Central injection of captopril inhibits the blood pressure response to intracerebroventricular choline

Isbil-Buyukcoskun, Naciye; Gulec, Guldal; Ozluk, Kasim; Ulus, İsmail H.

doi:10.1590/s0100-879x2001000600018

Cited by 5 publications

(5 citation statements)

References 32 publications

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“…The dose of choline used in this study was chosen based on reports in the literature that demonstrated that the pressor response induced by ICV choline is dose-dependent and that the highest documented dose (150 μg) immediately increases MABP, catecholamines, and AVP (20,24). The MABP response to 150 μg choline is sustained for approximately 15 minutes as shown by our preliminary studies as well as studies in the literature (36). Only animals that had a positive response to angiotensin II-induced polydipsia, reflecting accurate placement of the cannula in the lateral ventricle, were used in these studies.…”

Section: Methodssupporting

confidence: 75%

“…Reports in the literature suggest that the observed effects are mediated via central nicotinic receptors (35). In addition, the brain renin-angiotensin system may be involved in the pressor response elicited by ICV choline because ICV pretreatment with captopril, an angiotensin converting enzyme inhibitor, has been shown to inhibit the pressor response induced by ICV choline (36). …”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Transient Central Cholinergic Activation Enhances Sympathetic Nervous System Activity but Does Not Improve Hemorrhage-Induced Hypotension in Alcohol-Intoxicated Rodents

Mathis

Molina

2009

Shock

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Morbidity and mortality following traumatic injury and hemorrhagic shock is exacerbated in the alcohol-intoxicated individual. The level of hypotension at the time of admittance into the emergency department is a critical indicator of outcome from injury. Previously we have demonstrated that acute alcohol intoxication (AAI) decreases basal mean arterial blood pressure (MABP), exaggerates hypotension throughout hemorrhagic shock (HS), and attenuates the pressor response to fluid resuscitation (FR) in male rodents. This AAI-induced impaired hemodynamic counter-regulation to blood loss is associated with dampened neuroendocrine activation [i.e., epinephrine (EPI), norepinephrine (NE), and arginine vasopressin (AVP) release]. We hypothesize that the blunted neuroendocrine response is the principal mechanism involved in hemodynamic instability during and following HS in AAI. The present study investigates whether enhancing central cholinergic activity via intracerebroventricular (ICV) choline, a precursor of acetylcholine, would restore the neuroendocrine response, and as a result, improve hemodynamic compensation following HS. Chronically-catheterized, conscious, male Sprague-Dawley rats (225–250g) received a primed 15-h alcohol infusion (30% w/v; total ~8g/kg) prior to ICV choline (150μg) injection and were subsequently subjected to fixed-volume HS (50%) and FR with lactated Ringers (2× volume removed). There were a total of eight experimental groups (n=5–12 rats per group): alcohol-treated not hemorrhaged (alcohol/sham), dextrose-treated not hemorrhaged (dextrose/sham), alcohol-treated hemorrhaged (alcohol/hemorrhage), and dextrose-treated hemorrhaged (dextrose/hemorrhage), with ICV choline or water injection. ICV choline immediately increased basal MABP in both control (16%) and AAI animals (12%), but did not alter MABP following HS in either group. ICV choline increased basal plasma EPI (196%), NE (96%), and AVP (145%), and enhanced the HS-induced rise in EPI and AVP, without altering NE responses to HS, in control animals. AAI blunted choline-induced neuroendocrine activation and prevented the HS-induced rise in NE, without affecting post-HS EPI and AVP levels. ICV choline administration to AAI animals enhanced the HS-induced rise in EPI without affecting post-HS NE or AVP. These results indicate that ICV choline produced immediate neuroendocrine activation and elevation in MABP that was not sustained sufficiently to improve hemodynamic counter-regulation in alcohol-treated animals.

