Adrenergic nerve elements in the hypogatric ganglion of the guinea pig

1971 ◽  
Vol 130 (3) ◽  
pp. 305-329 ◽  
Author(s):  
Hiroshi Watanabe
Keyword(s):  
Guinea Pig ◽  
Adrenergic Nerve

Ultrastructural evidence for adrenergic nerve degeneration in the guinea pig uterus during pregnancy

1978 ◽  
Vol 195 (1) ◽  
Author(s):  
B. Sporrong ◽  
P. Alm ◽  
Ch. Owman ◽  
N.-O. Sj�berg ◽  
G. Thorbert
Keyword(s):  
Guinea Pig ◽  
Nerve Degeneration ◽  
Adrenergic Nerve ◽  
Ultrastructural Evidence

Activation of protein kinase C potentiates norepinephrine release from sinus node

1986 ◽  
Vol 251 (6) ◽  
pp. C833-C840 ◽  
Author(s):  
H. Shuntoh ◽  
C. Tanaka
Keyword(s):  
Protein Kinase C ◽  
Electrical Stimulation ◽  
Protein Kinase ◽  
Guinea Pig ◽  
Binding Sites ◽  
Sinus Node ◽  
Adrenergic Nerve ◽  
Nerve Terminals ◽  
Single Class ◽  
Kinase C

Localization of binding sites of [20-3H]phorbol-12,13-dibutyrate [( 3H]PDBu) and the involvement of Ca2+-phospholipid-dependent protein kinase (protein kinase C) in the release of norepinephrine (NE) from sympathetic nerve terminals in the guinea pig sinus node were investigated. There was a single class of specific [3H]PDBu binding sites in the heart. [3H]NE release from the sinus node preloaded with [3H]NE was evoked by electrical stimulation in superfusing medium containing Ca2+ or by the concomitant presence of Ca2+ ionophore and Ca2+, in Ca2+-free medium. 12-O-tetradecanoylphorbol-13-acetate (TPA) potentiated the evoked [3H]NE release. The effect of TPA was antagonized by both polymyxin B and H-7, inhibitors of protein kinase C. TPA increased the apparent affinities of electrical stimulation-evoked release for extracellular Ca2+. The possibility that protein kinase C plays a role in transmembrane signal transduction involved in the release of NE from peripheral adrenergic nerve terminals in the guinea pig sinus node warrants continued study.

Adrenergic presynaptic receptors: Examination of a hypothesis in guinea pig vas deferens

1979 ◽  
Vol 57 (7) ◽  
pp. 717-724 ◽  
Author(s):  
Stanley Kalsner
Keyword(s):  
Guinea Pig ◽  
Negative Feedback ◽  
Vas Deferens ◽  
Mechanical Response ◽  
Relative Effectiveness ◽  
Feedback System ◽  
Presynaptic Receptors ◽  
Adrenergic Nerve ◽  
Receptor Sites ◽  
Physiological Relevance

The hypothesis was examined that phenoxybenzamine enhances both the overflow of noradrenaline and the mechanical response in guinea pig vas deferens by blockade of presynaptic inhibitory receptors located on adrenergic nerve terminals which serve a negative-feedback function. Preparations were stimulated with a constant small number of pulses but at three different frequencies (1, 5, and 15 Hz) and the relative effectiveness of phenoxybenzamine in enhancing overflow assessed. According to the presynaptic receptor hypothesis inhibition of transmitter output should increase with increasing frequency due to increased activation of receptor sites by endogenously released noradrenaline. The antagonist enhanced the overflow of tritium but did so to a similar extent at all three frequencies, regardless of the length of the interval between pulses. Similarly, no evidence for a greater sensitization of the mechanical response by phenoxybenzamine at the higher frequencies was obtained. The conditions of the present experiment were considered optimal for the operation of the negative-feedback system and the results indicate that the physiological relevance of such a system is questionable.

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