Publication

Exogenous administration of thiosulfate, a donor of hydrogen sulfide, attenuates angiotensin II-induced hypertensive heart disease in rats

Snijder, P. M., Frenay, A. R., de Boer, R. A., Pasch, A., Hillebrands, J. L., Leuvenink, H. G. D. & van Goor, H., Mar-2015, In : British Journal of Pharmacology. 172, 6, p. 1494-1504 11 p.

Research output: Contribution to journalArticleAcademicpeer-review

APA

Snijder, P. M., Frenay, A. R., de Boer, R. A., Pasch, A., Hillebrands, J. L., Leuvenink, H. G. D., & van Goor, H. (2015). Exogenous administration of thiosulfate, a donor of hydrogen sulfide, attenuates angiotensin II-induced hypertensive heart disease in rats. British Journal of Pharmacology, 172(6), 1494-1504. https://doi.org/10.1111/bph.12825

Author

Snijder, P. M. ; Frenay, A. R. ; de Boer, R. A. ; Pasch, A. ; Hillebrands, J. L. ; Leuvenink, H. G. D. ; van Goor, H. / Exogenous administration of thiosulfate, a donor of hydrogen sulfide, attenuates angiotensin II-induced hypertensive heart disease in rats. In: British Journal of Pharmacology. 2015 ; Vol. 172, No. 6. pp. 1494-1504.

Harvard

Snijder, PM, Frenay, AR, de Boer, RA, Pasch, A, Hillebrands, JL, Leuvenink, HGD & van Goor, H 2015, 'Exogenous administration of thiosulfate, a donor of hydrogen sulfide, attenuates angiotensin II-induced hypertensive heart disease in rats', British Journal of Pharmacology, vol. 172, no. 6, pp. 1494-1504. https://doi.org/10.1111/bph.12825

Standard

Exogenous administration of thiosulfate, a donor of hydrogen sulfide, attenuates angiotensin II-induced hypertensive heart disease in rats. / Snijder, P. M.; Frenay, A. R.; de Boer, R. A.; Pasch, A.; Hillebrands, J. L.; Leuvenink, H. G. D.; van Goor, H.

In: British Journal of Pharmacology, Vol. 172, No. 6, 03.2015, p. 1494-1504.

Research output: Contribution to journalArticleAcademicpeer-review

Vancouver

Snijder PM, Frenay AR, de Boer RA, Pasch A, Hillebrands JL, Leuvenink HGD et al. Exogenous administration of thiosulfate, a donor of hydrogen sulfide, attenuates angiotensin II-induced hypertensive heart disease in rats. British Journal of Pharmacology. 2015 Mar;172(6):1494-1504. https://doi.org/10.1111/bph.12825


BibTeX

@article{24e865cf4b5a4461a8e3351d085256cc,
title = "Exogenous administration of thiosulfate, a donor of hydrogen sulfide, attenuates angiotensin II-induced hypertensive heart disease in rats",
abstract = "BACKGROUND AND PURPOSE: Hypertension is an important mediator of cardiac damage and remodelling. Hydrogen sulfide (H2S) is an endogenously produced gasotransmitter with cardioprotective properties. However, it is not yet in clinical use. We, therefore, investigated the protective effects of sodium thiosulfate (STS), a clinically applicable H2 S donor substance, in angiotensin II (Ang II)-induced hypertensive cardiac disease in rats.EXPERIMENTAL APPROACH: Male Sprague Dawley rats were infused with Ang II (435 ng kg min(-1)) or saline (control) for 3 weeks via s.c. placed osmotic minipumps. During these 3 weeks, rats received i.p. injections of either STS, NaHS or vehicle (0.9{\%} NaCl).KEY RESULTS: Compared with controls, Ang II infusion caused an increase in systolic and diastolic BP with associated cardiac damage as evidenced by cardiac hypertrophy, an increase in atrial natriuretic peptide (ANP) mRNA, cardiac fibrosis and increased oxidative stress. Treatment with NaHS and STS prevented the development of hypertension and the increase in ANP mRNA levels. Furthermore, the degree of cardiac hypertrophy, the extent of histological fibrosis in combination with the expression of profibrotic genes and the levels of oxidative stress were all significantly decreased.CONCLUSIONS AND IMPLICATIONS: Ang II-induced hypertensive cardiac disease can be attenuated by treatment with STS and NaHS. Although BP regulation is the most plausible mechanism of cardiac protection, the antifibrotic and antioxidant properties of released sulfide may also contribute to their effects. Our data show that H2 S might be a valuable addition to the already existing antihypertensive and cardioprotective therapies.",
keywords = "CYSTATHIONINE GAMMA-LYASE, CHRONIC KIDNEY-DISEASE, NITRIC-OXIDE SYNTHASE, SODIUM THIOSULFATE, BLOOD-PRESSURE, OXIDATIVE STRESS, CONCISE GUIDE, MOLECULAR-MECHANISMS, ARRIVE GUIDELINES, TYROSINE KINASE",
author = "Snijder, {P. M.} and Frenay, {A. R.} and {de Boer}, {R. A.} and A. Pasch and Hillebrands, {J. L.} and Leuvenink, {H. G. D.} and {van Goor}, H.",
note = "{\circledC} 2014 The British Pharmacological Society.",
year = "2015",
month = "3",
doi = "10.1111/bph.12825",
language = "English",
volume = "172",
pages = "1494--1504",
journal = "British Journal of Pharmacology",
issn = "0007-1188",
publisher = "Wiley-Blackwell",
number = "6",

}

RIS

TY - JOUR

T1 - Exogenous administration of thiosulfate, a donor of hydrogen sulfide, attenuates angiotensin II-induced hypertensive heart disease in rats

AU - Snijder, P. M.

