Effects of cervical sympathetic nerve stimulation and neuropeptide Y (NPY) on cranial blood flow in the cat

1991 ◽  
Vol 142 (1) ◽  
pp. 21-32 ◽  
Author(s):  
E. GRANSTAM ◽  
S. F. E. NILSSON
Keyword(s):  
Blood Flow ◽  
Neuropeptide Y ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Stimulation ◽  
Cervical Sympathetic ◽  
Cervical Sympathetic Nerve

Influence of sympathetic discharge pattern on norepinephrine and neuropeptide Y release

1989 ◽  
Vol 257 (3) ◽  
pp. H866-H872 ◽  
Author(s):  
J. Pernow ◽  
J. Schwieler ◽  
T. Kahan ◽  
P. Hjemdahl ◽  
J. Oberle ◽  
...  
Keyword(s):  
Neuropeptide Y ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Impulse Activity ◽  
Sympathetic Nerve Stimulation ◽  
Vasoconstrictor Response ◽  
Neuropeptide Y Release ◽  
Sympathetic Discharge ◽  
Stimulation Pattern

The effects of sympathetic nerve stimulation on vasoconstrictor responses and overflow of norepinephrine (NE) and neuropeptide Y-like immunoreactivity (NPY-LI) were studied in the dog gracilis muscle and pig spleen in vivo. A continuous regular impulse activity was compared with irregular human sympathetic and regular bursting patterns. During control conditions, stimulation with the irregular activity induced larger peak vasoconstriction than the regular activity at 0.59 Hz, but not at higher frequencies in the muscle, at 0.59 and 2.0 Hz in the spleen. The nerve stimulation-evoked overflow of NE and NPY-LI from the muscle were not influenced by the pattern of stimulation. The overflow of NPY-LI, but not that of NE, from the spleen was enhanced by the irregular activity at 0.59 and 2.0 Hz, and both NPY-LI and NE overflows were enhanced by regular burst activity at 2.0 Hz. After blockade of alpha- and beta-adrenoceptors by phenoxybenzamine and propranolol, respectively, which enhanced nerve stimulation-evoked overflow of both NE and NPY-LI, the NE overflow from the muscle evoked by the irregular activity was slightly larger at 0.59 Hz but smaller at higher frequencies compared with that evoked by regular activity, whereas the detectable overflow of NPY-LI was not largely influenced by the stimulation pattern. In conclusion, both the vasoconstrictor response and the overflow of NPY-LI and NE seem to be influenced by the pattern and frequency of sympathetic nerve stimulation.

Arteriolar network response to pressure reduction during sympathetic nerve stimulation in cat skeletal muscle

1994 ◽  
Vol 266 (3) ◽  
pp. H1251-H1259 ◽  
Author(s):  
P. Ping ◽  
P. C. Johnson
Keyword(s):  
Blood Flow ◽  
Shear Stress ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Similar Degree ◽  
Sartorius Muscle ◽  
Pressure Reduction ◽  
Third Order ◽  
Sympathetic Nerve Stimulation ◽  
Resistance Change

Previous studies in this laboratory have shown that autoregulation of blood flow and dilation of midsized (second-order) arterioles were significantly enhanced during sympathetic nerve stimulation of cat sartorius muscle apparently because of a greater myogenic response of the arterioles. Quite typically, blood flow increased with arterial pressure reduction to 80, 60, and 40 mmHg (superregulation) during sympathetic nerve stimulation. To determine the contribution of the various orders of arterioles to the enhanced autoregulation, we measured diameters in all orders of arterioles and measured red cell velocity in first-, second-, and third-order arterioles. Without sympathetic nerve stimulation, all orders of arterioles except the first order dilated to pressure reduction, but flow autoregulation was weak. With sympathetic nerve stimulation, arteriolar dilation to pressure reduction was significantly enhanced in all six orders of arterioles, and flow rose significantly. The resistance change in the arteriolar network during pressure reduction as calculated from diameter changes was greatest in third- and fourth-order arterioles. Experimentally determined flow changes to pressure reduction and to sympathetic nerve stimulation were quantitatively similar to those predicted from diameter changes in a model of the arteriolar network. Calculated wall shear stress (from viscosity and shear rate) for first-, second-, and third-order arterioles decreased during pressure reduction with and without sympathetic nerve stimulation. We concluded that endothelium-mediated dilation due to shear stress would tend to oppose autoregulation of blood flow to a similar degree under both circumstances.

Presynaptic inhibitory effects of sotalol, propranolol, and acebutolol on noradrenaline release upon cardiac sympathetic nerve stimulation in anesthetized dogs

1986 ◽  
Vol 64 (8) ◽  
pp. 1076-1084 ◽  
Author(s):  
Nobuharu Yamaguchi ◽  
Michel Naud ◽  
Daniel Lamontagne ◽  
Reginald Nadeau ◽  
Jacques de Champlain
Keyword(s):  
Blood Flow ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Inhibitory Effect ◽  
Cardiac Sympathetic Nerve ◽  
Sympathetic Nerve Stimulation ◽  
Flow Response ◽  
Anesthetized Dogs ◽  
Na Release

Effect of sotalol (STL) was compared with that of (±)-propranolol, (+)-propranolol (PPL), and acebutolol (ABL) on noradrenaline (NA) release as measured in coronary sinus (CS) blood during postganglionic stimulation (2 Hz, 30 s) of the left cardiac sympathetic nerves in anesthetized dogs. In control dogs receiving saline, increasing responses of CS-NA concentration, mean CS blood flow, and CS-NA output to repetitive stimulation were relatively stable throughout a given experimental period. Both STL (1, 2.5, and 5 mg/kg, i.v.) and (±)-PPL (0.5 and 2.5 mg/kg, i.v.) diminished the increased CS-NA concentration by approximately 35 (P < 0.05) to 60% (P < 0.01) in a dose-dependent fashion. However, (+)-PPL (0.02–2.5 mg/kg, i.v.) and ABL (0.5–5 mg/kg, i.v.) did not significantly alter the increasing response of CS-NA concentration upon stimulation. STL, (±)-PPL, and ABL markedly inhibited the CS blood flow response to stimulation at all doses tested, while (+)-PPL did not significantly diminish the flow response even at the highest dose tested. Consequently, CS-NA output decreased significantly (p < 0.01) in the presence of STL, (±)-PPL, and ABL at all doses tested but not with (+)-PPL at any dose tested. The inhibitory effect of STL and (±)-PPL on the increasing response of CS-NA concentration upon stimulation could be related to their beta-blocking effect, which exerts presumably on postulated presynaptic β-adrenoceptors, as (+)-PPL did not at all diminish the response. On the other hand, ABL does not seem to exert a similar presynaptic inhibitory effect, owing presumably either to its β-1 selectivity or to its intrinsic sympathetic activity. The results support the existence of facilitatory presynaptic β-adrenoceptors in the normal dog heart under in vivo conditions. The findings also suggest that NA release upon cardiac sympathetic nerve stimulation may be reflected more precisely by CS-NA concentration than by NA output.

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