The Effect of Angiotensin-Converting Enzyme Inhibition on ACTH Response to Corticotropin-Releasing Hormone (CRH) in Normal Men

Zacharieva, Sabina; Matrozov, P; Stoeva, Iva; K, Andonova

doi:10.1055/s-2007-1003665

Cited by 7 publications

(3 citation statements)

References 4 publications

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“…Regardless of the underlying mechanism(s) by which perindopril modulates the subjective effects of METH, it is also noteworthy that ACE inhibitors decrease depression in hypertensive patients ( Germain and Chouinard, 1989 ) and the release of stress hormones in healthy controls ( Zacharieva et al, 1991 ), which could play a role in reducing stress-related relapse to METH use. This idea is consistent with the current findings; all active perindopril doses reduced anxious ratings ( Figure 3 ).…”

Section: Discussionmentioning

confidence: 99%

Subjective and Cardiovascular Effects of Intravenous Methamphetamine during Perindopril Maintenance: A Randomized, Double-Blind, Placebo-Controlled Human Laboratory Study

Verrico

Haile

Garza

et al. 2016

IJNPPY

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Background:Our pilot study suggested that the angiotensin-converting enzyme inhibitor perindopril might reduce some subjective effects produced by i.v. methamphetamine. We characterized the impact of a wider range of perindopril doses on methamphetamine-induced effects in a larger group of non-treatment-seeking, methamphetamine-using volunteers.Methods:Before treatment, participants received 30mg methamphetamine. After 5 to 7 days of perindopril treatment (0, 4, 8, or 16mg/d), participants received 15 and 30mg of methamphetamine on alternate days. Before and after treatment, participants rated subjective effects and cardiovascular measures were collected.Results:Prior to treatment with perindopril, there were no significant differences between treatment groups on maximum or peak subjective ratings or on peak cardiovascular effects. Following perindopril treatment, there were significant main effects of treatment on peak subjective ratings of “anxious” and “stimulated”; compared to placebo treatment, treatment with 8mg perindopril significantly reduced peak ratings of both anxious (P=.0009) and stimulated (P=.0070). There were no significant posttreatment differences between groups on peak cardiovascular effects.Conclusions:Moderate doses of perindopril (8mg) significantly reduced peak subjective ratings of anxious and stimulated as well as attenuated many other subjective effects produced by methamphetamine, likely by inhibiting angiotensin II synthesis. Angiotensin II is known to facilitate the effects of norepinephrine, which contributes to methamphetamine’s subjective effects. The lack of a classic dose-response function likely results from either nonspecific effects of perindopril or from between-group differences that were not accounted for in the current study (i.e., genetic variations and/or caffeine use). The current findings suggest that while angiotensin-converting enzyme inhibitors can reduce some effects produced by methamphetamine, more consistent treatment effects might be achieved by targeting components of the renin-angiotensin system that are downstream of angiotensin-converting enzyme.

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Section: Discussionmentioning

confidence: 99%

Subjective and Cardiovascular Effects of Intravenous Methamphetamine during Perindopril Maintenance: A Randomized, Double-Blind, Placebo-Controlled Human Laboratory Study

Verrico

Haile

Garza

et al. 2016

IJNPPY

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“…Although to date it is not established with certainty whether both ACE and ATII are increased in ACE allele D carriers, 29 it was shown, that ACE inhibition also reduces basal and CRH stimulated ACTH levels, which in turn are modulated by ATII levels. 30 The fact that the literature is controversial with respect to the involvement of the ACE I/D polymorphism in genetic vulnerability to depression 11 could propose that other, maybe genetic variants are necessary for the expression of the phenotype.…”

Section: Combined Analysismentioning

confidence: 99%

Combined action of the ACE D- and the G-protein β3 T-allele in major depression: a possible link to cardiovascular disease?

