Skip header and navigation

2 records – page 1 of 1.

Acetylcholine-induced calcium signalling in adrenaline- and noradrenaline-containing adrenal chromaffin cells.

https://arctichealth.org/en/permalink/ahliterature9516
Source
Arch Biochem Biophys. 2004 Apr 1;424(1):23-32
Publication Type
Article
Date
Apr-1-2004
Author
O L Zaika
O M Pochynyuk
P G Kostyuk
E N Yavorskaya
E A Lukyanetz
Author Affiliation
International Center for Molecular Physiology, Kiev, Ukraine.
Source
Arch Biochem Biophys. 2004 Apr 1;424(1):23-32
Date
Apr-1-2004
Language
English
Publication Type
Article
Keywords
Acetylcholine - pharmacology
Adrenal Medulla - cytology
Animals
Atropine - pharmacology
Calcium - chemistry - metabolism
Calcium Signaling - drug effects - physiology
Cholinergic Agonists - pharmacology
Cholinergic Antagonists - pharmacology
Chromaffin Cells - chemistry - drug effects - metabolism - physiology
Cytophotometry - methods
Epinephrine - metabolism
Histocytochemistry - methods
Muscarine - pharmacology
Nicotine - pharmacology
Norepinephrine - metabolism
Rats
Receptors, Muscarinic - metabolism - physiology
Receptors, Nicotinic - metabolism - physiology
Research Support, Non-U.S. Gov't
Tubocurarine - pharmacology
Abstract
Adrenal chromaffin cells secrete catecholamines in response to cholinergic receptor activation by acetylcholine (ACh). Characteristics of Ca(2+) transients induced by activation of nicotinic (nAChRs) and muscarinic (mAChRs) receptors were analyzed using Fura-2 fluorescent measurements on rat chromaffin cells. We first found two populations of chromaffin cells, which differently responded on AChR stimulation. In the first group (n-cells), consecutive ACh applications evoked persistent Ca(2+) transients, whereas desensitizing transients were observed in the other group (m-cells). The AChR agonists and antagonists precisely imitated or abolished the ACh action on n- and m-type cells, respectively. Cytochemical staining showed that n-cells contained adrenaline, whereas m-cells-noradrenaline. Thus, for the first time we found that nAChRs and mAChRs are differentially expressed in adrenergic and noradrenergic chromaffin cells, respectively. Our data suppose that chromaffin cells can be differentially regulated by incoming ACh signals and in such way release different substances-adrenaline and noradrenaline.
PubMed ID
15019833 View in PubMed
Less detail

Dialysate calcium concentration and mineral metabolism in long and long-frequent hemodialysis: a systematic review and meta-analysis for a Canadian Society of Nephrology clinical practice guideline.

https://arctichealth.org/en/permalink/ahliterature114688
Source
Am J Kidney Dis. 2013 Jul;62(1):97-111
Publication Type
Article
Date
Jul-2013
Author
Deborah L Zimmerman
Gihad E Nesrallah
Christopher T Chan
Michael Copland
Paul Komenda
Philip A McFarlane
Azim Gangji
Robert Lindsay
Jennifer MacRae
Robert P Pauly
David N Perkins
Andreas Pierratos
Jean-Philippe Rioux
Andrew Steele
Rita S Suri
Reem A Mustafa
Author Affiliation
Division of Nephrology, Kidney Research Centre of the Ottawa Hospital Research Institute, Division of Nephrology, University of Ottawa, Ottawa, Ontario, Canada. dzimmerman@ottawahospital.on.ca
Source
Am J Kidney Dis. 2013 Jul;62(1):97-111
Date
Jul-2013
Language
English
Publication Type
Article
Keywords
Calcium - chemistry - metabolism
Canada
Hemodialysis Solutions - chemistry - metabolism - standards
Humans
Minerals - metabolism
Nephrology - methods - standards
Practice Guidelines as Topic - standards
Randomized Controlled Trials as Topic - methods - standards
Renal Dialysis - methods - standards
Societies, Medical - standards
Time Factors
Abstract
Patients treated with conventional hemodialysis (HD) develop disorders of mineral metabolism that are associated with increased morbidity and mortality. More frequent and longer HD has been associated with improvement in hyperphosphatemia that may improve outcomes.
Systematic review and meta-analysis to inform the clinical practice guideline on intensive dialysis for the Canadian Society of Nephrology.
Adult patients receiving outpatient long (=5.5 hours/session; 3-4 times per week) or long-frequent (=5.5 hours/session, =5 sessions per week) HD.
We included clinical trials, cohort studies, case series, case reports, and systematic reviews.
Dialysate calcium concentration =1.5 mmol/L and/or phosphate additive.
Fragility fracture, peripheral arterial and coronary artery disease, calcific uremic arteriolopathy, mortality, intradialytic hypotension, parathyroidectomy, extraosseous calcification, markers of mineral metabolism, diet liberalization, phosphate-binder use, and muscle mass.
21 studies were identified: 2 randomized controlled trials, 2 reanalyses of data from the randomized controlled trials, and 17 observational studies. Dialysate calcium concentration =1.5 mmol/L for patients treated with long and long-frequent HD prevents an increase in parathyroid hormone levels and a decline in bone mineral density without causing harm. Both long and long-frequent HD were associated with a reduction in serum phosphate level of 0.42-0.45 mmol/L and a reduction in phosphate-binder use. There was no direct evidence to support the use of a dialysate phosphate additive.
Almost all the available information is related to changes in laboratory values and surrogate outcomes.
Dialysate calcium concentration =1.5 mmol/L for most patients treated with long and long-frequent dialysis prevents an increase in parathyroid hormone levels and decline in bone mineral density without increased risk of calcification. It seems prudent to add phosphate to the dialysate for patients with a low predialysis phosphate level or very low postdialysis phosphate level until more evidence becomes available.
Notes
Comment In: Am J Kidney Dis. 2013 Nov;62(5):1018-924157274
Comment In: Am J Kidney Dis. 2013 Nov;62(5):1019-2024157276
PubMed ID
23591289 View in PubMed
Less detail