2011
DOI: 10.1016/j.autneu.2011.05.008
|View full text |Cite
|
Sign up to set email alerts
|

Central mechanisms involved in pilocarpine-induced pressor response

Abstract: Pilocarpine (cholinergic muscarinic agonist) injected peripherally may act centrally to produce pressor responses; in the present study, using c-fos immunoreactive expression, we investigated the forebrain and brainstem areas activated by pressor doses of intravenous (i.v.) pilocarpine. In addition, the importance of vasopressin secretion and/or sympathetic activation and the effects of lesions in the anteroventral third ventricle (AV3V) region in awake rats were also investigated. In male Holtzman rats, piloc… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2

Citation Types

0
2
0

Year Published

2013
2013
2017
2017

Publication Types

Select...
4

Relationship

0
4

Authors

Journals

citations
Cited by 4 publications
(2 citation statements)
references
References 38 publications
(59 reference statements)
0
2
0
Order By: Relevance
“…Inhibitory signals for sodium and water intake arise from arterial baroreceptors or cardiopulmonary receptors that are activated by increases in arterial pressure or body fluid volume (Johnson and Thunhorst, 1997;De Gobbi et al, 2008). Therefore, a reason for the absence of hypertonic NaCl intake in rats treated with central cholinergic agonists might be the inhibitory signals produced in response to the increases in arterial pressure caused by these treatments (Trendelenburg, 1961;Hoffman et al, 1977;Imai et al, 1989;Thunhorst and Johnson, 1994;Johnson and Thunhorst, 1997;Takakura et al, 2003Takakura et al, , 2005Takakura et al, , 2011Borella et al, 2008). Reducing the action of the inhibitory signals with bilateral injections of methysergide (serotonergic receptor antagonist) into the LPBN results in significant ingestion of hypertonic NaCl in rats treated with the cholinergic agonist carbachol intracerebroventricularly (i.c.v.)…”
Section: Introductionmentioning
confidence: 97%
“…Inhibitory signals for sodium and water intake arise from arterial baroreceptors or cardiopulmonary receptors that are activated by increases in arterial pressure or body fluid volume (Johnson and Thunhorst, 1997;De Gobbi et al, 2008). Therefore, a reason for the absence of hypertonic NaCl intake in rats treated with central cholinergic agonists might be the inhibitory signals produced in response to the increases in arterial pressure caused by these treatments (Trendelenburg, 1961;Hoffman et al, 1977;Imai et al, 1989;Thunhorst and Johnson, 1994;Johnson and Thunhorst, 1997;Takakura et al, 2003Takakura et al, , 2005Takakura et al, , 2011Borella et al, 2008). Reducing the action of the inhibitory signals with bilateral injections of methysergide (serotonergic receptor antagonist) into the LPBN results in significant ingestion of hypertonic NaCl in rats treated with the cholinergic agonist carbachol intracerebroventricularly (i.c.v.)…”
Section: Introductionmentioning
confidence: 97%
“…Peri-ictal, centrally originating or peripheral autonomic irregularities leading to cardiorespiratory collapse may be the immediate cause of death in SUDEP ( Ryvlin et al, 2013 ), but few studies have been aimed at identifying mechanisms underlying this autonomic failure. Seizures can increase activity of neurons in brainstem autonomic areas, independently of physical activity or peripheral metabolic influences ( Kanter et al, 1995 ; Takakura et al, 2011 ), and autonomic irregularities often develop over time in individuals with epilepsy, implicating central or peripheral autonomic reactive neuroplasticity as a potential driver of increased SUDEP risk in patients and in rodent epilepsy models ( Glasscock et al, 2010 ; Massey et al, 2014 ; Biet et al, 2015 ). Thus, recurrent seizures might induce changes in central or systemic physiologic functions that increase the risk for sudden death.…”
Section: Introductionmentioning
confidence: 99%