Effects of 6-hydroxydopamine on dopamine and noradrenaline content in dog blood vessels and heart

1985 ◽  
Vol 329 (3) ◽  
pp. 253-257 ◽  
Author(s):  
P. Soares-da-Silva ◽  
R. Davidson
Keyword(s):  
Blood Vessels ◽  
Noradrenaline Content ◽  
Dog Blood ◽  
6 Hydroxydopamine

scholarly journals Nerve Fibers Containing Neuropeptide Y in the Cerebrovascular Bed: Immunocytochemistry, Radioimmunoassay, and Vasomotor Effects

1987 ◽  
Vol 7 (1) ◽  
pp. 45-57 ◽  
Author(s):  
L. Edvinsson ◽  
J. R. Copeland ◽  
P. C. Emson ◽  
J. McCulloch ◽  
R. Uddman
Keyword(s):  
Neuropeptide Y ◽  
Blood Vessels ◽  
Superior Cervical Ganglion ◽  
Cerebral Arteries ◽  
Nerve Fibers ◽  
Calcium Entry Blocker ◽  
Cervical Ganglion ◽  
Prostaglandin F ◽  
6 Hydroxydopamine

Perivascular nerve fibers containing neuropeptide Y (NPY)-like immunoreactivity were identified around cerebral blood vessels of human, cat, guinea pig, rat, and mouse. The major cerebral arteries were invested by dense plexuses; veins, small arteries, and arterioles were accompanied by few fibers. Removal of the superior cervical ganglion resulted in a reduction of NPY-like material in pial vessels and dura mater. Pretreatment with 6-hydroxydopamine or reserpine reduced the number of visible NPY fibers and the concentration of NPY in rat cerebral vessels. Sequential immuno-staining with antibodies toward dopamine-β-hydroxylase (DBH) (an enzyme involved in the synthesis of noradrenaline) and NPY revealed an identical localization of DBH and NPY in nerve cell bodies in the superior cervical ganglion and in perivascular fibers of pial blood vessels, suggesting their coexistence. Administration of NPY in vitro resulted in concentration-dependent contractions that were not modified by a sympathectomy. The contractions induced by noradrenaline, 5-hydroxytryptamine, and prostaglandin F2α and the dilator responses to calcitonin gene-related peptide were not modified by NPY in rat cerebral arteries. However, the constrictor response to NPY was reduced by 70% in the presence of the calcium entry blocker nifedipine, and abolished following incubation in a calcium-free buffer. These data suggest an interaction of NPY at a postsynaptic site, which for induction of contraction may open calcium channels in the sarcolemma of cerebral arteries.

scholarly journals Heterogeneity of α1-adrenoceptor subtypes involved in noradrenaline-induced contractions of dog blood vessels.

1993 ◽  
Vol 61 ◽  
pp. 258
Author(s):  
Yoko Kohno ◽  
Hitoshi Saito ◽  
Manabu Takita ◽  
Shigeru Kigoshi ◽  
Ikunobu Muramatsu
Keyword(s):  
Blood Vessels ◽  
Dog Blood

scholarly journals Galanin is localized in sympathetic neurons of the dog liver

1997 ◽  
Vol 273 (6) ◽  
pp. E1194-E1202 ◽  
Author(s):  
Thomas O. Mundinger ◽  
C. Bruce Verchere ◽  
Denis G. Baskin ◽  
Michael R. Boyle ◽  
Stephan Kowalyk ◽  
...  
Keyword(s):  
Blood Vessels ◽  
Sympathetic Neurons ◽  
Sympathetic Nerves ◽  
Liver Parenchyma ◽  
Nerve Fibers ◽  
Adrenergic Nerve ◽  
Adrenergic Nerve Terminals ◽  
6 Hydroxydopamine ◽  
Hepatic Nerves ◽  
Dog Liver

Stimulation of canine hepatic nerves releases the neuropeptide galanin from the liver; therefore, galanin may be a sympathetic neurotransmitter in the dog liver. To test this hypothesis, we used immunocytochemistry to determine if galanin is localized in hepatic sympathetic nerves and we used hepatic sympathetic denervation to verify such localization. Liver sections from dogs were immunostained for both galanin and the sympathetic enzyme marker tyrosine hydroxylase (TH). Galanin-like immunoreactivity (GALIR) was colocalized with TH in many axons of nerve trunks as well as individual nerve fibers located both in the stroma of hepatic blood vessels and in the liver parenchyma. Neither galanin- nor TH-positive cell bodies were observed. Intraportal 6-hydroxydopamine (6-OHDA) infusion, a treatment that selectively destroys hepatic adrenergic nerve terminals, abolished the GALIR staining in parenchymal neurons but only moderately diminished the GALIR staining in the nerve fibers around blood vessels. To confirm that 6-OHDA pretreatment proportionally depleted galanin and norepinephrine in the liver, we measured both the liver content and the hepatic nerve-stimulated spillover of galanin and norepinephrine from the liver. Pretreatment with 6-OHDA reduced the content and spillover of both galanin and norepinephrine by >90%. Together, these results indicate that galanin in dog liver is primarily colocalized with norepinephrine in sympathetic nerves and may therefore function as a hepatic sympathetic neurotransmitter.

