scholarly journals An electrophysiological analysis of the uptake of noradrenaline at sympathetic nerve terminals

1973 ◽  
Vol 229 (2) ◽  
pp. 533-546 ◽  
Author(s):  
M. R. Bennett
Keyword(s):  
Sympathetic Nerve ◽  
Nerve Terminals ◽  
Electrophysiological Analysis ◽  
Uptake Of Noradrenaline

scholarly journals Sympathetic nerve terminals in the tunica media of human superficial temporal and middle cerebral arteries: wet histofluorescence.

Stroke ◽  
1983 ◽  
Vol 14 (1) ◽  
pp. 62-66 ◽  
Author(s):  
I Akiguchi ◽  
H Fukuyama ◽  
M Kameyama ◽  
T Koyama ◽  
H Kimura ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
Cerebral Arteries ◽  
Nerve Terminals ◽  
Tunica Media ◽  
Middle Cerebral Arteries

Chronic exposure to neuropeptide Y determines cardiac alpha 1-adrenergic responsiveness

1991 ◽  
Vol 261 (3) ◽  
pp. H969-H973 ◽  
Author(s):  
L. S. Sun ◽  
P. C. Ursell ◽  
R. B. Robinson
Keyword(s):  
Neuropeptide Y ◽  
Sympathetic Nerve ◽  
Chronic Exposure ◽  
Developmental Change ◽  
Sympathetic Innervation ◽  
Nerve Terminals ◽  
Cardiac Sympathetic Nerve ◽  
Cardiac Sympathetic Innervation ◽  
Chronotropic Response ◽  
Npy Antagonist

The onset of sympathetic innervation induces a developmental change in the cardiac alpha 1-adrenergic chronotropic response from an increase to a decrease in rate. The mechanism by which innervation induces this alteration is unknown. Neuropeptide Y (NPY), which is found abundantly in cardiac sympathetic nerve terminals, was considered as a possible mediator for this effect. Chronic conditioning by NPY in noninnervated myocyte cultures stimulated the effect of sympathetic innervation in inducing the alpha 1-inhibitory chronotropic response. Chronic conditioning by the NPY antagonist PYX-2 blocked the effect of innervation. Thus endogenous NPY may modulate alpha 1-adrenergic responsiveness during the ontogeny of cardiac sympathetic innervation.

scholarly journals Sympathetic nerves and the endothelium influence the vasoconstrictor effect of low concentrations of ouabain in pressurized small arteries

2010 ◽  
Vol 298 (6) ◽  
pp. H2093-H2101 ◽  
Author(s):  
Hema Raina ◽  
Qingli Zhang ◽  
Albert Y. Rhee ◽  
Thomas L. Pallone ◽  
W. Gil Wier
Keyword(s):  
Smooth Muscle ◽  
Sympathetic Nerve ◽  
Arterial Wall ◽  
Sympathetic Nerves ◽  
Nerve Terminals ◽  
Arterial Smooth Muscle ◽  
Low Concentrations ◽  
Endogenous Ouabain ◽  
Adrenoceptor Blocker ◽  
Arterial Endothelium

We hypothesized that in salt-dependent forms of hypertension, endogenous ouabain acts on arterial smooth muscle to cause enhanced vasoconstriction. Here, we tested for the involvement of the arterial endothelium and perivascular sympathetic nerve terminals in ouabain-induced vasoconstriction. Segments of rat mesenteric or renal interlobar arteries were pressurized to 70 mmHg at 37°C and exposed to ouabain (10−11–10−7 M). Removal of the endothelium enhanced ouabain-induced vasoconstriction by as much as twofold (at an ouabain concentration of 10−9 M). A component of the ouabain-induced vasoconstriction is due to the enhanced spontaneous release of norepinephrine (NE) from nerve terminals in the arterial wall. The α1-adrenoceptor blocker prazosin (10−6 M) decreased ouabain-induced vasoconstrictions by as much as 50%. However, neither the contraction induced by sympathetic nerve activity (SNA) nor the NE release evoked by SNA (measured directly by carbon fiber amperometry) was increased by ouabain (<10−7 M). Nevertheless, the converse case was true: after brief bursts of SNA, vasoconstrictor responses to ouabain were transiently increased (1.75-fold). This effect may be mediated by neuropeptide Y and Y1 receptors on smooth muscle. In arteries lacking the endothelium and exposed to prazosin, ouabain (10−11 M and greater) caused vasoconstriction, indicating a direct effect of very “low” concentrations of ouabain on arterial smooth muscle. In conclusion, in intact arteries, the endothelium opposes ouabain (10−11–10−7M)-induced vasoconstriction, which is caused by both enhanced spontaneous NE release and direct effects on smooth muscle. Ouabain (<10−7M) does not enhance SNA-mediated contractions, but SNA enhances ouabain-induced contractions. The effects of endogenous ouabain may be accentuated in forms of hypertension that involve sympathetic nerve hyperactivity and/or endothelial dysfunction.

The processing of secretogranin II in the peripheral nervous system: release of secretoneurin from porcine sympathetic nerve terminals

1999 ◽  
Vol 818 (2) ◽  
pp. 459-467 ◽  
Author(s):  
Fei Liang ◽  
Jia-Yi Li ◽  
Paola Lovisetti-Scamihorn ◽  
Edmond Coen ◽  
Jan Depreitere ◽  
...  
Keyword(s):  
Nervous System ◽  
Peripheral Nervous System ◽  
Sympathetic Nerve ◽  
Nerve Terminals ◽  
Secretogranin Ii
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