Blockade of the Antiadrenergic Action of Bretylium by an Aqueous Extract of the Leaves of Rhoeo spathacea

1971 ◽  
Vol 49 (12) ◽  
pp. 1106-1110 ◽  
Author(s):  
M. Garcia ◽  
C. Miyares ◽  
E. Menendez ◽  
F. Sainz
Keyword(s):  
Aqueous Extract ◽  
Inhibitory Response ◽  
Adrenergic Nerve ◽  
Nerve Supply ◽  
Rabbit Ileum ◽  
Dopamine Content ◽  
Stimulation Of

In isolated rabbit ileum, bretylium-induced blockade of the inhibitory response to stimulation of the adrenergic nerve supply is prevented by an aqueous extract of the leaves of Rhoeo spathacea, apparently as a result of its dopamine content.

Peripheral muscarinic control of norepinephrine release in the cardiovascular system

1980 ◽  
Vol 239 (6) ◽  
pp. H713-H720 ◽  
Author(s):  
E. Muscholl
Keyword(s):  
Physiological Role ◽  
Sympathetic Nerves ◽  
Adrenergic Nerve ◽  
Sequence Of Events ◽  
Adrenergic Response ◽  
Adrenergic Nerve Terminals ◽  
Muscarinic Cholinergic ◽  
Related Compounds ◽  
Stimulation Of

Activation of muscarinic cholinergic receptors located at the terminal adrenergic nerve fiber inhibits the process of exocytotic norepinephrine (NE) release. This neuromodulatory effect of acetylcholine and related compounds has been discovered as a pharmacological phenomenon. Subsequently, evidence for a physiological role of the presynaptic muscarinic inhibition was obtained on organs known to be innervated by the autonomic ground plexus (Hillarp, Acta. Physiol. Scand. 46, Suppl. 157: 1-68, 1959) in which terminal adrenergic and cholinergic axons run side by side. Thus, in the heart electrical vagal stimulation inhibits the release of NE evoked by stimulation of sympathetic nerves, and this is reflected by a corresponding decrease in the postsynaptic adrenergic response. On the other hand, muscarinic antagonists such as atropine enhance the NE release evoked by field stimulation of tissues innervated by the autonomic ground plexus. The presynaptic muscarine receptor of adrenergic nerve terminals probably restricts the influx of calcium ions that triggers the release of NE. However, the sequence of events between recognition of the muscarinic compound by the receptor and the process of exocytosis still remains to be clarified.

Endothelium inhibits norepinephrine release from adrenergic nerves of rabbit carotid artery

1988 ◽  
Vol 254 (5) ◽  
pp. H871-H878 ◽  
Author(s):  
R. A. Cohen ◽  
R. M. Weisbrod
Keyword(s):  
Carotid Artery ◽  
Adrenergic Nerves ◽  
Adrenergic Nerve ◽  
Norepinephrine Release ◽  
Physical Barrier ◽  
Rabbit Carotid Artery ◽  
Vessel Lumen ◽  
Donor Artery ◽  
The Difference ◽  
Stimulation Of

The overflow of endogenous norepinephrine caused by transmural electrical stimulation or depolarization with potassium was smaller in superfused segments of the rabbit carotid artery with intact endothelium than in segments denuded of endothelium. In segments preincubated with [3H]norepinephrine, the lesser overflow was found to be partially due to metabolism by the endothelium of the neurotransmitter. Even after treatment to block the disposition of norepinephrine, the endothelium acted as a partial physical barrier to the overflow of norepinephrine into the lumen of arteries superfused and perfused selectively. However, a lesser overflow of norepinephrine to the adventitia of the artery accounted for the majority of the difference in overflow between segments with and without endothelium. The inhibition by the endothelium of the overflow of norepinephrine from adrenergic nerves was unaffected by blocking prejunctional alpha 2-adrenoceptors, prostaglandin synthesis, free radicals, or guanylate cyclase. Vasodilators released from the endothelium of a donor artery inhibited contractions caused by adrenergic nerve stimulation of a bioassay artery but failed to inhibit norepinephrine release. These observations indicate that the endothelium 1) metabolizes norepinephrine, 2) acts as a physical barrier to its overflow into the blood vessel lumen, and 3) inhibits the release of the adrenergic transmitter from adrenergic nerves.

