Oxidant Stress Stimulates Na/K Pump Activity in Bovine Pulmonary Arterial Endothelial Cells

Rounds, Sharon; Cutaia, Michael; Charles, A.; Meharg, Joseph; Dawicki, Doloretta D.; Oldmixon, E. H.; Kuhn, Charles

doi:10.1378/chest.114.1_supplement.22s

Cited by 2 publications

(1 citation statement)

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“…The Na + pump mediates transient post-excitatory depression of activity in a variety of sensory nerves (Nakajima & Takahashi, 1966; Sokolove & Cooke, 1971) including baroreceptor terminals (Saum et al, 1976), and its activation is enhanced by H 2 O 2 (Matsuoka et al, 1990; Rounds et al, 1998). The stability of H 2 O 2 may account for the relatively prolonged period of inhibition of baroreceptor activity observed after antidromic stimulation of ADN.…”

Section: Discussionmentioning

confidence: 99%

Autocrine/paracrine modulation of baroreceptor activity after antidromic stimulation of aortic depressor nerve in vivo

Santana‐Filho¹,

Davis²,

Castania³

et al. 2014

Autonomic Neuroscience

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Activation of the sensory nerve endings of nonmyelinated C-fiber afferents evokes release of autocrine/paracrine factors that cause localized vasodilation, neurogenic inflammation, and modulation of sensory nerve activity. The aims of this study were to determine the effect of antidromic electrical stimulation on afferent baroreceptor activity in vivo, and investigate the role of endogenous prostanoids and hydrogen peroxide (H2O2) in mediating changes in nerve activity. Baroreceptor activity was recorded from the left aortic depressor nerve (ADN) in anesthetized rats before and after stimulating the ADN for brief (5–20 s) periods. The rostral end of the ADN was crushed or sectioned beforehand to prevent reflex changes in blood pressure. Antidromic stimulation of ADN using parameters that activate both myelinated A-fibers and nonmyelinated C-fibers caused pronounced and long-lasting (>1 min) inhibition of baroreceptor activity (n=9, P<0.05), with the magnitude and duration of inhibition dependent on the duration of the stimulation period (n=5). Baroreceptor activity was only transiently inhibited after selective stimulation of A-fibers. The inhibition of activity after antidromic stimulation of A and C fibers was prolonged after administration of the cyclooxygenase inhibitor indomethacin (5 mg/kg, IV, n=7) and abolished after administration of PEG-catalase (104 units/kg, IV, n=7), an enzyme that catalyzes the decomposition of H2O2 to water and oxygen. The results demonstrate a long-lasting inhibition of baroreceptor activity after antidromic stimulation of ADN and suggest that endogenous prostanoids and H2O2 oppose and mediate the inhibition, respectively. These mechanisms may contribute to rapid baroreceptor resetting during acute hypertension and be engaged during chronic baroreceptor activation therapy in patients with hypertension.

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