A role of the central catecholamine neuron in cerebral circulation

1986 ◽  
Vol 65 (3) ◽  
pp. 370-375 ◽  
Author(s):  
Hideyoshi Yokote ◽  
Toru Itakura ◽  
Kunio Nakai ◽  
Ichiro Kamei ◽  
Harumichi Imai ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Blood Vessels ◽  
Cerebral Circulation ◽  
Intracerebral Injection ◽  
Neuron System ◽  
Content Type ◽  
6 Hydroxydopamine ◽  
Catecholamine Neuron

✓ The effect of the central catecholaminergic neurons on the cerebral microcirculation was investigated by means of a unilateral intracerebral injection of 6-hydroxydopamine (6-OHDA) which produced the degeneration of catecholamine (CA) nerve terminals. Subsequent observation with CA histofluorescence revealed an absence of CA fibers in the vicinity of the 6-OHDA injection site. A significant increase in regional cerebral blood flow (rCBF), measured by the hydrogen clearance method, was demonstrated in the CA-depleted cortex under normocapnia as compared with rCBF in the control cortex (CA-depleted cortex 47.0 ± 2.8 ml/100 gm/min; control cortex 38.5 ± 3.5 ml/100 gm/min; p < 0.005). The increased rCBF in the cortex treated with 6-OHDA was suppressed by the iontophoretic replacement of noradrenaline (NA) to the CA-depleted cortex. An iontophoretic replacement of 10−5 M dopamine (DA) mildly suppressed the increased rCBF in the 6-OHDA-treated cortex. The CO2 reactivity in the CA-depleted cortex was significantly lower than that of the control cortex (CA-depleted cortex 2.13% ± 0.67%/mm Hg; control cortex 3.53% ± 0.70%/mm Hg). No change was noticeable in the cerebral glucose metabolism in the CA-depleted cortex in an investigation based on tritiated (3H)-deoxyglucose uptake. It is suggested that the 6-OHDA-induced change in cerebral blood flow (CBF) is not secondary to alterations in cerebral metabolic rate, and that the central NA neuron system innervating intraparenchymal blood vessels regulates CBF through a direct vasoconstrictive effect on the cerebral blood vessels. The central DA neuron system may modulate the cerebral circulation as a mild vasoconstrictor.

Relaxant Effects of Butylidenephthalide in Isolated Dog Blood Vessels

Planta Medica ◽  
2002 ◽  
Vol 68 (11) ◽  
pp. 1004-1009 ◽  
Author(s):  
Wun Chang Ko ◽  
Chao-Chiun Liao ◽  
Chih-Hsien Shih ◽  
Chien-Bang Lei ◽  
Chi-Ming Chen
Keyword(s):  
Blood Vessels ◽  
Dog Blood

Supersensitivity of the Isolated Rat Heart after Chemical Sympathectomy with 6-Hydroxydopamine

1971 ◽  
Vol 49 (1) ◽  
pp. 36-44 ◽  
Author(s):  
R. A. Nadeau ◽  
J. De Champlain ◽  
G. M. Tremblay
Keyword(s):  
Nerve Fibers ◽  
Isolated Rat Heart ◽  
Adrenergic Nerve ◽  
Noradrenaline Content ◽  
Chronotropic Response ◽  
Endogenous Noradrenaline ◽  
6 Hydroxydopamine ◽  
Perfused Hearts ◽  
Supersensitivity To Noradrenaline ◽  
Isolated Rat

Presynaptic supersensitivity was demonstrated in isolated rat atria and perfused hearts 2 h after an intravenous injection of 6-hydroxydopamine (6-OH-DA), 100 mg/kg. This coincided with a maximum depletion of cardiac endogenous noradrenaline, a disappearance of the fluorescence of terminal adrenergic nerve fibers in the atrial myocardium, and an abolished chronotropic response to tyramine. The chronotropic response to dopamine was also significantly diminished. Maximal supersensitivity to the chronotropic effect of noradrenaline was observed 72 h after the injection of 6-OH-DA. Two weeks after the administration of 6-OH-DA, supersensitivity to noradrenaline was less marked, and the response to tyramine was restored. These changes corresponded to an increasing noradrenaline content in the heart and to the reappearance of histofluorescent fibers in the atria.

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