Platelet-derived Products and Adrenergic Neurotransmission

1990 ◽  
pp. 159-190
Author(s):  
Tony J. Verbeuren
Keyword(s):  
Adrenergic Neurotransmission

INFLUENCE OF HYPERTENSION ON DYSFUNCTION OF REGULATION OF ADRENERGIC NEUROTRANSMISSION IN SHR.Cg-Leprcp/NDmcr RATS

2007 ◽  
Vol 34 (s1) ◽  
pp. S33-S34
Author(s):  
Namie Nejime ◽  
Satomi Kagota ◽  
Ryoko Yoshihara ◽  
Naoko Tanaka ◽  
Ami Tei ◽  
...  
Keyword(s):  
Adrenergic Neurotransmission

Endothelium Inhibits Adrenergic Neurotransmission

2015 ◽  
pp. 206-212
Author(s):  
Richard A. Cohen ◽  
Belay Tesfamariam ◽  
Robert M. Weisbrod
Keyword(s):  
Adrenergic Neurotransmission

scholarly journals Inhibitory modulation of adrenergic neurotransmission via prejunctional P3 like purinoceptors in rat mesenteric artery

1998 ◽  
Vol 76 ◽  
pp. 57
Author(s):  
Young Mi Kwon ◽  
Yoshie Tanioka ◽  
Masako Fukuda ◽  
Kazuki Nakamura ◽  
Kazumasa Shinozuka ◽  
...  
Keyword(s):  
Mesenteric Artery ◽  
Inhibitory Modulation ◽  
Rat Mesenteric Artery ◽  
Adrenergic Neurotransmission

Prejunctional adrenergic inhibition by aggregating platelets in canine blood vessels

1985 ◽  
Vol 249 (3) ◽  
pp. H685-H689 ◽  
Author(s):  
R. R. Lorenz ◽  
P. M. Vanhoutte
Keyword(s):  
Blood Vessels ◽  
Inhibitory Effect ◽  
Adrenergic Nerve ◽  
Saphenous Veins ◽  
Other Substances ◽  
Adrenergic Nerve Endings ◽  
Adrenergic Neurotransmission ◽  
Prejunctional Inhibition ◽  
Serotonergic Antagonist ◽  
Stimulation Of

Experiments were performed to determine the effect of aggregating platelets on adrenergic neurotransmission. Rings of canine saphenous veins and left circumflex coronary arteries were incubated with [3H]norepinephrine and suspended for superfusion. Aggregating platelets and exogenous 5-hydroxytryptamine decreased the overflow of [3H]norepinephrine evoked by electrical stimulation of the adrenergic nerve endings. The reduction of transmitter overflow caused by 5-hydroxytryptamine was prevented by the serotonergic antagonist methiothepin in a concentration that did not significantly affect the release of 5-hydroxytryptamine or thromboxane B2 from the aggregating platelets. Methiothepin decreased but did not abolish the inhibitory effect of aggregating platelets on neurotransmitter overflow. These experiments demonstrate that 5-hydroxytryptamine and other substances released from aggregating platelets can exert prejunctional inhibition of adrenergic neurotransmission in isolated blood vessels.

Effects of maturation on adrenergic neurotransmission in ovine cerebral arteries

1999 ◽  
Vol 277 (4) ◽  
pp. R931-R937 ◽  
Author(s):  
William J. Pearce ◽  
Sue P. Duckles ◽  
John Buchholz
Keyword(s):  
Cerebral Arteries ◽  
Age Groups ◽  
Peptidergic Neurons ◽  
Synaptic Density ◽  
Vasoactive Substances ◽  
Age Related ◽  
Middle Cerebral Arteries ◽  
Adrenergic Neurotransmission ◽  
Fractional Release ◽  
Two Age Groups

The present studies examine the hypothesis that multiple adrenergic neuroeffector mechanisms are not fully developed in fetal, compared with adult, ovine middle cerebral arteries. In arteries denuded of endothelium and pretreated with 1 μM atropine to block involvement of muscarinic receptors, 10 μM capsaicin to deplete sensory peptidergic neurons, and 10 μM nitro-l-arginine methyl ester (l-NAME) to block possible influences from nitric oxidergic innervation, transmural stimulation at 16 Hz increased contractile tensions to 9.5 ± 3.7% ( n = 6) of the potassium maximum in adult arteries. Corresponding values in fetal arteries, however, were significantly less and averaged only 1.1 ± 0.6% ( n =10). However, postsynaptic sensitivity to norepinephrine (NE) was similar in the two age groups; NE pD2 values (−log EC50) averaged 6.11 ± 0.12 ( n = 6) and 6.33 ± 0.09 M ( n = 9) in fetal and adult arteries, respectively. Similarly, NE content measured via HPLC was also similar in the two age groups and averaged 32.4 ± 5.0 ( n = 17) and 32.5 ± 3.9 ng/ng wet wt ( n = 13) in fetal and adult middle cerebral arteries, respectively. In contrast, stimulation-induced NE release was greater in fetal than in adult arteries, whether calculated as total mass released [883 ± 184 ( n = 17) vs. 416 ± 106 pg NE/mg wet wt ( n = 13)] or as fractional release [51.1 ± 5.3 ( n = 17) vs. 22.8 ± 3.8 pg/pg NE content per pulse × 10−6]. Measured as an index of synaptic density, neuronal cocaine-sensitive NE uptake was similar in fetal and adult arteries [1.55 ± 0.40 ( n = 10) and 1.84 ± 0.51 pmol/mg wet wt ( n = 7), respectively]. Overall, age-related differences in postsynaptic sensitivity to NE, NE release, and NE uptake capacity cannot explain the corresponding age-related differences in response to stimulation. The data thus suggest that total synaptic volume and cleft width, in particular, are probably greater and/or that adrenergic corelease of vasoactive substances other than NE is altered in fetal compared with adult middle cerebral arteries.

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