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Open AccessArticle

Pretreatment with Relaxin Does Not Restore NO-Mediated Modulation of Calcium Signal in Coronary Endothelial Cells Isolated from Spontaneously Hypertensive Rats

1
Departments of Clinical & Experimental Medicine, Research Unit of Histology & Embryology University of Florence, Viale G. Pieraccini 6, 50139 Florence, Italy
2
NEUROFARBA, Section of Pharmacology & Toxicology, University of Florence, Viale G. Pieraccini 6, 50139 Florence, Italy
*
Author to whom correspondence should be addressed.
Academic Editor: Claudio Battilocchio
Molecules 2015, 20(6), 9524-9535; https://doi.org/10.3390/molecules20069524
Received: 18 March 2015 / Revised: 11 May 2015 / Accepted: 15 May 2015 / Published: 26 May 2015
(This article belongs to the Special Issue Nitric Oxide (NO) Release Chemistry)
We demonstrated that in coronary endothelial cells (RCEs) from normotensive Wistar Kyoto rats (WKY), the hormone relaxin (RLX) increases NO production and reduces calcium transients by a NO-related mechanism. Since an impairment of the NO pathway has been described in spontaneously hypertensive rats (SHR), the present study was aimed at exploring RLX effects on RCEs from SHR, hypothesizing that RLX could restore calcium responsiveness to NO. RCEs were isolated from WKY and SHR. Calcium transients were evaluated by image analysis after the administration of angiotensin II or α-thrombin. Angiotensin II (1 µM) caused a prompt rise of [Ca2+]i in WKY and SHR RCEs and a rapid decrease, being the decay time higher in SHR than in WKY. NOS inhibition increased calcium transient in WKY, but not in SHR RCEs. Whereas RLX pretreatment (24 h, 60 ng/mL) was ineffective in SHR, it strongly reduced calcium transient in WKY in a NO-dependent way. A similar behavior was measured using 30 U/mL α-thrombin. The current study offers evidence that RLX cannot restore NO responsiveness in SHR, suggesting an accurate selection of patients eligible for RLX treatment of cardiovascular diseases. View Full-Text
Keywords: angiotensin II; cGMP-dependent protein kinase I; cardiovascular diseases; NG-nitro-l-arginine methylester; normotensive Wistar Kyoto rats; S-nitroso-N-acetylpenicillamine; α-thrombin; W1400 angiotensin II; cGMP-dependent protein kinase I; cardiovascular diseases; NG-nitro-l-arginine methylester; normotensive Wistar Kyoto rats; S-nitroso-N-acetylpenicillamine; α-thrombin; W1400
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MDPI and ACS Style

Nistri, S.; Di Cesare Mannelli, L.; Ghelardini, C.; Zanardelli, M.; Bani, D.; Failli, P. Pretreatment with Relaxin Does Not Restore NO-Mediated Modulation of Calcium Signal in Coronary Endothelial Cells Isolated from Spontaneously Hypertensive Rats. Molecules 2015, 20, 9524-9535.

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