| 1. |
- Chang, W, et al.
(författare)
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Parathyroid Ca(2+)-conducting currents are modulated by muscarinic receptor agonists and antagonists.
- 1997
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Ingår i: The American journal of physiology. - 0002-9513. ; 273:5 Pt 1
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Tidskriftsartikel (refereegranskat)abstract
- Parathyroid cells express Ca(2+)-conducting cation currents, which are activated by raising the extracellular Ca2+ concentration ([Ca2+]o) and blocked by dihydropyridines. We found that acetylcholine (ACh) inhibited these currents in a reversible, dose-dependent manner (50% inhibitory concentration approximately equal to 10(-8) M). The inhibitory effects could be mimicked by the agonist (+)-muscarine. The effects of ACh were blunted by the antagonist atropine and reversed by removing ATP from the pipette solution (+)-Muscarine enhanced the adenosine 3',5'-cyclic monophosphate (cAMP) production by 30% but had no effect on inositol phosphate accumulation in parathyroid cells. Oligonucleotide primers, based on sequences of known muscarinic receptors (M1-M5), were used in reverse transcriptase-polymerase chain reaction (RT-PCR) to amplify receptor cDNA from parathyroid poly (A)+ RNA. RT-PCR products displayed > 90% nucleotide sequence identity to human M2- and M4-receptor cDNAs. Expression of M2-receptor protein was further confirmed by immunoblotting and immunocytochemistry. Thus parathyroid cells express muscarinic receptors of M2 and possibly M4 subtypes. These receptors may couple to dihydropyridine-sensitive, cation-selective currents through the activation of adenylate cyclase and ATP-dependent pathways in these cells.
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| 2. |
- Skantze, H B, et al.
(författare)
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Endothelial injury in vivo: a technical and statistical approach to the study of aortic integrity.
- 1996
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Ingår i: The American journal of physiology. - 0002-9513. ; 270:5 Pt 2
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Tidskriftsartikel (refereegranskat)abstract
- The endothelium can be a link connecting risk factors with the development of cardiovascular disease, and methods for studying endothelial integrity are therefore important. We describe a method of studying endothelial injury in vivo by combining immunohistochemistry with an improved technique of producing "enface" preparations (Häutchens) aortic endothelium of rabbits and guinea pigs. These Häutchens enabled the study of large numbers of endothelial cells and adherent cells (probably leukocytes) at different locations along the aorta. The statistical distributions of the number of injured endothelial cells and adherent cells in a visual field were also investigated, and both closely followed a log-normal distribution. Based on this distribution, a method to estimate endothelial injury by grouping the cell count data, instead of exact counting, was developed. The grouped cell count data were then used to calculate the grouped mean and grouped standard deviation for each animal. The improvements of the technical and statistical methods offer good opportunities to study various aspects of endothelial integrity in a time efficient manner.
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| 3. |
- Stenlöf, Kaj, 1965, et al.
(författare)
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Energy expenditure in obstructive sleep apnea: effects of treatment with continuous positive airway pressure.
- 1996
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Ingår i: The American journal of physiology. - 0002-9513. ; 271:6 Pt 1
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Tidskriftsartikel (refereegranskat)abstract
- We examined 24-h energy expenditure (EE) in a chamber for indirect calorimetry in five male patients with obstructive sleep apnea (OSA) and six snoring control subjects (snorers). The 24-h EE was remeasured in patients with OSA after 3-mo treatment with nasal continuous positive airway pressure (CPAP). Patients with OSA had a greater degree of severe sleep-breathing disturbance than snorers. Patients with OSA had higher 24-h EE [39.2 +/- 3.0 vs. 33.9 +/- 2.7 kcal.24 h-1.kg fat-free mass (FFM)-1, P < 0.05], daytime urinary norepinephrine and vanillylmandelic acid (VMA), and aminoterminal procollagen III peptide (PIIIp) levels, and they tended to have higher sleeping EE (32.4 +/- 4.1 vs. 26.3 +/- 1.9 kcal.24 h-1.kg FFM-1, P < 0.1) than snorers. CPAP treatment normalized sleep architecture and breathing. CPAP treatment also decreased sleep EE (from 32.4 +/- 4.1 to 27.2 +/- 1.4 kcal.24 h-1.kg FFM-1, P < 0.05) and EE variability during sleep (from 1.6 +/- 0.5 to 1.0 +/- 0.5 kcal.24 h-1.kg FFM-1, P < 0.05) and increased the basal metabolic rate-to-sleep EE ratio in all subjects. Serum PIIIp and plasma norepinephrine decreased after CPAP in all patients. We conclude that OSA is associated with an increased sleep EE, which is normalized by treatment with CPAP.
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| 4. |
- Svanberg, Elisabeth, 1961, et al.
(författare)
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Role of insulin and IGF-I in activation of muscle protein synthesis after oral feeding.
- 1996
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Ingår i: The American journal of physiology. - 0002-9513. ; 270:4 Pt 1
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Tidskriftsartikel (refereegranskat)abstract
- The aim was to evaluate the role of insulin and insulin-like growth factor I (IGF-I) in activation of muscle protein synthesis after oral feeding. Synthesis rate of globular and myofibrillar proteins in muscle tissue was quantified by a flooding dose of radioactive phenylalanine. Muscle tissue expression of IGF-I mRNA was measured. Normal (C57 Bl) and diabetic mice (type I and type II) were subjected to an overnight fast (18 h) with subsequent refeeding procedures for 3 h with either oral chow intake or provision of insulin, IGF-I, glucose, and amino acids. Anti-insulin and anti-IGF-I were provided intraperitoneally before oral refeeding in some experiments. An overnight fast reduced synthesis of both globular (38 +/- 3%) and myofibrillar proteins (54 +/- 3%) in skeletal muscles, which was reversed by oral refeeding. Muscle protein synthesis, after starvation/ refeeding, was proportional and similar to changes in skeletal muscle IGF-I mRNA expression. Diabetic mice responded quantitatively similarly to starvation/refeeding in muscle protein synthesis compared with normal mice (C57 Bl). Both anti-insulin and anti-IGF-I attenuated significantly the stimulation of muscle protein synthesis in response to oral feeding, whereas exogenous provision of either insulin or IGF-I to overnight-starved and freely fed mice did not clearly stimulate protein synthesis in skeletal muscles. Our results support the suggestion that insulin and IGF-I either induce or facilitate the protein synthesis machinery in skeletal muscles rather than exerting a true stimulation of the biosynthetic process during feeding.
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