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.5; KCl, 4.6; KH 2 PO 4 , 1.2; MgSO 4 .7H 2 O, 1.2; NaHCO 3 , 25; glucose, 11.1; Na 2 EDTA, 0.03) at 4 °C. The endothelium was removed to eliminate the main source of vasoactive substances, including NO. This avoided possible actions on endothelial cells
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balance, further contributing to systemic metabolic control ( Graupera & Claret 2018 ). Through mediating insulin delivery and facilitating monocyte transmigration, the adipose microvascular endothelium plays a crucial role in the development of high
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Unit of Clinical Pharmacology, Turku University Hospital, Turku, Finland
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–80% of the maximal reference contraction to KCl and endothelium-dependent vasodilatation response to acetylcholine was determined. Endothelium-independent relaxation was studied in a similar fashion using cumulative doses of sodium nitroprusside (SNP
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) cells of pancreatic islet and (B) the endothelium of pancreatic blood vessels. (C) Ovary was used as positive control. (D) Pancreatic tissue without the addition of primary antibody was used as negative control. Confocal microscopy of double
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artery), potassium (KCl; 2.5×10 −3 −3.2 mol/l for aortae; high-potassium PSS (KPSS), 2.5 × 10 −3 −0.125 mol/l for mesenteric arteries), Ang II (10 −11 − 1 × 10 −6 mol/l) and AVP (10 −11 −1× 10 −6 mol/l). Responses to the endothelium
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). Endothelium-dependent responses were examined using acetylcholine (Sigma Chemical Co.). To measure the maximal relaxation, 100 μmol/l SNP were added following the relaxation experiments to CGRP and acetylcholine. Contractile responses were investigated with
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- or micro-vascular endothelium or each individual microvascular endothelium. Given the fact that different origins of endothelia are highly heterogeneous in global gene expression profiles, possibly leading to different cell phenotypes including
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SUMMARY
The adrenal histology of Chelonia amyda is described and emphasis placed upon the interpenetration of the interrenal and chromaffin tissues and on their structural relationships with the vascular endothelium. Diastase-resistant polysaccharide complexes are present within the chromaffin-reactive cells. Alkaline glycerophosphatase is absent from the interrenal tissues but present in the chromaffin tissues, especially in the intercellular material.
Department of Pharmacology, Korea University College of Medicine, Seoul, Republic of Korea
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Department of Pharmacology, Korea University College of Medicine, Seoul, Republic of Korea
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Department of Pharmacology, Korea University College of Medicine, Seoul, Republic of Korea
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humans or rodents compared to those in younger ones, which could partly be due to the impairment of endothelium-dependent dilation ( Donato et al. 2009 , Seals et al. 2011 ). Therefore, the results suggest that vascular endothelial dysfunction
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Endothelial cells (EC) are hypoxia-tolerant and their capacity to proliferate in low oxygen tension is essential to maintain vascular endothelium integrity. The present study addresses whether hypoxia alters the expression of insulin-like growth factor (IGF) and IGF binding protein (IGFBP) genes in bovine aortic EC (BAEC) and bovine pulmonary artery EC (BPAEC). EC were cultured in normoxic (21%) conditions and exposed to 0% oxygen for 24, 48, or 72 h; some cells were reoxygenated by exposure to 21% oxygen for 24 or 48 h following hypoxia. IGF-I peptide and mRNA levels were very low in both cell types, and decreased further with exposure to hypoxia. Ligand blotting showed that both cell types synthesized 24 kDa (IGFBP-4), 30 kDa (IGFBP-5 and/or IGFBP-6), 43 kDa and 48 kDa IGFBPs (IGFBP-3 glycosylation variants). IGFBP-4 was the predominant IGFBP expressed by both cell types and did not change with exposure to hypoxia. Hypoxia caused a significant increase in IGFBP-3 secretion in BPAEC but not in BAEC. IGFBP-3 stable mRNA levels in BPAEC were increased correspondingly. IGFBP-5 was expressed only in BAEC and decreased with exposure to hypoxia. IGFBP-6 mRNA expression was low and increased in both cell types with exposure to hypoxia. These results demonstrate that EC IGFBP baseline expression as well as its expression in hypoxia vary in different vascular beds and suggest that the IGFBPs may be the dominant paracrine regulators of proliferation of EC as well as maintenance of endothelium integrity during hypoxia.