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Section: Methodssupporting

confidence: 75%

Section: Discussionmentioning

confidence: 99%

Transient Central Cholinergic Activation Enhances Sympathetic Nervous System Activity but Does Not Improve Hemorrhage-Induced Hypotension in Alcohol-Intoxicated Rodents

Mathis

Molina

2009

Shock

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“…However, studies by IsbilBuyukcoskun et al demonstrated that captopril given i.c.v. blocked choline-induced pressor effect in conscious rats [8].…”

Section: Resultsmentioning

confidence: 89%

Interactions between the histaminergic and angiotensinergic systems in the central cardiovascular regulation in rats

et al. 2006

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“…Furthermore, central choline administration enhances plasma catecholamine and vasopressin responses to haemorrhage in conscious rats 5,7,12 . Although we have demonstrated a link between the central renin–angiotensin (RAS) and cholinergic systems 13 suggesting that the central RAS may be involved in the pressor response to central choline, 2 changes in plasma renin activity (PRA; as an index of peripheral RAS activity) following choline administration have not been investigated in a systematic manner. In previous studies, we observed that PRA showed a tendency to decrease following intracerebroventricular (i.c.v.)…”

Section: Introductionmentioning

confidence: 94%

“…In past years, considerable evidence has accumulated from experimental studies in rats showing that central administration of choline, a precursor of the neurotransmitter acetylcholine (ACh), increases blood pressure in normotensive rats 1–4 and restores blood pressure when rats are made hypotensive by acute haemorrhage, 5–7 endotoxin treatment, 8 chemical sympathectomy, 9 peripheral α‐adrenoceptor or autonomic ganglionic blockade 10 or spinal cord transection shock 11 . Elevations in plasma catecholamines and vasopressin have been shown to be associated with and involved in the pressor response to choline in either normotensive 1 or hypotensive 5,7–12 states.…”

Section: Introductionmentioning

confidence: 99%

Central Choline Suppresses Plasma Renin Response to Graded Haemorrhage in Rats

Isbil-Buyukcoskun

İlçöl²,

Cansev

et al. 2008

Clin Exp Pharma Physio

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Central administration of choline increases blood pressure in normotensive and hypotensive states by increasing plasma concentrations of vasopressin and catecholamines. We hypothesized that choline could also modulate the renin-angiotensin pathway, the third main pressor system in the body. Plasma renin activity (PRA), which serves as an index of the function of the peripheral renin-angiotensin system, was determined in rats subjected to graded haemorrhage following central choline administration. Intracerebroventricular (i.c.v.) injection of choline (12.5-150 microg), a precursor of the neurotransmitter acetylcholine (ACh), inhibited the increase in PRA in rats subjected to graded haemorrhage by sequential removal of 0.55 mL blood/100 g bodyweight. Choline, in the range 50-150 microg, increased blood pressure. Intraperitoneal (i.p.) administration of 150 microg choline failed to alter blood pressure and plasma renin responses to graded haemorrhage. Administration of a higher dose (90 mg/kg, i.p.) of choline decreased blood pressure and enhanced PRA in the first two blood samples obtained during the graded haemorrhage. Physostigmine (10 microg, i.c.v.), ACh (10 microg, i.c.v.), carbamylcholine (10 microg, i.c.v.) and cytidine 5'-diphosphocholine (CDP-choline; 250 microg, i.c.v.) increased blood pressure and attenuated plasma renin responses to graded haemorrhage. Inhibition of PRA by i.c.v. choline was abolished by i.c.v. pretreatment with mecamylamine (50 microg), but not atropine (10 microg). Blood pressure responses to choline (150 microg) were attenuated by pretreatment with both mecamylamine and atropine. Inhibition of PRA in response to central choline administration was associated with enhanced plasma vasopressin and catecholamine responses to graded haemorrhage. Pretreatment of rats with a vasopressin antagonist reversed central choline-induced inhibition of plasma renin responses to graded haemorrhage without altering the blood pressure response. In conclusion, central administration of choline inhibits the plasma renin response to graded haemorrhage. Nicotinic receptor activation and an increase in plasma vasopressin appear to be involved in this effect.

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Central injection of captopril inhibits the blood pressure response to intracerebroventricular choline

Cited by 5 publications

References 32 publications

Transient Central Cholinergic Activation Enhances Sympathetic Nervous System Activity but Does Not Improve Hemorrhage-Induced Hypotension in Alcohol-Intoxicated Rodents

Transient Central Cholinergic Activation Enhances Sympathetic Nervous System Activity but Does Not Improve Hemorrhage-Induced Hypotension in Alcohol-Intoxicated Rodents

Interactions between the histaminergic and angiotensinergic systems in the central cardiovascular regulation in rats

Central Choline Suppresses Plasma Renin Response to Graded Haemorrhage in Rats

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