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Ganglion stimulant activity

Actions Carbachol has profound effects on both the cardiovascular system and the gastrointestinal system because of its ganglion-stimulating activity and may first stimulate and then depress these systems. It can cause release of epinephrine from the adrenal medulla by its nicotinic action. Locally instilled into the eye, it mimics the effects of acetylcholine, causing miosis. [Pg.51]

The answer is d. (Hardman, pp 142—M3.) ACh will stimulate both muscarinic and nicotinic receptors. Skeletal muscle contraction is mediated through NM receptors, and ganglionic stimulation is an effect of NN receptors All of the other effects listed in the question occur following muscarinic receptor activation and will be blocked by atropine and scopolamine, both of which are muscarinic receptor antagonists. Skeletal muscle contraction will not be affected by these drugs rather, a neuromuscular blocker (e.g., tubocurarine) is required to antagonize this effect of ACh. [Pg.193]

At a low concentration, the tobacco alkaloid nicotine acts as a ganglionic stimulant by causing a partial depolarization via activation of ganglionic cholinocep-tors (p. 108). A similar action is evident at diverse other neural sites, considered below in more detail. [Pg.110]

Autonomic ganglia. Ganglionic stimulation occurs in both the sympathetic and parasympathetic divisions of the autonomic nervous system. Parasympathetic activation results in increased production of gastric juice (smoking ban in peptic ulcer) and enhanced bowel motility ( laxative effect of the first morning cigarette defecation diarrhea in the novice). [Pg.110]

Levamisole acts as a ganglion-stimulating compound and induces a neuromuscular inhibition of the depolarizing type. However, it is possible that its ability to act as an immune stimulant may also contribute to its activity. [Pg.203]

Additionally, pair 112a/l 12b was tested on the isolated guinea pig ileum. Both compounds, which can be regarded as derivatives of the ganglionic stimulant phenoxy-ethyl-trimethylammonium (113), were found to exhibit similar anticholinergic activity. [Pg.37]

It was concluded that the nicotinic activity of choline phenyl ether and of choline o-tolyl ether is a reflection of the ability of the molecule to assume a "planar" conformation when interacting with the ganglionic nicotinic receptor. In contrast, the inactive 2,6-xylyl ether of choline cannot assume this planar disposition. Evaluation of additional conformation-ally restricted aiyl choline ethers (44-47) revealed that only the piperidine derivative (47) is a ganglionic stimulant (98). [Pg.48]

Some aromatic ethers of choline display marked nicotinic activity, but they are inactive at muscarinic sites (94). The o-tolyl ether of choline is a potent ganglionic stimulant (95), but the 2,6-xylyl ether of choline is inert as a nicotinic agent (96). [Pg.48]

Reflex changes in heart rate involve ganglionic transmission. Activation of alphaj receptors on blood vessels by phenylephrine elicits a reflex bradycardia since mean blood pressure is increased. One of the characteristic effects of tubocurarine is its block of autonomic ganglia—this action can interfere with reflex changes in heart rate. Tubocurarine would not prevent bradycardia due to neostigmine (an inhibitor of acetylcholinesterase) since this occurs via stimulation by acetylcholine of cardiac muscarinic receptors. [Pg.251]

TK NKxr displays a broad distribution in both peripheral tissues and in the central nervous system (CNS). In both CNS and enteric neurons, NKxr stimulation increase their excitability, whereas in trigeminal ganglion neurons SP has no intrinsic electrophysio-logical effects but is capable to enhance the amplitude of the inward current induced by the stimulation of serotonin 5-HT3 recqrtors. This enhancement dqjends on the activation of PKC via the stimulation of NKX recqrtors. This is an interesting case of receptor cross talk. Other functions of NKxr have been also highlighted. [Pg.1187]

