Central and peripheral effects of arecoline in patients with autonomic failure.

Polinsky, Ronald J.; Brown, Robert T.; Curras, M. T.; Baser, Susan M.; Baucom, Celeste E.; Hooper, David R.; Marini, A

doi:10.1136/jnnp.54.9.807

Cited by 11 publications

(8 citation statements)

References 34 publications

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“…The adreno-medullary response to hypoglycaemia, for example, requires activation of central glucose receptors and an efferent pre-ganglionic sympathetic arc [23]. This response is blunted in both PAF and MSA, but can be restored in MSA subjects through the application of post-ganglionic stimuli [28]. The pressor response to a low-dose CO 2 challenge was lost in MSA subjects compared to controls presumably due to impaired or absent responses of sympathetic autonomic nervous system structures in the brainstem or cervical trunk [5].…”

Section: Discussion J Neuroendocrine Responsementioning

confidence: 97%

Neuroendocrine and behavioural responses to CO2 inhalation in central versus peripheral autonomic failure

et al. 2006

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Multiple system atrophy (MSA) and pure autonomic failure (PAF) represent distinct pathological models of autonomic failure in humans. We have investigated the neuroendocrine, behavioural and autonomic cardiovascular responses to the 35% CO2 challenge. Nine patients with MSA, nine with PAF and five control subjects received a single breath of 35% CO2. Peripheral autonomic failure (i.e., PAF) was associated with significantly lower resting noradrenaline levels. All groups demonstrated a significant pressor response to CO2. In controls, the mean pressor response was +60.2 mm Hg, which was significantly smaller in both the PAF (+26.8 mm Hg, P < 0.01) and MSA (+18.3 mm Hg, P < 0.001) patients. In addition, the onset of the response was significantly delayed in both MSA (140.2 s) and PAF (154.2 s) patients compared with controls (32.4 s, P = 0.04 and P = 0.03, respectively). Noradrenaline levels increased only in controls. Central autonomic impairment (i.e., MSA) was associated with lower cortisol release (+8.8% in MSA compared with +35.2% in control and +23.7% in PAF) and fewer somatic symptoms of emotional arousal. Both MSA and PAF exhibit marked sympathetic autonomic impairment, however, residual (albeit differing) sympathetic pathways can still maintain a partial cardiovascular response. A central autonomic lesion, however, also appears to be associated with blunting of both cortisol and emotional responses to this stress paradigm.

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Section: Discussion J Neuroendocrine Responsementioning

confidence: 97%

Neuroendocrine and behavioural responses to CO2 inhalation in central versus peripheral autonomic failure

et al. 2006

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“…It has been reported that arecoline increases plasma epinephrine levels in normal subjects and patients with multiple system atrophy, which may result from nicotinic adrenal stimulation [18] . Therefore, in order to compare the effects of nicotine with those of arecoline, it was of interest to examine the effect of nicotine on CA secretion from isolated perfused rat adrenal glands evoked by ACh, high K + , and DMPP.…”

Section: Effect Of Nicotine On Ca Secretion Evoked By Ach Excess K +mentioning

confidence: 99%

“…It has been concluded that the pressor effects brought about by quaternary compounds can be attributed to the stimulation of nicotinic and muscarinic receptors in the sympathetic ganglia of both pithed and anesthetized rats [17] . Moreover, Polinsky and coworkers found that the increased plasma epinephrine levels following arecoline treatment in normal subjects and patients with multiple system atrophy might result from nicotinic adrenal stimulation [18] . It has also been reported that betel chewing increases plasma concentrations of norepinephrine and epinephrine [19] .…”

