Anti-Ischemic Potential of Drugs related to the Renin-Angiotensin System

Ertl, Georg; Hu, Kai

doi:10.1097/00005344-200109011-00003

Cited by 25 publications

(28 citation statements)

References 107 publications

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“…The catalytic activity of ACE may influence the balance within the RA system, and indirectly of the RA system with ET-1 and VP. 1,11,12 The enzymatic activity and plasma concentration of ACE is genetically determined 34 by ACE I/D polymorphism. 13,27 An association of ACE I/D gene polymorphism with an increased risk of CAD in the Caucasian population has been controversial.…”

Section: Discussionmentioning

confidence: 99%

“…Dysfunction of the RA system promotes the development of cardiovascular disease. 1,2 Renin secretion, physiologically triggered by a reduction in blood pressure, intravasal volume or renal perfusion, initiates the RA system cascade by converting angiotensinogen to angiotensin I. Angiotensin Iconverting enzyme (ACE) converts angiotensin I into angiotensin II (AT-II), which physiologically induces vasoconstriction and aldosterone secretion. 1 However, AT-II may also exert a strong atherogenic effect by promoting vascular cell proliferation and neointima formation.…”

Section: Introductionmentioning

confidence: 99%

“…1,2 Renin secretion, physiologically triggered by a reduction in blood pressure, intravasal volume or renal perfusion, initiates the RA system cascade by converting angiotensinogen to angiotensin I. Angiotensin Iconverting enzyme (ACE) converts angiotensin I into angiotensin II (AT-II), which physiologically induces vasoconstriction and aldosterone secretion. 1 However, AT-II may also exert a strong atherogenic effect by promoting vascular cell proliferation and neointima formation. 1,2 The release of other vasoactive substances with a distinct atherogenic potential is induced by the RA system, such as endothelins (ETs) and vasopressin (VP).…”

Section: Introductionmentioning

confidence: 99%

“…1 However, AT-II may also exert a strong atherogenic effect by promoting vascular cell proliferation and neointima formation. 1,2 The release of other vasoactive substances with a distinct atherogenic potential is induced by the RA system, such as endothelins (ETs) and vasopressin (VP).…”

Section: Introductionmentioning

confidence: 99%

“…Pharmacological inhibition of ACE leads to a decrease in AT-II, ET-1 and VP plasma levels. 1,11,12 The insertion/deletion (I/D) polymorphism in intron 16 of the human ACE gene leads to changes in plasma ACE concentration and activity. Homozygotes for the shorter allele (DD) show increased ACE plasma concentrations and activity.…”

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confidence: 99%

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Endothelin-1 and vasopressin plasma levels are not associated with the insertion/deletion polymorphism of the human angiotensin I-converting enzyme gene in patients with coronary artery disease

et al. 2003

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The objective was to investigate whether the reninangiotensin (RA) system and related peptides endothelin-1 (ET-1) and vasopressin (VP) influence the development of coronary artery disease (CAD). Angiotensin I-converting enzyme (ACE) insertion/deletion (I/D) gene polymorphism has been associated with the risk of CAD. The ACE I/D polymorphism determines ACE activity, but plasma levels of other RA system components remain unchanged. However, ET-1 and VP production could be increased by RA system-dependent stimulation, continually promoted by paracrine stimulation and sustained by neointimal growth. ET-1 and VP have not been associated with the ACE I/D polymorphism so far. The present study investigated the association of the ACE I/D polymorphism with plasma concentrations of ET-1 and VP, as well as with renin, angiotensin-II (AT-II) and ACE activity in 98 Caucasian individuals with CAD. ACE I/D polymorphism showed no association with plasma levels of VP, ET-1, AT-II or renin. These parameters were also not associated taking into consideration different patient variables, such as diabetes mellitus, hypertension or severity of CAD. Only plasma ACE activity was associated with the D allele. In conclusion, the ACE I/D polymorphism could not be related to plasma concentrations of VP, ET-1, renin or AT-II, but as previously demonstrated, it could only be related to ACE activity in patients with CAD. Differences in ACE activity between ACE I/D genotype subgroups are probably compensated within the RA system itself or within non-ACE pathways, so that plasma concentrations of the related peptides ET-1 and VP remain unaffected.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

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Endothelin-1 and vasopressin plasma levels are not associated with the insertion/deletion polymorphism of the human angiotensin I-converting enzyme gene in patients with coronary artery disease

et al. 2003

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Integrated Coronary Physiology and Pathophysiology

Bassenge¹,

Schwemmer²

2002

Pan Vascular Medicine

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Role of central angiotensin receptors in scopolamine-induced impairment in memory, cerebral blood flow, and cholinergic function

et al. 2012

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Rational Inhibition of renin-angiotensin system (RAS) improves cognitive functions in hypertensive patients. However, role of AT1 and AT2 receptors in memory impairment due to cholinergic hypofunction is unexplored. Objective This study investigated the role of AT1 and AT2 receptors in cerebral blood flow (CBF), cholinergic neurotransmission, and cerebral energy metabolism in scopolamineinduced amnesic mice. Methods Scopolamine was given to male Swiss albino mice to induce memory impairment tested in passive avoidance and Morris water maze tests after a weeklong administration of blocker of AT1 receptor, candesartan, and AT2 receptor, PD123, 319. CBF was measured by laser Doppler flowmetry. Biochemical and molecular studies were done in cortex and hippocampus of mice brain. Results Scopolamine caused memory impairment, reduced CBF, acetylcholine (ACh) level, elevated acetylcholinesterase (AChE) activity, and malondialdehyde (MDA). Administration of vehicle had no significant effect on any parameter in comparison to control. Candesartan prevented scopolamineinduced amnesia, restored CBF and ACh level, and decreased AChE activity and MDA level. In contrast, PD123, 319 was not effective. However, the effect of AT1 receptor blocker on memory, CBF, ACh level, and oxidative stress was blunted by concomitant blockade of AT2 receptor. Angiotensin-converting enzyme (ACE) activity, ATP level, and mRNA expression of AT1, AT2, and ACE remained unaltered. Conclusion The study suggests that activation of AT1 receptors appears to be involved in the scopolamine-induced amnesia and that AT2 receptors contribute to the beneficial effects of candesartan. Theses finding corroborated the number of clinical studies that RAS inhibition in hypertensive patients could be neuroprotective.

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Anti-Ischemic Potential of Drugs related to the Renin-Angiotensin System

Cited by 25 publications

References 107 publications

Endothelin-1 and vasopressin plasma levels are not associated with the insertion/deletion polymorphism of the human angiotensin I-converting enzyme gene in patients with coronary artery disease

Endothelin-1 and vasopressin plasma levels are not associated with the insertion/deletion polymorphism of the human angiotensin I-converting enzyme gene in patients with coronary artery disease

Integrated Coronary Physiology and Pathophysiology

Role of central angiotensin receptors in scopolamine-induced impairment in memory, cerebral blood flow, and cholinergic function

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