Evidence supporting the existence of presynaptic ?-adrenoceptors in the regulation of endogenous noradrenaline release upon hepatic sympathetic nerve stimulation in the dog liver in vivo

1982 ◽  
Vol 321 (3) ◽  
pp. 177-184 ◽  
Author(s):  
Nobuharu Yamaguchi
Keyword(s):  
Nerve Stimulation ◽  
Noradrenaline Release ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Stimulation ◽  
Endogenous Noradrenaline ◽  
Presynaptic Adrenoceptors ◽  
Dog Liver

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.

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.

Comparative Effects of Prostaglandins A2 and B2 on Vascular and Airway Resistances and Adrenergic Neurotransmission

1974 ◽  
Vol 52 (3) ◽  
pp. 699-705 ◽  
Author(s):  
Stanley Greenberg ◽  
Linda Howard ◽  
William R. Wilson
Keyword(s):  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Neurotransmitter Release ◽  
Airway Resistance ◽  
Autologous Blood ◽  
Sympathetic Nerve Stimulation ◽  
Systemic Pressure ◽  
Low Concentrations ◽  
Pressor Responses

Prostaglandin B2 (PGB2) may be formed from PGA2in vivo. The following study compares the effects of equivalent concentrations of PGA2 and PGB2 on systemic pressure, heart rate, airway resistance, cutaneous vascular resistance, and responses to sympathetic nerve stimulation and to norepinephrine and tyramine in the acutely denervated canine hind paw perfused with autologous blood at constant flow. Intra-arterial (i.a.) PGB2 (1 and 10 μg/min) produced concentration-dependent vasoconstriction. Fifteen minutes after PGB2 administration the pressor responses of the paw to sympathetic nerve stimulation were enhanced, whereas the pressor responses to norepinephrine and tyramine were unchanged. In contrast, low concentrations of PGA2 produced systemic and transient cutaneous dilation whereas the higher concentration (10 μg/min i.a.) produced systemic dilation and constriction of the acutely denervated paw. The pressor responses of the perfused paw to sympathetic nerve stimulation were enhanced with the higher infusion rate of PGA2. However, the pressor responses to norepinephrine and tyramine were unchanged during PGA2. In addition, PGB2, but not PGA2, increased airway resistance. These results suggest that: (1) PGB2 and PGA2 have different effects on systemic pressure and airway resistance but have similar effects on the cutaneous vascular bed; (2) both PGB2 and PGA2 selectively enhance neurotransmitter release from the catecholamine pool susceptible to activation by the nerve action potential; and (3) PGB2 is more potent in its ability to enhance neurotransmitter release than PGA2. The vasoconstriction and facilitation of sympathetic neurotransmission by PGA2 may be related to formation of PGB2 within the paw.

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