Hydrogen sulfide ameliorates vascular calcification induced by vitamin D3 plus nicotine in rats1

Sheng-ying, WU; Pan, Chun‐Shui; Geng, Bin; Zhao, Jing; Yu, Fang; Pang, Yilin; Tang, Chaoshu; Qi, Yongfen

doi:10.1111/j.1745-7254.2006.00283.x

Cited by 61 publications

(47 citation statements)

References 38 publications

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“…Several animal studies reported that VDN treatment brought 5-to 10-fold increase of arterial Ca content to young male Sprague-Dawley (SD) rats (36,41,42). However, our data unexpectedly showed a slight increase but no significant difference in the arterial Ca content of the 0.6% Ca intake group in OVX with VDN rats compared with the 0.6% Ca intake group in OVX without VDN.…”

Section: Discussioncontrasting

confidence: 71%

The Effect of Different Amounts of Calcium Intake on Bone Metabolism and Arterial Calcification in Ovariectomized Rats

Agata

Park

Hattori

et al. 2013

J Nutr Sci Vitaminol

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Summary Low calcium (Ca) intake is the one of risk factors for both bone loss and medial elastocalcinosis in an estrogen deficiency state. To examine the effect of different amounts of Ca intake on the relationship between bone mass alteration and medial elastocalcinosis, 6-wk-old female SD rats were randomized into ovariectomized (OVX) control or OVX treated with vitamin D3 plus nicotine injection (VDN) groups. The OVX treated with VDN group was then divided into 5 groups depending on the different Ca content in their diet, 0.01%, 0.1%, 0.6%, 1.2%, and 2.4% Ca intakes. After 8 wk of experimentation, the low Ca intake groups of 0.01% and 0.1% showed a low bone mineral density (BMD) and bone properties significantly different from those of the other groups, whereas the high Ca intake groups of 1.2% and 2.4% showed no difference compared with the OVX control. Only in the 0.01% Ca intake group, a significantly higher Ca content in the thoracic artery was found compared with that of the OVX control. Arterial tissues of the 0.01% Ca intake group showed an increase of bone-specific alkaline phosphatase (BAP) activity, a marker of bone mineralization, associated with arterial Ca content. However, the high Ca intake did not affect arterial Ca content nor arterial BAP activity. These results suggested that a low Ca intake during periods of rapid bone loss caused by estrogen deficiency might be one possible cause for the complication of both bone loss and medial elastocalcinosis.

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Section: Discussioncontrasting

confidence: 71%

The Effect of Different Amounts of Calcium Intake on Bone Metabolism and Arterial Calcification in Ovariectomized Rats

Agata

Park

Hattori

et al. 2013

J Nutr Sci Vitaminol

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“…The inconsistency between the results of previous studies and our results were presumably because of using different animal models for in vivo studies. VDN treatment reportedly results in an approximately 15-fold increase in arterial Ca levels in young male Wistar rats 8 wk of age (18)(19)(20)(21), whereas this treatment results in ,10-fold increase in arterial Ca levels in young male SD rats of various ages (22)(23)(24). In female rats, the investigation of the calcification paradox by means of OVX plus VDN treatment in vivo has not been studied, except in our previous studies with SD rats of 6 wk (7,25).…”

mentioning

confidence: 99%

The Impact of Different Amounts of Calcium Intake on Bone Mass and Arterial Calcification in Ovariectomized Rats

Agata

Park

Hattori

et al. 2015

J Nutr Sci Vitaminol

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SummaryReduced estrogen secretion and low calcium (Ca) intake are risk factors for bone loss and arterial calcification in female rodents. To evaluate the effects of Ca intake at different amounts on bone mass changes and arterial calcification, 8-wk-old female Wistar rats were randomly placed in ovariectomized (OVX) control and OVX with vitamin D3 plus nicotine (VDN) treatment groups. The OVX with VDN rats were then divided into six groups to receive different amounts of Ca in their diets: 0.01%, 0.1%, 0.3%, 0.6%, 1.2%, or 2.4% Ca. After 8 wk of administration, low Ca intake groups with 0.01% and 0.1% Ca diets had significantly reduced bone mineral density (BMD) and bone mechanical properties as compared with those of the other groups, whereas high Ca intake groups with 1.2% and 2.4% Ca diets showed no differences as compared with the 0.6% Ca intake group. For both the 0.01% and 2.4% Ca intake groups, Ca levels in their thoracic arteries were significantly higher as compared with those of the 0.6% Ca diet group, and that was highly correlated with serum PTH levels. An increase in relative BMP-2 mRNA expression in the arterial tissues of the 0.01% and 2.4% Ca diet groups was also observed. These results suggested that extremely low Ca intake during periods of estrogen deficiency may be a possible risk for the complications of reduced BMD and arterial calcification and that extremely high Ca intake may promote arterial calcification with no changes in BMD.

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“…Experimental angiosteosis induced by combined introduction of vitamin D and nicotine in rats is accompanied by a drop in the expression of CSE, the activity of the latter, and the level of H 2 S in tissues of the aortal wall. Exogenous H 2 S prevents the process of angiosteosis; this fact is confirmed by a decrease in the calcium concentration in the vessels and also by drops in the activity of acidic phosphatase and expression of osteopontin under conditions of the corresponding experiments [80].…”

Section: Importance Of H 2 S For Pathologies Of the Nervousmentioning

confidence: 88%

Hydrogen Sulfide as a Regulator of Systemic Functions in Vertebrates

Вараксин

Puschina

2011

Neurophysiology

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This review deals with new published data and also with our own findings related to the physiological and pathological effects of hydrogen sulfide (H 2 S), a gasotransmitter, which has recently attracted intense attention. In the organism, hydrogen sulfide is synthesized from cysteine with the involvement of pyridoxal-5′-phosphate-dependent enzymes, cystathionine-β-synthase (CBS) or cystathionine-γ-lyase (CSE). Under the action of H 2 S, ATP-dependent potassium channels (K АТР ) are activated in vascular smooth muscle cells, neurons, cardiomyocytes, and pancreatic β-cells; this explains the important and extensive role of this agent in the control of vascular tone and contractile activity of cardiomyocytes, in the processes of neurotransmission, and in secretion of insulin. Possible roles of Н 2 S-producing systems in the pathogenesis of arterial and pulmonary hypertension, Alzheimer's disease, and hepatocirrhosis are discussed. A description of some aspects of the action of H 2 S "beyond the nervous system" should, probably, also attract the interest of readers, allowing them to form a clearer view of the role of this gasotransmitter in the control of systemic functions.

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Hydrogen sulfide ameliorates vascular calcification induced by vitamin D3 plus nicotine in rats1

Cited by 61 publications

References 38 publications

The Effect of Different Amounts of Calcium Intake on Bone Metabolism and Arterial Calcification in Ovariectomized Rats

The Effect of Different Amounts of Calcium Intake on Bone Metabolism and Arterial Calcification in Ovariectomized Rats

The Impact of Different Amounts of Calcium Intake on Bone Mass and Arterial Calcification in Ovariectomized Rats

Hydrogen Sulfide as a Regulator of Systemic Functions in Vertebrates

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