AU - Frenay, A. R.

AU - de Boer, R. A.

AU - Pasch, A.

AU - Hillebrands, J. L.

AU - Leuvenink, H. G. D.

AU - van Goor, H.

N1 - © 2014 The British Pharmacological Society.

PY - 2015/3

Y1 - 2015/3

N2 - BACKGROUND AND PURPOSE: Hypertension is an important mediator of cardiac damage and remodelling. Hydrogen sulfide (H2S) is an endogenously produced gasotransmitter with cardioprotective properties. However, it is not yet in clinical use. We, therefore, investigated the protective effects of sodium thiosulfate (STS), a clinically applicable H2 S donor substance, in angiotensin II (Ang II)-induced hypertensive cardiac disease in rats.EXPERIMENTAL APPROACH: Male Sprague Dawley rats were infused with Ang II (435 ng kg min(-1)) or saline (control) for 3 weeks via s.c. placed osmotic minipumps. During these 3 weeks, rats received i.p. injections of either STS, NaHS or vehicle (0.9% NaCl).KEY RESULTS: Compared with controls, Ang II infusion caused an increase in systolic and diastolic BP with associated cardiac damage as evidenced by cardiac hypertrophy, an increase in atrial natriuretic peptide (ANP) mRNA, cardiac fibrosis and increased oxidative stress. Treatment with NaHS and STS prevented the development of hypertension and the increase in ANP mRNA levels. Furthermore, the degree of cardiac hypertrophy, the extent of histological fibrosis in combination with the expression of profibrotic genes and the levels of oxidative stress were all significantly decreased.CONCLUSIONS AND IMPLICATIONS: Ang II-induced hypertensive cardiac disease can be attenuated by treatment with STS and NaHS. Although BP regulation is the most plausible mechanism of cardiac protection, the antifibrotic and antioxidant properties of released sulfide may also contribute to their effects. Our data show that H2 S might be a valuable addition to the already existing antihypertensive and cardioprotective therapies.

AB - BACKGROUND AND PURPOSE: Hypertension is an important mediator of cardiac damage and remodelling. Hydrogen sulfide (H2S) is an endogenously produced gasotransmitter with cardioprotective properties. However, it is not yet in clinical use. We, therefore, investigated the protective effects of sodium thiosulfate (STS), a clinically applicable H2 S donor substance, in angiotensin II (Ang II)-induced hypertensive cardiac disease in rats.EXPERIMENTAL APPROACH: Male Sprague Dawley rats were infused with Ang II (435 ng kg min(-1)) or saline (control) for 3 weeks via s.c. placed osmotic minipumps. During these 3 weeks, rats received i.p. injections of either STS, NaHS or vehicle (0.9% NaCl).KEY RESULTS: Compared with controls, Ang II infusion caused an increase in systolic and diastolic BP with associated cardiac damage as evidenced by cardiac hypertrophy, an increase in atrial natriuretic peptide (ANP) mRNA, cardiac fibrosis and increased oxidative stress. Treatment with NaHS and STS prevented the development of hypertension and the increase in ANP mRNA levels. Furthermore, the degree of cardiac hypertrophy, the extent of histological fibrosis in combination with the expression of profibrotic genes and the levels of oxidative stress were all significantly decreased.CONCLUSIONS AND IMPLICATIONS: Ang II-induced hypertensive cardiac disease can be attenuated by treatment with STS and NaHS. Although BP regulation is the most plausible mechanism of cardiac protection, the antifibrotic and antioxidant properties of released sulfide may also contribute to their effects. Our data show that H2 S might be a valuable addition to the already existing antihypertensive and cardioprotective therapies.

KW - CYSTATHIONINE GAMMA-LYASE

KW - CHRONIC KIDNEY-DISEASE

KW - NITRIC-OXIDE SYNTHASE

KW - SODIUM THIOSULFATE

KW - BLOOD-PRESSURE

KW - OXIDATIVE STRESS

KW - CONCISE GUIDE

KW - MOLECULAR-MECHANISMS

KW - ARRIVE GUIDELINES

KW - TYROSINE KINASE

U2 - 10.1111/bph.12825

DO - 10.1111/bph.12825

M3 - Article

VL - 172

SP - 1494

EP - 1504

JO - British Journal of Pharmacology

JF - British Journal of Pharmacology

SN - 0007-1188

IS - 6

ER -

ID: 20519429