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Modulation of endothelin-1 coronary vasoconstriction in spontaneously hypertensive rats by the nitric oxide system.
Am J Hypertens. 2000 Jan; 13(1 Pt 1):83-7.AJ

Abstract

To determine whether nitric oxide contributes to the augmented vasoconstrictive response to endothelin-1 (ET-1) in coronary vessels of hypertensive hearts, and also whether L-arginine administration can inhibit the augmented response to ET-1, we designed experiments to measure coronary perfusion resistance in isolated hearts of spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY) with or without L-arginine administration (0.5 g/L) for 2 weeks. The hearts were paced at a constant rate and perfused by the Langendorff technique at constant pressure (75 mm Hg). Perfusion flow and pressure were monitored, and coronary vascular resistance (CVR) was calculated. ET-1 infusion elicited dose-dependent increases in CVR in both WKY and SHR. At an ET-1 concentration of 1.5 x 10(-9) mol/L, the response was significantly greater in SHR. In L-NAME-treated WKY and SHR, responses to ET-1 were augmented, compared with those of nontreated rats, and this augmentation was greater in WKY. L-arginine administration reduced the CVR response to ET-1 in SHR, whereas it did not change responses to ET-1 in WKY. These findings suggest that the augmented vasoconstriction of the coronary artery induced by ET-1 in hypertensive hearts was due to a reduction in nitric oxide release in coronary vessels and that L-arginine can partially inhibit the vasoconstrictive response of the coronary artery.

Authors+Show Affiliations

Second Department of Medicine, Kyoto Prefectural University of Medicine, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

10678275

Citation

Miki, S, et al. "Modulation of Endothelin-1 Coronary Vasoconstriction in Spontaneously Hypertensive Rats By the Nitric Oxide System." American Journal of Hypertension, vol. 13, no. 1 Pt 1, 2000, pp. 83-7.
Miki S, Takeda K, Kiyama M, et al. Modulation of endothelin-1 coronary vasoconstriction in spontaneously hypertensive rats by the nitric oxide system. Am J Hypertens. 2000;13(1 Pt 1):83-7.
Miki, S., Takeda, K., Kiyama, M., Hatta, T., Moriguchi, J., Kawa, T., Morimoto, S., Nakamura, K., Itoh, H., Nakata, T., Sasaki, S., & Nakagawa, M. (2000). Modulation of endothelin-1 coronary vasoconstriction in spontaneously hypertensive rats by the nitric oxide system. American Journal of Hypertension, 13(1 Pt 1), 83-7.
Miki S, et al. Modulation of Endothelin-1 Coronary Vasoconstriction in Spontaneously Hypertensive Rats By the Nitric Oxide System. Am J Hypertens. 2000;13(1 Pt 1):83-7. PubMed PMID: 10678275.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Modulation of endothelin-1 coronary vasoconstriction in spontaneously hypertensive rats by the nitric oxide system. AU - Miki,S, AU - Takeda,K, AU - Kiyama,M, AU - Hatta,T, AU - Moriguchi,J, AU - Kawa,T, AU - Morimoto,S, AU - Nakamura,K, AU - Itoh,H, AU - Nakata,T, AU - Sasaki,S, AU - Nakagawa,M, PY - 2000/3/11/pubmed PY - 2000/3/11/medline PY - 2000/3/11/entrez SP - 83 EP - 7 JF - American journal of hypertension JO - Am J Hypertens VL - 13 IS - 1 Pt 1 N2 - To determine whether nitric oxide contributes to the augmented vasoconstrictive response to endothelin-1 (ET-1) in coronary vessels of hypertensive hearts, and also whether L-arginine administration can inhibit the augmented response to ET-1, we designed experiments to measure coronary perfusion resistance in isolated hearts of spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY) with or without L-arginine administration (0.5 g/L) for 2 weeks. The hearts were paced at a constant rate and perfused by the Langendorff technique at constant pressure (75 mm Hg). Perfusion flow and pressure were monitored, and coronary vascular resistance (CVR) was calculated. ET-1 infusion elicited dose-dependent increases in CVR in both WKY and SHR. At an ET-1 concentration of 1.5 x 10(-9) mol/L, the response was significantly greater in SHR. In L-NAME-treated WKY and SHR, responses to ET-1 were augmented, compared with those of nontreated rats, and this augmentation was greater in WKY. L-arginine administration reduced the CVR response to ET-1 in SHR, whereas it did not change responses to ET-1 in WKY. These findings suggest that the augmented vasoconstriction of the coronary artery induced by ET-1 in hypertensive hearts was due to a reduction in nitric oxide release in coronary vessels and that L-arginine can partially inhibit the vasoconstrictive response of the coronary artery. SN - 0895-7061 UR - https://www.unboundmedicine.com/medline/citation/10678275/Modulation_of_endothelin_1_coronary_vasoconstriction_in_spontaneously_hypertensive_rats_by_the_nitric_oxide_system_ L2 - https://academic.oup.com/ajh/article-lookup/doi/10.1016/s0895-7061(99)00100-4 DB - PRIME DP - Unbound Medicine ER -