2017
DOI: 10.1152/ajpheart.00745.2016
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The human coronary vasodilatory response to acute mental stress is mediated by neuronal nitric oxide synthase

Abstract: Acute mental stress induces vasodilation of the coronary microvasculature. Here, we show that this response involves neuronal nitric oxide synthase in the human coronary circulation.

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Cited by 13 publications
(9 citation statements)
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References 44 publications
(58 reference statements)
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“…PRG1-1 treatment increased the expression levels of iNOS and COX-2, both of which are associated with NO production. The release of NO is involved in many physiological processes, such as vasodilatation (Khan et al, 2017), neurotransmission (Kusek et al, 2017), immune responses (Cinzia, Maria Pia, Angela, & Marco, 2016), and platelet aggregation (Smyth et al, 2017). Furthermore, activated macrophages produce cytokines, including IL-6 and TNF-α, that play important roles in the cellular immune process by aiding in the elimination of abnormal cells (Ying et al, 2009).…”
Section: Discussionmentioning
confidence: 99%
“…PRG1-1 treatment increased the expression levels of iNOS and COX-2, both of which are associated with NO production. The release of NO is involved in many physiological processes, such as vasodilatation (Khan et al, 2017), neurotransmission (Kusek et al, 2017), immune responses (Cinzia, Maria Pia, Angela, & Marco, 2016), and platelet aggregation (Smyth et al, 2017). Furthermore, activated macrophages produce cytokines, including IL-6 and TNF-α, that play important roles in the cellular immune process by aiding in the elimination of abnormal cells (Ying et al, 2009).…”
Section: Discussionmentioning
confidence: 99%
“…Indeed, an nNOS-selective inhibitor, S-methyl-L-thiocitrulline (SMTC), reduced basal CBF, and epicardial coronary diameter ( Seddon et al., 2009 ). Recently, it has been established that nNOS plays a role in mental stress-induced vasodilatation in human coronary circulation ( Khan et al., 2017 ). In contrast, SMTC had no effect on substance P- and pacing-induced increases in CBF, although these responses were significantly attenuated by the nonselective NOS inhibitor L-NMMA, suggesting the involvement of eNOS but not nNOS ( Seddon et al., 2009 ; Shabeeh et al., 2013 ).…”
Section: Introductionmentioning
confidence: 99%
“…It has been shown that the Stroop task excites cardiopulmonary baroreceptors which then attenuate sympathetic outflow to the forearm vasculature causing muscle vasodilation [29]. Other Stroop-induced vasodilatory mechanisms such as Stroop-induced elevations in shear stress causing release of vasodilatory substances such as nitric oxide [28,30] may also have contributed to the rise in skeletal muscle blood flow and vascular conductance.…”
Section: Discussionmentioning
confidence: 99%