EXPERIMENTS ON ATROPINE-RESISTANT VASODILATATION IN SALIVARY GLANDS

1963 ◽  
Vol 41 (2) ◽  
pp. 519-524 ◽  
Author(s):  
B. C. R. Strömblad ◽  
Peter E. Dresel
Keyword(s):  
Salivary Glands ◽  
Blocking Effect ◽  
Nerve Supply ◽  
Parotid Glands ◽  
Cholinergic Nerves ◽  
Parasympathetic Nerve ◽  
Ganglionic Transmission ◽  
Stimulation Of

Vasodilatation induced by stimulation of the parasympathetic nerve supply to the submaxillary and the parotid glands has long been known to be resistant to the blocking effect of atropine. We have found that dichloroisoproterenol does not block this vasodilatation, that d-tubocurarine blocks it by interfering with ganglionic transmission, and that a hemicholinium, HC-3, blocks it gradually under conditions in which interference with ganglionic transmission is excluded. It is concluded that the mechanism of vasodilatation includes the action of cholinergic nerves.

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.

scholarly journals Responses of Neurons in the Insular Cortex to Gustatory, Visceral, and Nociceptive Stimuli in Rats

1998 ◽  
Vol 79 (5) ◽  
pp. 2535-2545 ◽  
Author(s):  
Takamitsu Hanamori ◽  
Takato Kunitake ◽  
Kazuo Kato ◽  
Hiroshi Kannan
Keyword(s):  
Electrical Stimulation ◽  
Intravenous Injection ◽  
Anterior Commissure ◽  
Insular Cortex ◽  
Inhibitory Response ◽  
Inhibitory Neurons ◽  
Excitatory Response ◽  
Tail Pinch ◽  
Posterior Tongue ◽  
Stimulation Of

Hanamori, Takamitsu, Takato Kunitake, Kazuo Kato, and Hiroshi Kannan. Responses of neurons in the insular cortex to gustatory, visceral, and nociceptive stimuli in rats. J. Neurophysiol. 79: 2535–2545, 1998. Extracellular unit responses to baroreceptor and chemoreceptor stimulation, gustatory stimulation of the posterior tongue, electrical stimulation of the superior laryngeal (SL) nerve, and tail pinch were recorded from the insular cortex of anesthetized and paralyzed rats. Forty-three neurons identified responded to stimulation by at least one of the stimuli used in the present study. Of the 43 neurons, 33 responded to tail pinch, and the remaining 10 had no response; 18 showed an excitatory response, and 15 showed an inhibitory response. Of the 43 neurons, 35 responded to electrical stimulation of the SL nerve; 27 showed an excitatory response, and 8 showed an inhibitory response. Of the 20 neurons that responded to baroreceptor stimulation by an intravenous injection of methoxamine hydrochloride (Mex), 11 were excitatory and 9 were inhibitory. Twenty-seven neurons were responsive to an intravenous injection of sodium nitroprusside (SNP); 10 were excitatory and 17 were inhibitory. Ten neurons were excited and 16 neurons were inhibited by arterial chemoreceptor stimulation by an intravenous injection of sodium cyanide (NaCN). Twenty-six neurons were responsive to at least one of the gustatory stimuli (1.0 M NaCl, 30 mM HCl, 30 mM quinine HCl, and 1.0 M sucrose): four to six excitatory neurons and three to nine inhibitory neurons for each stimulus. A large number of the neurons (42/43) received convergent inputs from more than one stimulus among the nine stimuli used in the present study. Most neurons (38/43) were responsive to two or more stimulus groups when the natural stimuli used in the present study are grouped into three, gustatory, visceral, and nociceptive stimuli. The neurons recorded were located in the insular cortex between 2.8 mm anterior and 1.1 mm posterior to the anterior edge of the joining of the anterior commissure (AC); the mean location was 1.0 mm ( n = 43) anterior to the AC. This indicates that most of the neurons identified in the present study were located in the region posterior to the taste area and anterior to the visceral area in the insular cortex. These results indicate that the insular cortex neurons distributing between the taste area and the visceral area receive convergent inputs from baroreceptor, chemoreceptor, gustatory, and nociceptive organs and may have roles in taste aversion or in regulation of visceral responses.

Projections from the Ventral Tegmental Area to the Olfactory Tubercle in the Rat

1987 ◽  
Vol 96 (2) ◽  
pp. 151-157 ◽  
Author(s):  
Kenneth E. Mooney ◽  
Akira Inokuchi ◽  
James B. Snow ◽  
Charles P. Kimmelman
Keyword(s):  
Ventral Tegmental Area ◽  
Inhibitory Response ◽  
Inhibitory Influence ◽  
Olfactory Tubercle ◽  
Mixed Response ◽  
Neural Connection ◽  
Ventral Tegmental ◽  
Excitatory Responses ◽  
Stimulation Of

