The effects of enalapril maleate and cold stress exposure on tyrosine hydroxylase activity in some rat tissues

Talas, Zeliha Selamoğlu; Yürekli, Muhittin

doi:10.1002/cbf.1256

Cited by 11 publications

(6 citation statements)

References 15 publications

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“…Tyrosine, the precursor of catecholamines (the sympathetic nervous system (SNS) neurotransmitters such as dopamine, noradrenaline, and adrenaline), was significantly decreased, whereas homovanillate, a catecholamine product, was increased in the urine samples of animals exposed to cold stress. These alterations indicate enhanced SNS activity, leading to an up-regulated catecholamine metabolic pathway (Figure A), and is in agreement with previous reports of increased levels of plasma catecholamines (noradrenaline and adrenaline) and activated tyrosine hydroxylase (which catalyzes tyrosine to dopa) in tissues of animals exposed to cold stress . Increased SNS activity during cold stress contributes to a number of instant physiologic effects such as rapid heart rate, tensed muscles, constricted peripheral vasculature, and increased alertness.…”

Section: Discussionsupporting

confidence: 91%

“…1 It has been reported that cold stress, commonly occurring in clammy weather for human beings, is closely connected with cardiovascular and respiratory diseases, chilblain, diarrhea, and so forth, thereby causing higher mortality, especially among the elderly. 2 Numerous works have centered on individual gene expression, protein structure, and function, 3,4 as well as conventional pathophysiological studies on the hypothalamicpituitary-adrenal (HPA), neuroendocrine, circulatory systems, and immunological responses. 5 Panax ginseng is a highly favored herb restorative in many countries, particularly in China, as it possesses a variety of beneficial anti-inflammatory, antioxidant, glycolipid metabolic, and anti-cancer effects.…”

Section: Introductionmentioning

confidence: 99%

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Metabolic Regulatory Network Alterations in Response to Acute Cold Stress and Ginsenoside Intervention

Wang

Qiu

et al. 2007

J. Proteome Res.

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Acute stress may trigger systemic biochemical and physiological changes in living organisms, leading to a rapid loss of homeostasis, which can be gradually reinstated by self-regulatory mechanisms and/ or drug intervention strategy. However, such a sophisticated metabolic regulatory process has so far been poorly understood, especially from a holistic view. Urinary metabolite profiling of SpragueDawley rats exposed to cold temperature (-10°C) for 2 h using GC/MS in conjunction with modern multivariate statistical techniques revealed drastic biochemical changes as evidenced by fluctuations of urinary metabolites and demonstrated the protective effect of total ginsenosides (TGs) in ginseng extracts on stressed rats. The metabonomics approach enables us to visualize significant alterations in metabolite expression patterns as a result of stress-induced metabolic responses and post-stress compensation, and drug intervention. Several major metabolic pathways including catecholamines, glucocorticoids, the tricarboxylic acid (TCA) cycle, tryptophan (nicotinate), and gut microbiota metabolites were identified to be involved in metabolic regulation and compensation required to restore homeostasis.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Metabolic Regulatory Network Alterations in Response to Acute Cold Stress and Ginsenoside Intervention

Wang

Qiu

et al. 2007

J. Proteome Res.

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“…30 Interestingly, Bregonzio et al and Talas and Yurekli have shown that angiotensin receptor blockers and enalapril treatment were able to prevent the increase of tyrosine hydroxylase activity in the adrenal medulla of rats exposed to cold stress, suggesting a possible attenuation of insulinmediated inhibition of noradrenaline release by these treatments. 16,31 Our data from the present study showed that plasma insulin response to neuroglucopenic stress was modified by enalapril treatment although no significant change in the hyperglycaemic stress response could be observed. We postulate that the chronic treatment with enalapril might have attenuated the sympathetic effect on insulin secretion, very likely by potentiating glucoseinduced insulin secretion in this experiment.…”

Section: Discussionmentioning

confidence: 49%

Angiotensin-converting enzyme inhibition changes the metabolic response to neuroglucopenic stress