Bondy¹,

Baghai²,

Zill³

et al. 2002

Mol Psychiatry

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Although it is well established that depression is a major risk factor for the development of coronary artery disease and that cerebrovascular disease can be a major contributing factor for the development of depression, the information about the interplay between the central nervous system and cardiovascular disease is still limited. We investigated the angiotensin I converting enzyme (ACE) ID and the G-protein ␤3-subunit (G␤3) C825T polymorphism in 201 patients with unipolar major depression and 161 ethnically and age-matched controls. Both gene variants have earlier been associated with either cardiovascular disease or affective disorders, making them good candidates for a combined analysis. We found a significant increase in the G␤3 T allele (OR = 1.61, 95% CI 1.17-2.2, P = 0.0035) and a marginal altered genotype distribution of the ACE ID polymorphism with decrease in the II genotypes ( 2 = 6.43, df=3, P = 0.04) in the patients' group. Analysing the data for both genes we found that the combined actions of ACE and G␤3 genotypes accumulate in carriers of the ACE D allele (ID and DD) and G␤3 TT homozygotes with ID/DD-TT carriers showing a more than five-fold increase in risk for major depression (crude OR = 5.83, 95% CI 1.99-17.08, P = 0.0002). As our study was carried out with depressive patients without serious cardiac impairment at the time of the investigation, we are presently unable to predict whether this combined action of the ACE ID/DD-G␤3 TT genotype is increasing the risk for both disorders. Nevertheless our study reports for the first time that the same allelic combination of two genes that have been shown to increase the risk for myocardial infarction (Naber et al, 2000) increase the vulnerability for depressive disorder.

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“…ACE inhibition had little or no effect on CRF metabolism in any of the membrane preparations. Zacharieva et al (1991) previously studied the effects of ACE inhibition (by captopril) on the ACTH response to CRF in humans by conducting CRF challenge tests (100 mg r/h CRF administered at 0900 h) both before and after 3 days of captopril treatment (100 mg/day) in 10 normal men. Figure 5 Summary of CRF hydrolysis by three ectopeptidases and cleavage products recovered.…”

Section: Discussionmentioning

confidence: 99%

Action of Three Ectopeptidases on Corticotropin-Releasing Factor: Metabolism and Functional Aspects

Ritchie

Davis

Nemeroff

2002

Neuropsychopharmacol

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Using purified enzyme preparations, we investigated the actions of angiotensin-converting enzyme, aminopeptidase N, and endopeptidase 24.11 on corticotropin-releasing factor (CRF). The effects of inhibition of these enzymes on CRF action in rat anterior pituitary cultures were also determined. Finally, specific inhibitors were used to evaluate ectopeptidase action on the regional brain metabolism of CRF. K m values for CRF were 165, 90, and 42 mM for angiotensin-converting enzyme, aminopeptidase N, and endopeptidase 24.11, respectively. A CRF metabolite profile for each enzyme was determined. In pituitary cultures, inhibition of endopeptidase 24.11 and aminopeptidase N potentiated CRF-stimulated release of adrenocorticotropic hormone (ACTH). In rat pituitary and hypothalamus membrane preparations, specific inhibitor experiments indicated that CRF hydrolysis involved members of the neutral endopeptidase and aminopeptidase enzyme families. In cortex membranes, similar peptidase inhibition was without effect. These data support the hypothesis that ectopeptidases play a major role in CRF metabolism and biological function.

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The Effect of Angiotensin-Converting Enzyme Inhibition on ACTH Response to Corticotropin-Releasing Hormone (CRH) in Normal Men

Cited by 7 publications

References 4 publications

Subjective and Cardiovascular Effects of Intravenous Methamphetamine during Perindopril Maintenance: A Randomized, Double-Blind, Placebo-Controlled Human Laboratory Study

Subjective and Cardiovascular Effects of Intravenous Methamphetamine during Perindopril Maintenance: A Randomized, Double-Blind, Placebo-Controlled Human Laboratory Study

Combined action of the ACE D- and the G-protein β3 T-allele in major depression: a possible link to cardiovascular disease?

Action of Three Ectopeptidases on Corticotropin-Releasing Factor: Metabolism and Functional Aspects

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