2007
DOI: 10.1016/j.ejphar.2006.11.012
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Participation of CGRP and prostanoids in the sex-linked differences of vascular anandamide effects in mesenteric beds of Sprague-Dawley rats

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Cited by 16 publications
(15 citation statements)
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References 26 publications
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“…The presence of this antagonist did not modify the vasoconstrictor response to EFS in female WKY rats, as has also been observed in male rats [5], and this indicates that sensory innervation is not involved in this response in normotension. These results do not concur with previous studies indicating an increased sensory function in females [30,31]. The differences between our data and these studies may be because we used endothelium-denuded arteries, and the vasodilator effect of CGRP is mediated by endothelial NO [32,33] the production of which is greater in females than males [34].…”
Section: Discussioncontrasting
confidence: 82%
“…The presence of this antagonist did not modify the vasoconstrictor response to EFS in female WKY rats, as has also been observed in male rats [5], and this indicates that sensory innervation is not involved in this response in normotension. These results do not concur with previous studies indicating an increased sensory function in females [30,31]. The differences between our data and these studies may be because we used endothelium-denuded arteries, and the vasodilator effect of CGRP is mediated by endothelial NO [32,33] the production of which is greater in females than males [34].…”
Section: Discussioncontrasting
confidence: 82%
“…We hypothesized that hypoxia-induced IUGR would cause changes in vascular function that would affect the mechanisms of endothelium-dependent vasodilation. Since vascular endothelial function is also known to be affected by age (5,20) and sex (32,36), we also investigated whether changes associated with IUGR were age or sex dependent.…”
mentioning
confidence: 99%
“…The experiments were performed according to [6]. Deeply anaesthetized rats were fixed by transcardiac perfusion with PBS containing 4% w/v paraformaldehyde, and mesenteric vascular beds were dissected.…”
Section: Methodsmentioning
confidence: 99%
“…Inhibition of the fatty acid amide hydrolase, enzyme involved in intracellular anandamide degradation, normalizes the cardiovascular function in hypertensive rats without producing adverse metabolic effects [4]. Estrogens are also positive modulators of the anandamide effects at the vascular wall since they stimulate the release of anandamide from human endothelial cells [5] as well as potentiate the anandamide-induced vasorelaxations by increasing the bioavailability of the calcitonin-related peptide (CGRP) in the rat mesenteric vasculature [6]. This potent vasodilator peptide is released, at least in part, as a consequence of the activation of the transient receptor potential vanilloid type 1 (TRPV1) by anandamide [7].…”
Section: Introductionmentioning
confidence: 99%