Alfacalcidol suppresses α-receptor–mediated vasoconstriction via an endothelium dependent mechanism

İsmail ÜN; Akif Hakan KURT; Ali BATUŞ; Kansu BÜYÜKAFŞAR

doi:https://doi.org/10.3906/sag-1205-92

Article Details

Alfacalcidol suppresses α-receptor–mediated vasoconstriction via an endothelium dependent mechanism

Authors:

İsmail ÜN | Akif Hakan KURT | Ali BATUŞ | Kansu BÜYÜKAFŞAR

Publisher:

TUBITAK

Main Topics:

Promotion of health

Journal:

Turkish Journal of Medical Sciences 2013 Vol.43 Issue 2, pp.238-244

Document Type:

Article

Publication Date:

1/2013

Document Language:

English

Document ID (Org No.):

2000753789

Frequency:

Bimonthly

eISSN:

1303-6165

pISSN:

1300-0144

DOI:

https://doi.org/10.3906/sag-1205-92

Keywords:

Abstract:

 

Vitamin D level could be related to blood pressure and cardiovascular health. However, the direct suppressor effect of vitamin D on vascular contraction has not yet been explored. Therefore, the effects of alfacalcidol (1a-hydroxyvitamin D3) and calcitriol (1a,25-dihydroxyvitamin D3) on contractions induced by phenylephrine (10-8 to 10-5 M) in mice aorta were investigated.  Materials and methods: Arterial rings were suspended in isolated organ chambers filled with Krebs bicarbonate solution gassed with 95% O2 and 5% CO2 maintained at 37 °C. Tissue responses were recorded isometrically with a force transducer and displayed on an acquisition system. Alfacalcidol and calcitriol were applied on phenylephrine-induced active tone. Furthermore, aortic rings were preincubated with alfacalcidol and calcitriol and thereafter contracted with phenylephrine. Incubation studies were conducted by endothelium removal and in the presence of L-nitro-arginine methyl ester (L-NAME).   Results: Phenylephrine-induced active tones were significantly suppressed by alfacalcidol (P < 0.05 and P < 0.01) and calcitriol (both 10-5 and 10-6 M). The pEC50 values of alfacalcidol and calcitriol were 7.06 ± 0.91 and 7.13 ± 0.60, respectively. Furthermore, preincubation of aortic rings with alfacalcidol (10-5 M) but not calcitriol (10-5 M) significantly inhibited phenylephrine-induced contractions (10-8 to 10-5 M, P < 0.05 and P < 0.001). The suppressive effect of alfacalcidol incubation disappeared with endothelium removal. Furthermore, alfacalcidol was unable to inhibit phenylephrine-induced contractions in the presence of L-NAME, an inhibitor of nitric oxide biosynthesis.   Conclusion: In this study we report for the first time that alfacalcidol may prevent phenylephrine-induced vasoconstriction in mice aorta with an endothelium-dependent nitric oxide-mediated mechanism.

 

Vitamin D level could be related to blood pressure and cardiovascular health. However, the direct suppressor effect of vitamin D on vascular contraction has not yet been explored. Therefore, the effects of alfacalcidol (1a-hydroxyvitamin D3) and calcitriol (1a,25-dihydroxyvitamin D3) on contractions induced by phenylephrine (10-8 to 10-5 M) in mice aorta were investigated.  Materials and methods: Arterial rings were suspended in isolated organ chambers filled with Krebs bicarbonate solution gassed with 95% O2 and 5% CO2 maintained at 37 °C. Tissue responses were recorded isometrically with a force transducer and displayed on an acquisition system. Alfacalcidol and calcitriol were applied on phenylephrine-induced active tone. Furthermore, aortic rings were preincubated with alfacalcidol and calcitriol and thereafter contracted with phenylephrine. Incubation studies were conducted by endothelium removal and in the presence of L-nitro-arginine methyl ester (L-NAME).   Results: Phenylephrine-induced active tones were significantly suppressed by alfacalcidol (P < 0.05 and P < 0.01) and calcitriol (both 10-5 and 10-6 M). The pEC50 values of alfacalcidol and calcitriol were 7.06 ± 0.91 and 7.13 ± 0.60, respectively. Furthermore, preincubation of aortic rings with alfacalcidol (10-5 M) but not calcitriol (10-5 M) significantly inhibited phenylephrine-induced contractions (10-8 to 10-5 M, P < 0.05 and P < 0.001). The suppressive effect of alfacalcidol incubation disappeared with endothelium removal. Furthermore, alfacalcidol was unable to inhibit phenylephrine-induced contractions in the presence of L-NAME, an inhibitor of nitric oxide biosynthesis.   Conclusion: In this study we report for the first time that alfacalcidol may prevent phenylephrine-induced vasoconstriction in mice aorta with an endothelium-dependent nitric oxide-mediated mechanism.

Article Details

Alfacalcidol suppresses α-receptor–mediated vasoconstriction via an endothelium dependent mechanism

Authors:

İsmail ÜN | Akif Hakan KURT | Ali BATUŞ | Kansu BÜYÜKAFŞAR

Publisher:

TUBITAK

Main Topics:

Promotion of health

Journal:

Turkish Journal of Medical Sciences 2013 Vol.43 Issue 2, pp.238-244

Document Type:

Article

Publication Date:

1/2013

Document Language:

English

Document ID (Org No.):

2000753789

Frequency:

Bimonthly

eISSN:

1303-6165

pISSN:

1300-0144

DOI:

https://doi.org/10.3906/sag-1205-92

Key words: Alfacalcidol

calcitriol

mice

aorta

contraction

Issues

Article Details

Alfacalcidol suppresses α-receptor–mediated vasoconstriction via an endothelium dependent mechanism

Authors: İsmail ÜN | Akif Hakan KURT | Ali BATUŞ | Kansu BÜYÜKAFŞAR

Publisher: TUBITAK

Main Topics: Promotion of health

Journal: Turkish Journal of Medical Sciences 2013 Vol.43 Issue 2, pp.238-244

Document Type: Article

Publication Date: 1/2013

Document Language: English

Document ID (Org No.): 2000753789

Frequency: Bimonthly

eISSN: 1303-6165

pISSN: 1300-0144

DOI: https://doi.org/10.3906/sag-1205-92

Key words: Alfacalcidol

calcitriol

mice

aorta

contraction

Issues

Authors:

İsmail ÜN | Akif Hakan KURT | Ali BATUŞ | Kansu BÜYÜKAFŞAR

Publisher:

TUBITAK

Main Topics:

Promotion of health

Journal:

Turkish Journal of Medical Sciences 2013 Vol.43 Issue 2, pp.238-244

Document Type:

Article

Publication Date:

1/2013

Document Language:

English

Document ID (Org No.):

2000753789

Frequency:

Bimonthly

eISSN:

1303-6165

pISSN:

1300-0144

DOI:

https://doi.org/10.3906/sag-1205-92