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2015 ; 6
(ä): 243
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English Wikipedia
The new nitric oxide donor cyclohexane nitrate induces vasorelaxation,
hypotension, and antihypertensive effects via NO/cGMP/PKG pathway
#MMPMID26379557
Mendes-Júnior Ld
; Guimarães DD
; Gadelha DD
; Diniz TF
; Brandão MC
; Athayde-Filho PF
; Lemos VS
; França-Silva Mdo S
; Braga VA
Front Physiol
2015[]; 6
(ä): 243
PMID26379557
show ga
We investigated the cardiovascular effects induced by the nitric oxide donor
Cyclohexane Nitrate (HEX). Vasodilatation, NO release and the effects of acute or
sub-chronic treatment with HEX on cardiovascular parameters were evaluated. HEX
induced endothelium-independent vasodilatation (Maximum effect [efficacy, ME] =
100.4 ± 4.1%; potency [pD2] = 5.1 ± 0.1). Relaxation was attenuated by scavenging
nitric oxide (ME = 44.9 ± 9.4% vs. 100.4 ± 4.1%) or by inhibiting the soluble
guanylyl cyclase (ME = 38.5 ± 9.7% vs. 100.4 ± 4.1%). In addition, pD2 was
decreased after non-selective blockade of K(+) channels (pD2 = 3.6 ± 0.1 vs. 5.1
± 0.1) or by inhibiting KATP channels (pD2 = 4.3 ± 0.1 vs. 5.1 ± 0.1). HEX
increased NO levels in mesenteric arteries (33.2 ± 2.3 vs. 10.7 ± 0.2 au, p <
0.0001). Intravenous acute administration of HEX (1-20 mg/kg) induced hypotension
and bradycardia in normotensive and hypertensive rats. Furthermore, starting at 6
weeks after the induction of 2K1C hypertension, oral treatment with the HEX (10
mg/Kg/day) for 7 days reduced blood pressure in hypertensive animals (134 ± 6 vs.
170 ± 4 mmHg, respectively). Our data demonstrate that HEX is a NO donor able to
produce vasodilatation via NO/cGMP/PKG pathway and activation of the
ATP-sensitive K(+) channels. Furthermore, HEX acutely reduces blood pressure and
heart rate as well as produces antihypertensive effect in renovascular
hypertensive rats.