Original articlesHyperpolarization contributes to vascular hyporeactivity in rats with lipopolysaccharide-induced endotoxic shock
References (0)
Cited by (51)
Cecal inoculum peritonitis: An alternative model for sepsis vascular dysfunction study
2015, Life SciencesCitation Excerpt :Confirming this, we also observed a similar inhibition following the direct addition of penitrem A to a muscle bath containing aortae exhibiting oscillatory activity (data not shown). Hyper-activated voltage dependent potassium (Kv) channels have been shown to alter membrane potential and basal tone in LPS and CLP aortae [21,29] however, the exact Kv isoform responsible for sepsis-induced vascular dysfunction has not been identified. We hypothesized that Kv1.5 could be a potential target for sepsis induced vascular hyporesponsiveness to PE since the Kv1.5 channel has been suggested as one of the major components of delayed rectifier K+ currents in a variety of vascular beds [33,34].
Role of non-MLC20 phosphorylation pathway in the regulation of vascular reactivity during shock
2014, Journal of Surgical ResearchCitation Excerpt :Elucidating the mechanism for vascular hyporesponsiveness has appreciable implications for the treatment of these critical conditions. Previous studies have demonstrated that the mechanisms for the vascular hyporeactivity after shock are related to receptor desensitization, membrane hyperpolarization of vascular smooth muscle cells (VSMCs), and calcium desensitization [4–6]. These mechanisms are all involved in the inhibition of 20-kDa myosin light chain (MLC20) phosphorylation.
Stress response in critical illness
2013, Current Problems in Pediatric and Adolescent Health CareCitation Excerpt :Vasopressin has myriad end-organ effects that are mediated through several different receptors. Endotoxins diminish the contractile response of arteries to norepinephrine in vitro.40 Vasopressin is capable of reversing this diminished responsiveness through the V1 receptor.41
Role of adenosine A2A receptor in organ-specific vascular reactivity following hemorrhagic shock in rats
2013, Journal of Surgical ResearchCitation Excerpt :Research has shown that vascular reactivity is significantly decreased following severe trauma, shock, or sepsis. This vascular hyporeactivity interferes with the development, therapy, and outcome of these critical illnesses, especially with the application of vasoactive agents [1–7]. Many studies have focused on single blood vessels such as the aorta or the pulmonary, renal, or mesenteric artery [5–10], and a few studies have identified different responses to vasoactive agents among different vessels.
Role of V<inf>1a</inf> Receptor in AVP-Induced Restoration of Vascular Hyporeactivity and Its Relationship to MLCP-MLC<inf>20</inf> Phosphorylation Pathway
2010, Journal of Surgical ResearchCitation Excerpt :Studies have demonstrated that vascular hyporeactivity plays an important role in the incidence, development, and the outcome of shock and interferes with the application of vasoactive agents in the therapy of shock. Vascular hyporeactivity may be related to the functional disorder of the multiple receptors and ion channels in VSMC, the hyperpolarization of cell membrane [24], or calcium desensitization of VSMC [13]. Our previous study showed that AVP significantly restored the decreased vascular reactivity and calcium sensitivity of VSMC following hemorrhagic shock [5].