects.

The effects of electrical stimulation of the stellate ganglia on the arterio-venous concentration differences of neuropeptide Y (NPY)-like immunoreactivity (LI) over the pig heart were studied in vivo in relation to changes in heart rate and left ventricular pressure. Furthermore, the effects of NPY on coronary vascular tone were analysed in vivo and in vitro. Stellate ganglion stimulation at a high frequency (10 Hz) caused a clear-cut, long lasting increase in plasma levels of NPY-LI in the coronary sinus compared to the aorta, suggesting release of this peptide from sympathetic terminals within the heart. The stimulation-evoked overflow of NPY-LI from the heart was enhanced about 3-fold by alpha-adrenoceptor blockade using phenoxybenzamine, suggesting that NPY release is under prejunctional inhibitory control by noradrenaline (NA). Combined alpha- and beta-adrenoceptor blockade abolished most of the positive inotropic response of the heart upon stellate ganglion stimulation, while a considerable positive chronotropic effect remained. After guanethidine treatment, stellate ganglion stimulation still produced a small positive inotropic and chronotropic effect on the heart. The stimulation evoked NPY overflow was markedly reduced by guanethidine indicating an origin from sympathetic nerve terminals. Injection of NPY into the constantly perfused left anterior descending artery in vivo caused a long lasting, adrenoceptor antagonist resistant increase in perfusion pressure, suggesting coronary vasoconstriction. NPY contracted coronary arteries in vitro via a nifedipine-sensitive mechanism. NA dilated coronary vessels both in vivo and in vitro via beta-adrenoceptor activation. It is concluded that sympathetic nerve stimulation increases overflow of NPY-LI from the heart suggesting release from cardiac nerves in vivo.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMedDate not supplied

Exogenous adenosine induces flowmotion in skeletal muscle microcirculation of the anesthetized rat.

The aim of this study was to investigate the characteristics of the microcirculatory blood flow with laser-Doppler flowmetry (LDF) in skeletal muscle during both regional and systemic infusions of adenosine. A laser-Doppler flowmeter probe was placed on the left gastrocnemius muscle in anesthetized rats. Adenosine was given either systemically in the jugular vein (group A) or administered regionally in the iliac artery (group B). The infusion of adenosine was increased stepwise by 50 micrograms/kg/min, every 10 min, up to 400 micrograms/kg/min. In group A there was a dose-dependent decrease in mean arterial pressure as well as in LDF flow; flowmotion of the LDF signal with a frequency of 1.6 cycles/min was seen at a mean adenosine dose of 240 micrograms/kg/min at a blood pressure of 60 mm Hg. In group B there was a dose-dependent decrease of mean arterial blood pressure but not as marked compared to group A, meanwhile the LDF flow was unchanged; flowmotion was seen at a mean adenosine dose of 220 microgram/kg/min at a blood pressure of 72 mm Hg, with a frequency of 1.5 cycles/min. This study demonstrates that adenosine, given either regionally intraarterially with maintained blood flow, or intravenously with reduced blood flow, induces flowmotion in skeletal muscle microcirculation with a frequency of approximately 1.5 cycles/min.

Adenosine↗