The projection between the ventral tegmental area (VTA) and the olfactory tubercle (OT) was examined electrophysiologically in the rat. Stimulation of the olfactory bulb (OB) determined if the OT neurons were olfactory-related. Ipsilateral VTA stimulation produced a change in neuronal activity in 77% of the neurons tested, with 41% being inhibited, 24% excited, and 12% had mixed response. Contralateral VTA stimulation produced changes in only 38%. Intravenous administration of haloperidol was used in examination of the role of dopamine in this neural connection. The results suggest that the VTA-induced inhibitory response on OT neurons is mediated by dopamine, whereas excitatory responses are not. The VTA inhibitory influence projects primarily to olfactory-related neurons, since 60% of olfactory-related OT neurons were inhibited—as compared to 34% of non-olfactory-related neurons. This study documents electrophysiologically the VTA-OT connection and suggests that the dopaminergic input may modulate olfactory information projected to the OT from the OB. It also supports the concept that the OT acts as an integration center in central olfactory processing.

scholarly journals Combination Effects of Curcumin and Aqueous Extract of Lignosus rhinocerotis Mycelium on Neurite Outgrowth Stimulation Activity in PC-12 Cells

2013 ◽  
Vol 8 (6) ◽  
pp. 1934578X1300800 ◽  
Author(s):  
Priscilla A. John ◽  
Kah - Hui Wong ◽  
Murali Naidu ◽  
Vikineswary Sabaratnam ◽  
Pamela David
Keyword(s):  
Small Molecules ◽  
Neurite Outgrowth ◽  
Aqueous Extract ◽  
Neurotrophic Factors ◽  
Neuronal Function ◽  
Pc 12 Cells ◽  
Neurite Extension ◽  
High Concentrations ◽  
Lignosus Rhinocerotis ◽  
Stimulation Of

Neurotrophic factors are necessary for neuronal navigation to form viable neuronal networks. These factors are high molecular weight polypeptides that cannot cross the blood brain-barrier. Therefore, small molecules from mushrooms and plants are utilized to maintain neuronal function or up-regulate neurotrophic factors. The present study investigated whether a combination of Lignosus rhinocerotis mycelium aqueous extract and curcumin was more effective than L. rhinocerotis mycelium or curcumin alone in the stimulation of neurite outgrowth of PC-12 cells. The maximum neurite extension for L. rhinocerotis and curcumin was at 21.1% at 20 μg/mL and 29.5% at 10 μg/mL, respectively. Combining 20 μg/mL of L. rhinocerotis with one μg/mL curcumin gave 27.2% neurite extension. This combination was preferred because high concentrations of curcumin were toxic to cells. In the combination, 20 μg/mL of L. rhinocerotis enhanced neurite outgrowth activity at a lower dosage of curcumin at one μg/mL, and produced a comparable percentage of neurite outgrowth stimulation activity to L. rhinocerotis and curcumin alone in PC-12 cells.

Pontine-evoked inspiratory inhibitions after antagonism of NMDA, GABAA, or glycine receptor

1993 ◽  
Vol 74 (3) ◽  
pp. 1265-1273 ◽  
Author(s):  
L. Ling ◽  
D. R. Karius ◽  
D. F. Speck
Keyword(s):  
Electrical Stimulation ◽  
Glycine Receptor ◽  
Inhibitory Response ◽  
Glycine Receptors ◽  
Onset Latency ◽  
Nerve Activity ◽  
Systemic Injection ◽  
Mk 801 ◽  
Inspiratory Motor ◽  
Stimulation Of

Single-shock stimulation of the pontine respiratory group (PRG) produces a transient short-latency inhibition of inspiratory motor activity. Stimulus trains delivered to the PRG can elicit a premature termination of inspiration. This study examined the involvement of N-methyl-D-aspartate (NMDA), gamma-aminobutyrateA (GABAA), or glycine receptors in these inhibitory responses. Experiments were conducted in decerebrate, paralyzed, and ventilated cats. Control responses to PRG stimulation were obtained from recordings of the left phrenic nerve activity. After systemic injection of MK-801, bicuculline, or strychnine (antagonists to NMDA, GABAA, or glycine receptors, respectively), responses to stimulation were again recorded. Inspiratory termination elicited by the PRG stimulation persisted after antagonism of NMDA, GABAA, or glycine receptors. The onset latency and duration of the transient inhibition were not changed after administration of bicuculline, but MK-801 administration did significantly prolong the duration of the transient inhibition. Strychnine significantly prolonged both the onset latency and the duration. These data suggest that none of the three receptor types is required in the inspiratory termination response elicited by electrical stimulation of the PRG region and that NMDA, GABAA, or glycine receptor-mediated neurotransmission is not solely responsible for the transient inhibitory response. However, the prolonged onset and duration of the transient inhibition after strychnine administration suggest that glycine does normally participate in this response.

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