Miranda

Silva

Longo

et al. 2011

J Renin Angiotensin Aldosterone Syst

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Neuroglucopenia induced by 2-deoxy-D-glucose (2DG) activates hypothalamic glucoreceptors leading to increased hepatic glucose production and insulin inhibition. This response is similar to what is observed with intravenous injection of angiotensin II (Ang II). However, the involvement of an angiotensin-converting enzyme inhibitor on neuroglucopenia has not been investigated. The aim of this study was to determine the effects of chronic enalapril treatment on plasma glucose, insulin and lipid levels in response to neuroglucopenia. Male Holtzman rats (120-170 g) were chronically treated with enalapril (10 mg/kg per day) in the drinking water for two weeks. On the day of experiment the animals received an i.v. enalapril final dose one hour before the neuroglucopenic stress by 2DG infusion (500 mg/kg), and blood samples were drawn before and 5, 10, 20, 30 and 60 minutes following infusion. The hyperglycaemic response to 2DG was not significantly changed by enalapril treatment. The enalapril-treated group exhibited a peak of plasma insulin higher than controls. Plasma triglyceride showed a significant increase only in the enalapril group after neuroglucopenic stress (p < 0.05).These data show that chronic enalapril treatment changes insulin and triglyceride responses to neuroglucopenia, suggesting an effect on glucose-induced insulin secretion and the storage of triglycerides.

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“…Different mechanisms could underlie the enalapril‐induced changes in glucose metabolism during restraint. Studies have suggested that enalapril prevents increase in tyrosine hydroxylase activity in the adrenal medulla of rats exposed to cold stress and, thus, it could have attenuated the noradrenaline‐mediated inhibition of insulin release in enalapril‐treated rats submitted to restraint in the present study. Alternative mechanisms may be involved in this regulation, especially those related to the primary effects of RAS inhibitors in reducing angiotensin II levels and increasing levels of both bradykinin and angiotensin‐(1–7) .…”

Section: Discussionmentioning

confidence: 52%

Angiotensin‐converting enzyme inhibition increases glucose‐induced insulin secretion in response to acute restraint

Schweizer¹,

Miranda²,

Fóscolo³

et al. 2012

Clin Exp Pharma Physio

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There is increasing evidence suggesting involvement of the renin-angiotensin system (RAS) in carbohydrate metabolism and its response to stress. Thus, the aim of the present study was to evaluate the effects of chronic inhibition of the RAS on glucose and insulin levels during acute restraint stress. Male Holtzman rats were treated with 10 mg/kg per day enalapril solution or vehicle for 14 days. After 14 days, rats were divided into three experimental groups: enalapril + restraint (ER), vehicle + restraint (VR) and enalapril + saline (ES). Rats in the restraint groups were subjected to 30 min restraint stress, whereas rats in the ES groups were given saline infusion instead. Blood samples were collected at baseline and after 5, 10, 20 and 30 min restraint stress or saline infusion. After restraint, a hyperglycaemic response was observed in the ER and VR groups that peaked at 20 and 10 min, respectively (P < 0.05 compared with baseline). The area under the glucose curve was markedly increased in the ER and VR groups compared with that in the ES group (P < 0.05 for both). Importantly, restraint induced a marked increase in insulin secretion in the ER group compared with only a mild elevation in the VR group; insulin secretion in both groups peaked at 20 min (P < 0.05 compared with baseline). Analysis of the area under the insulin curve confirmed an increase in insulin secretion in the ER compared with the VR and ES groups (P < 0.05 for both). The results of the present study reinforce that the RAS is involved in modulating responses to stress and suggest that RAS inhibition with enalapril may increase glucose-induced insulin secretion in response to acute restraint.

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The effects of enalapril maleate and cold stress exposure on tyrosine hydroxylase activity in some rat tissues

Cited by 11 publications

References 15 publications

Metabolic Regulatory Network Alterations in Response to Acute Cold Stress and Ginsenoside Intervention

Metabolic Regulatory Network Alterations in Response to Acute Cold Stress and Ginsenoside Intervention

Angiotensin-converting enzyme inhibition changes the metabolic response to neuroglucopenic stress

Angiotensin‐converting enzyme inhibition increases glucose‐induced insulin secretion in response to acute restraint

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