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confidence: 99%

Arecoline inhibits catecholamine release from perfused rat adrenal gland1

Lim

Kim

2006

Acta Pharmacologica Sinica

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Aim: To study the effect of arecoline, an alkaloid isolated from Areca catechu, on the secretion of catecholamines (CA) evoked by cholinergic agonists and the membrane depolarizer from isolated perfused rat adrenal gland. Methods: Adrenal glands were isolated from male Sprague‐Dawley rats. The adrenal glands were perfused with Krebs bicarbonate solution by means of a peristaltic pump. The CA content of the perfusate was measured directly using the fluorometric method. Results: Arecoline (0.1–1.0 mmol/L) perfused into an adrenal vein for 60 min produced dose‐ and time‐dependent inhibition in CA secretory responses evoked by acetylcholine (ACh) (5.32 mmol/L), 1.1‐dimethyl‐4‐phenyl piperazinium iodide (DMPP) (100 μmol/L for 2 min) and 3‐(m‐choloro‐phenyl‐carbamoyl‐oxy)‐2‐butynyl trimethyl ammonium chloride (McN‐A‐343) (100 μmol/L for 2 min). However, lower doses of arecoline did not affect CA secretion of high K+ (56 mmol/L); higher doses greatly reduced CA secretion of high K+. Arecoline also failed to affect basal catecholamine output. Furthermore, in adrenal glands loaded with arecoline (0.3 mmol/L), CA secretory response evoked by Bay‐K‐8644 (10 μmol/L), an activator of L‐type Ca2+ channels, was markedly inhibited, whereas CA secretion by cyclopiazonic acid (10 μmol/L), an inhibitor of cytoplasmic Ca2+‐ATPase, was not affected. Nicotine (30 μmol/L), which was perfused into the adrenal gland for 60 min, however, initially enhanced ACh‐evoked CA secretory responses. As time elapsed, these responses became more inhibited, whereas the initially enhanced high K+‐evoked CA release diminished. CA secretion evoked by DMPP and McN‐A‐343 was significantly depressed in the presence of nicotine. Conclusion: Arecoline dose‐dependently inhibits CA secretion from isolated perfused rat adrenal gland evoked by activation of cholinergic receptors. At lower doses arecoline does not inhibit CA secretion through membrane depolarization, but at larger doses it does. This inhibitory effect of arecoline may be mediated by blocking the calcium influx into the rat adrenal medullary chromaffin cells without the inhibition of Ca2+ release from the cytoplasmic calcium store. There seems to be a difference in the mode of action of nicotine and arecoline in rat adrenomedullary CA secretion.

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“…Arecoline causes a reduction in the level of norepinephrine level in the cortex and subcortex of mice (22). Plasma epinephrine level is also increased after arecoline treatment in normal human subject (23). Betel nut chewing increases plasma concentrations of norepinephrine and epinephrine in humans (24).…”

Section: Introductionmentioning

confidence: 97%

Ultrastructural and hormonal modulations of adrenal gland with alterations of glycemic and liver glycogen profiles following arecoline administration in albino mice

Nag¹

2010

Acta Endo (Buc)

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Background. Arecoline, a plant alkaloid of betel nut, is consumed by millions of people, for increased capacity of work. It causes immunosuppression, hepatotoxicity, and disturbance in antioxidant production, but it stimulates HPA axis and induces thyroid dysfunction.Aim. To investigate the role of arecoline on adrenal activity, glycemia and glycogen profile in mice.Materials and methods. Arecoline was injected intraperitoneally at a dose of 10 mg/ kg body wt for 20-60 min for acute administration. In chronic administration the same dose was used daily for 15 days. Corticosterone, epinephrine, norepinephrine, blood glucose and liver glycogen profiles were measured after 20, 40 and 60 min, in acute administration and after 15 days in chronic administration.Results. Arecoline in acute administration increased corticosterone, norepinephrine and epinephrine levels and induced hyperglycemia with depletions of liver glycogen. But chronic arecoline administration with the same dose for 15 days caused ultrastructural degenerations of adrenal cortex and medulla with the elevation of corticosterone, and depletions of norepinephrine and epinephrine levels. Arecoline also caused hypoglycemia and elevated liver glycogen. Atropine (arecoline receptor antagonist) prevented arecoline action on adrenal activity or blood glucose -liver glycogen interaction.Conclusion. The findings indicate that arecoline initially stimulates adrenal activity, but subsequently inhibits it with alterations of glycemic and glycogen profiles. Arecoline action is mediated by arecoline receptor in mice. Arecoline may have immunological action via adrenal hormonal suppression in mice.

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Central and peripheral effects of arecoline in patients with autonomic failure.

Cited by 11 publications

References 34 publications

Neuroendocrine and behavioural responses to CO2 inhalation in central versus peripheral autonomic failure

Neuroendocrine and behavioural responses to CO2 inhalation in central versus peripheral autonomic failure

Arecoline inhibits catecholamine release from perfused rat adrenal gland1

Ultrastructural and hormonal modulations of adrenal gland with alterations of glycemic and liver glycogen profiles following arecoline administration in albino mice

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