The Cyclic AMP-Mediated Action of Epinephrine on the Activity of Carbonic Anhydrase in Avian Erythrocytes

Siegmund, Peter; Tüllmann, A; Holke, Monika

doi:10.1055/s-0028-1093863

Cited by 11 publications

(3 citation statements)

References 2 publications

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“…Several earlier pieces of evi dence pointed in this direction. It is known from the pioneering work of Sutherland and his colleagues, in which they first demon strated the existence of the cAMP second messenger system, that epinephrine increases cAMP in pigeon [ The model we selected was the Japanese quail erythrocyte similar to that used by Siegmund et al [4], Earlier we had reported that in this model epinephrine increased CA activ ity by 14% [5]; the present study focused on an attempt to increase the size of this response by employing two strategies: use of the padrenergic agonist isoproterenol instead of epinephrine, and pretreatment with reserpine to decrease circulating catecholamines at the time of removal of the erythrocytes.…”

Section: Discussionmentioning

confidence: 99%

“…The following method was modified from that described by Siegmund et al [4] for chicken erythro cytes. Heparinized blood was collected by cardiac puncture from halothane-anesthctizcd birds and was centrifuged at 2,000 rpm for 15 min at 4°C.…”

Section: Incubation O F Intact Erythrocytesmentioning

confidence: 99%

“…The model selected was the Japanese quail erythrocyte similar to that used by Siegmund et al [4], Blood is removed by heart puncture under anesthesia; the eryth rocytes are washed and resuspended in heated quail plasma and incubated with the appro priate catecholamine agonist. There are sever al reports, reviewed by Harvey et al [6], that stressing chickens prior to blood collection results in a relase of the adrenal medullary hormones, epinephrine and norepinephrine, into the circulation.…”

Section: Introductionmentioning

confidence: 99%

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Effect of Reserpine Pretreatment on Avian Erythrocyte Carbonic Anhydrase Activation by Isoproterenol

et al. 1994

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We studied the action of β-adrenergic agonists on Japanese quail erythrocyte carbonic anhydrase (CA) in vitro. Earlier we had reported that epinephrine increased CA activity by 14%; the present study focused on an attempt to increase the size of this response. Washed erythrocytes from reserpine-treated (1 mg/kg daily i.m. for 3 days) and control birds were incubated for 40 min in the presence of isoproterenol 10^–6 mol/l. The activity of CA expressed as Wilbur-Anderson units/mg hemoglobin was increased by as much as 42% in reserpine-treated birds over the control depending on the conditions. Addition of 10^–5 mol/l of the β-adrenergic antagonist propranolol inhibited the isoproterenol-induced effect in nonreserpinized birds. We conclude that pretreatment with reserpine, which was accompanied by a fall in plasma catecholamine levels, particularly epinephrine levels, enhanced the activation of CA by isoproterenol.

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Section: Discussionmentioning

confidence: 99%

Section: Incubation O F Intact Erythrocytesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Effect of Reserpine Pretreatment on Avian Erythrocyte Carbonic Anhydrase Activation by Isoproterenol

et al. 1994

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Unveiling tomorrow: Carbonic anhydrase activators and inhibitors pioneering new frontiers in Alzheimer's disease

Mishra,

Sethi

2024

Archiv der Pharmazie

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Alzheimer's disease (AD) is a neurodegenerative disorder and a principal basis of dementia in the elderly population globally. Recently, human carbonic anhydrases (hCAs, EC 4.2.1.1) were demonstrated as possible new targets for treating AD. hCAs are vital for maintaining pH balance and performing other physiological processes as they catalyze the reversible hydration of carbon dioxide to bicarbonate and a proton. Current research indicates that hCA plays a role in brain functions critical for transmitting neural signals. Activation of carbonic anhydrase (CA) has emerged as a promising avenue in addressing memory loss and cognitive issues. Conversely, the exploration of CA inhibition represents a novel frontier in this field. By enhancing glial fitness and cerebrovascular health and blocking amyloid‐β (Aβ)‐induced mitochondrial dysfunction pathways, cytochrome C (CytC) release, caspase 9 activation, and H2O2 generation in neurons, CA inhibitors improve cognition and lessen the pathology caused by Aβ. Recent research has pushed hCAs into the spotlight as critical players in AD pathogenesis and precise therapeutic targets. The captivating dilemma of choosing between hCA inhibitors and activators looms large, as inhibitors reduce Aβ aggregation and improve cerebral blood flow, while activators enhance cerebrovascular functions and restore pH balance. The current review sheds light on the clinical evidence for hCAs and the roles of inhibitors and activators in AD. Additionally, this review offers a fascinating outlook on the data that may aid medicinal chemists in designing and developing new leads that are more effective and selective for upcoming in vitro and in vivo studies, allowing for the discovery and introduction of novel drug candidates for the treatment of AD to the market and into the clinical pipeline.

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Parathyroid Hormone, Carbonic Anhydrase and Calcium Homeostasis

Dietsch¹

1987

Generalized Bone Diseases

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The Cyclic AMP-Mediated Action of Epinephrine on the Activity of Carbonic Anhydrase in Avian Erythrocytes

Cited by 11 publications

References 2 publications

Effect of Reserpine Pretreatment on Avian Erythrocyte Carbonic Anhydrase Activation by Isoproterenol

Effect of Reserpine Pretreatment on Avian Erythrocyte Carbonic Anhydrase Activation by Isoproterenol

Unveiling tomorrow: Carbonic anhydrase activators and inhibitors pioneering new frontiers in Alzheimer's disease

Parathyroid Hormone, Carbonic Anhydrase and Calcium Homeostasis

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