Different response of connective tissue matrix of abdominal and thoracic aorta to an injury caused by vasopressin hypertension or hypercholesterolemia

Drobnik, Jacek; Dąbrowski, R.; Szczepanowska, A; Giernat, L; Lorenc, J

doi:10.1016/s0753-3322(98)80051-6

Cited by 4 publications

(5 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, the elevation of serum AVP level is known to be induced by cigarette smoking, which is associated with hyperlipidemia and atherogenic changes of arteries [45]. It has also been suggested that AVP-induced hypertension causes the altered response of aorta connective tissue to vascular injury [46]. These findings as a whole suggest that elevated serum AVP level may take part in the progress of atherogenic change of arterial wall including arterial calcification under certain pathological conditions.…”

Section: Discussionmentioning

confidence: 99%

Vasopressin Stimulates Na-dependent Phosphate Transport and Calcification in Rat Aortic Smooth Muscle Cells

et al. 2007

View full text Add to dashboard Cite

Abstract. We investigated the effect of arginine vasopressin (AVP) on inorganic phosphate (Pi) transport in A-10 rat aortic vascular smooth muscle cells (VSMCs). AVP time-and dose-dependently stimulated Na-dependent Pi transport in A-10 cells. This stimulatory effect of AVP on Pi transport was markedly suppressed by V1 receptor antagonist. A protein kinase C (PKC) inhibitor calphostin C partially suppressed the stimulatory effect of AVP. The selective inhibitors of cJun-NH 2 -terminal mitogen-activated protein (MAP) kinase (Jun kinase) attenuated AVP-induced Pi transport, but Erk kinase or p38 MAP kinase inhibitors did not. Wortmannin, a phosphatidylinositol (PI) 3-kinase inhibitor, suppressed AVP-induced Pi transport. Rapamycin, a selective inhibitor of S 6 kinase, reduced this effect of AVP, while Akt kinase inhibitor did not. The combination of inhibitors for PKC, Jun kinase and PI 3-kinase completely suppressed the AVPenhanced Pi transport. Furthermore, AVP rescued the VSMC from high phosphate-induced cell death and enhanced mineralization of these cells. In summary, these results suggest that AVP stimulates both Na-dependent Pi transport and mineralization in VSMCs. The mechanism is mediated by the activation of multiple signaling pathways including PKC, PI 3-kinase, S 6 kinase and Jun kinase.

show abstract

Section: Discussionmentioning

confidence: 99%

Vasopressin Stimulates Na-dependent Phosphate Transport and Calcification in Rat Aortic Smooth Muscle Cells

et al. 2007

View full text Add to dashboard Cite

show abstract

“…In mice, defective HS polymerization leads to a decrease in sodium and water content within the skin as well as to a higher heart rate, increased fluid intake, increased plasma osmolality, and to an abnormal response to sodium loading 70 . In vasopressin induced HT, total GAGs and HS was increased in thoracic but not in abdominal aorta 71 . Weissgerber et al demonstrated that circulating HS levels as a measure of endothelial glycocalyx degradation was higher in women with early‐onset preeclampsia compared to late‐onset preeclampsia and normotensive women 72 …”

Section: Experimental and Clinical Studiesmentioning

confidence: 99%

“…70 In vasopressin induced HT, total GAGs and HS was increased in thoracic but not in abdominal aorta. 71 Weissgerber et al demonstrated that circulating HS levels as a measure of endothelial glycocalyx degradation was higher in women with early-onset preeclampsia compared to late-onset preeclampsia and normotensive women. 72 Heparin is very similar to HS widely used as an anticoagulant.…”

Section: Heparin Sulfate and Heparinmentioning

confidence: 99%

The role of glycosaminoglycans in blood pressure regulation

Afsar,

Afsar

2023

Microcirculation

View full text Add to dashboard Cite

Essential hypertension (HT) is the global health problem and is a major risk factor for the development of cardiovascular and kidney disease. High salt intake has been associated with HT and impaired kidney sodium excretion is considered to be a major mechanism for the development of HT. Although kidney has a very important role in regulation of BP, this traditional view of BP regulation was challenged by recent findings suggesting that nonosmotic tissue sodium deposition is very important for BP regulation. This new paradigm indicates that sodium can be stored and deposited nonosmotically in the interstitium without water retention and without increased BP. One of the major determinants of this deposition is glycosaminoglycans (GAGs). By binding to GAGs found in the endothelial surface layer (ESL) which contains glycocalyx, sodium is osmotically inactivated and not induce concurrent water retention. Thus, GAGs has important function for homeostatic BP and sodium regulation. In the current review, we summarized the role of GAGs in ESL and BP regulation.

show abstract

“…Rabbit aorta is commonly used to investigate lipid deposition and vascular changes. Although rabbits do not develop spontaneous atherosclerosis, they are useful because they are highly responsive to cholesterol manipulation and develop lesions in a relatively short period of time . The high‐cholesterol‐diet rabbit model has been widely used for inducing experimental atherosclerosis.…”

Section: Rabbit Modelmentioning

confidence: 99%

Animal models for periodontal regeneration and peri‐implant responses

Kantarcı¹,

Hastürk²,

Dyke³

2015

Periodontology 2000

107

View full text Add to dashboard Cite

Translation of experimental data to the clinical setting requires the safety and efficacy of such data to be confirmed in animal systems before application in humans. In dental research, the animal species used is dependent largely on the research question or on the disease model. Periodontal disease and, by analogy, peri‐implant disease, are complex infections that result in a tissue‐degrading inflammatory response. It is impossible to explore the complex pathogenesis of periodontitis or peri‐implantitis using only reductionist in‐vitro methods. Both the disease process and healing of the periodontal and peri‐implant tissues can be studied in animals. Regeneration (after periodontal surgery), in response to various biologic materials with potential for tissue engineering, is a continuous process involving various types of tissue, including epithelia, connective tissues and alveolar bone. The same principles apply to peri‐implant healing. Given the complexity of the biology, animal models are necessary and serve as the standard for successful translation of regenerative materials and dental implants to the clinical setting. Smaller species of animal are more convenient for disease‐associated research, whereas larger animals are more appropriate for studies that target tissue healing as the anatomy of larger animals more closely resembles human dento‐alveolar architecture. This review focuses on the animal models available for the study of regeneration in periodontal research and implantology; the advantages and disadvantages of each animal model; the interpretation of data acquired; and future perspectives of animal research, with a discussion of possible nonanimal alternatives. Power calculations in such studies are crucial in order to use a sample size that is large enough to generate statistically useful data, whilst, at the same time, small enough to prevent the unnecessary use of animals.

show abstract

Different response of connective tissue matrix of abdominal and thoracic aorta to an injury caused by vasopressin hypertension or hypercholesterolemia

Cited by 4 publications

References 0 publications

Vasopressin Stimulates Na-dependent Phosphate Transport and Calcification in Rat Aortic Smooth Muscle Cells

Vasopressin Stimulates Na-dependent Phosphate Transport and Calcification in Rat Aortic Smooth Muscle Cells

The role of glycosaminoglycans in blood pressure regulation

Animal models for periodontal regeneration and peri‐implant responses

Contact Info

Product

Resources

About