Noradrenaline-Induced Restoration of Acidosis-Inhibited Neurogenic Vasoreactivity at Using Different Electrical Stimulation Frequencies

Yartsev, V. N.; Karachentseva, O. V.

doi:10.1007/s11055-016-0383-x

Cited by 1 publication

(1 citation statement)

References 29 publications

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“…The signaling peptides responsible for the observed pharmacological events were investigated using proteomics tools, including 2D-GE and MS. A recent study showed that induction of hypercapnia through exposure to CO 2 for 5 min was sufficient to induce cerebrovascular dilation through activation of acid-sensing ion channel-1A (ASIC1A), a proton-gated cation channel, resulting in cerebrovascular hypoperfusion [28]. The current study used an ex vivo model of acute acidosis, which involved incubating arterial rings for 90 min at acidic pH o , a standard experimental tool to study the effects of acidosis on the contractile response in isolated arterial rings [18,19,29,30]. Consequently, the findings from our study will help in understanding the pathophysiological alterations contributing to hypotension and hypovolemic shock during acidosis.…”

Section: Discussionmentioning

confidence: 99%

Proteomic Profiling and Pathway Analysis of Acid Stress-Induced Vasorelaxation of Mesenteric Arteries In Vitro

Mohanty

Banerjee

Mahanty

et al. 2022

Genes

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Although metabolic acidosis is associated with numerous pathophysiological conditions and its vasorelaxation effects have been well described in different animal and culture models, the molecular mechanisms of acidosis-induced vasorelaxation are not fully understood. Mesenteric artery models have been used extensively to examine the vascular response to various pathophysiological conditions. Our previous studies and several other reports have suggested the vascular responses of goat mesenteric arteries and human arteries to various stimuli, including acidic stress, are highly similar. In this study, to further identify the signaling molecules responsible for altered vasoreactivity in response to acidic pH, we examined the proteomic profile of acid stress-induced vasorelaxation using a goat mesenteric artery model. The vascular proteomes under acidic pH were compared using 2D-GE with 7 cm IPG strips and mini gels, LC-MS/MS, and MALDI TOF MS. The unique proteins identified by mass spectroscopy were actin, transgelin, WD repeat-containing protein 1, desmin, tropomyosin, ATP synthase β, Hsp27, aldehyde dehydrogenase, pyruvate kinase, and vitamin K epoxide reductase complex subunit 1-like protein. Out of five protein spots identified as actin, three were upregulated > 2-fold. ATP synthase β was also upregulated (2.14-fold) under acid stress. Other actin-associated proteins upregulated were transgelin, desmin, and WD repeat-containing protein 1. Isometric contraction studies revealed that both receptor-mediated (histamine) and non-receptor-mediated (KCl) vasocontraction were attenuated, whereas acetylcholine-induced vasorelaxation was augmented under acidosis. Overall, the altered vasoreactivity under acidosis observed in the functional studies could possibly be attributed to the increase in expression of actin and ATP synthase β.

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