Hydrogen ions accumulate in tissue damaged by inflammation and ischaemia and so pH is lowered. These protons may activate nociceptors directly via their own family of ion channels as well as sensitising them to mechanical stimulation. Acid-sensing ion channels (ASICS) are a family of sodium channels that are activated by protons — of special interest is one type found only in small dorsal root ganglion neurons that possibly are responsible for activation of nociceptors. Although the transduction of mechanical stimuli is poorly understood, ASICs are closely related to channels that respond to stretch. [Pg.457]

A1 adenosine receptors are inhibitory in the central nervous system. A receptors were originally characterized on the basis of their ability to inhibit adenylyl cyclase in adipose tissue. A number of other G-protein-mediated effectors of A receptors have subsequently been discovered these include activation of K+ channels, extensively characterized in striatal neurons [13], and inhibition of Ca2+ channels, extensively characterized in dorsal root ganglion cells [14]. Activation of A receptors has been shown to produce a species-dependent stimulation or inhibition of the phosphatidylinositol pathway in cerebral cortex. In other tissues, activation of A receptors results in synergistic activation of the phosphatidylinositol pathway in concert with Ca2+-mobilizing hormones or neurotransmitters [15]. The effectors of A adenosine receptors and other purinergic receptor subtypes are summarized in Table 17-2. [Pg.313]

In moths, it was discovered in Helicoverpa zea that a peptide produced in the subesophageal ganglion portion of the brain complex regulates pheromone production in female moths (19). This factor has been purified and characterized in three species, Helicoverpa zea (20), Bombyx mori (21, 22), and Lymantria dispar (23). They are all a 33- or 34-amino acid peptide (named pheromone biosynthesis activating neuropeptide, PBAN) and have in common an amidated C-terminal 5-amino acid sequence (FXPRL-amide), which is the minimum peptide fragment required for pheromon-tropic activity. In the redbanded leafroller moth, it was shown that PBAN from the brain stimulates the release of a different peptide from the bursae copulatrix that is used to stimulate pheromone production in the pheromone gland found at the posterior tip of the abdomen (24). [Pg.120]

Dopamine-sensitive adenylate cyclase activity was early demonstrated in both the retina and the cervical ganglion of the cow [47] and later in homogenates of the caudate-putamen of the rat brain [48]. Kebabian has recently reviewed the biochemical components of dopamine-sensitive adenylate cyclase and the physiological role of the D1 receptor [49]. D1 and D2 agonists stimulate and inhibit adenylate cyclase activity, respectively. [Pg.190]

The ganglionic effects of ACh can be blocked by tetraethylammonium, hexa-methonium, and other substances (ganglionic blockers). None of these has intrinsic activity, that is, they fail to stimulate ganglia even at low concentration some of them (e.g hexamethonium) actually block the cholinoceptor-linked ion channel, but others (mecamyla-mine, trimethaphan) are typical receptor antagonists. [Pg.108]

E. The effect of ganglionic blockade depends upon the predominant autonomic tone exerted within various organ systems. Since the activity of the parasympathetic nervous system predominates in the eye, the effect of ganglionic blockade is mydriasis, not miosis. Similarly, stimulation of the genital tract and urinary retention would be decreased. Since sympathetic nervous system activity predominates in blood vessels and the ventricles, vasodilation and a decreased cardiac output would follow ganglionic blockade. [Pg.147]


See other pages where Ganglion stimulant activity is mentioned: [Pg.24]    [Pg.108]    [Pg.298]    [Pg.302]    [Pg.128]    [Pg.513]    [Pg.1787]    [Pg.201]    [Pg.84]    [Pg.62]    [Pg.317]    [Pg.64]    [Pg.197]    [Pg.243]    [Pg.226]    [Pg.119]    [Pg.27]    [Pg.190]    [Pg.492]    [Pg.158]    [Pg.32]    [Pg.296]    [Pg.342]    [Pg.115]    [Pg.142]    [Pg.100]    [Pg.108]    [Pg.135]    [Pg.541]    [Pg.182]   
See also in sourсe #XX -- [ Pg.64 ]




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