Pharmacological evidence that NaHS inhibits the vasopressor responses induced by stimulation of the preganglionic sympathetic outflow in pithed rats

Centurión, David; Cruz, Saúl Huerta de la; Gutiérrez-Lara, Erika J.; Beltrán-Ornelas, Jesús H.; Sánchez-López, Araceli

doi:10.1016/j.ejphar.2015.11.057

Cited by 17 publications

(4 citation statements)

References 23 publications

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“… Liang et al (2017) have previously shown that chronic PVN infusion of a separate H 2 S donor, GYY4137, decreased BP and plasma noradrenaline levels in rodent salt HTN while simultaneously reducing reactive oxygen species and IL-1β in the PVN. However, H 2 S may also have direct neuronal effects ( Szabo, 2021 ), warranting further investigation of H 2 S in regulation of activity of pre-sympathetic neurons ( Guo et al, 2011 ; Centurion et al, 2016 ; Dominguez-Rodriguez et al, 2017 ).…”

Section: Discussionmentioning

confidence: 99%

Central Administration of Hydrogen Sulfide Donor NaHS Reduces Iba1-Positive Cells in the PVN and Attenuates Rodent Angiotensin II Hypertension

et al. 2021

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Hydrogen sulfide (H2S) is a gaseous signaling molecule with neuromodulatory, anti-inflammatory, and anti-hypertensive effects. Here, we investigate whether chronic intracerebroventricular (ICV) infusion of sodium hydrosulfide (NaHS), an H2S donor, can alleviate angiotensin II (Ang II)–induced hypertension (HTN), improve autonomic function, and impact microglia in the paraventricular nucleus (PVN) of the hypothalamus, a brain region associated with autonomic control of blood pressure (BP) and neuroinflammation in HTN. Chronic delivery of Ang II (200 ng/kg/min, subcutaneous) for 4 weeks produced a typical increase in BP and sympathetic drive and elevated the number of ionized calcium binding adaptor molecule 1–positive (Iba1+) cells in the PVN of male, Sprague–Dawley rats. ICV co-infusion of NaHS (at 30 and/or 60 nmol/h) significantly attenuated these effects of Ang II. Ang II also increased the abundance of cecal Deltaproteobacteria and Desulfovibrionales, among others, which was prevented by ICV NaHS co-infusion at 30 and 60 nmol/h. We observed no differences in circulating H2S between the groups. Our results suggest that central H2S may alleviate rodent HTN independently from circulating H2S via effects on autonomic nervous system and PVN microglia.

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Section: Discussionmentioning

confidence: 99%

Central Administration of Hydrogen Sulfide Donor NaHS Reduces Iba1-Positive Cells in the PVN and Attenuates Rodent Angiotensin II Hypertension

et al. 2021

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“…In addition, the input from preganglionic neurons is increased through a presynaptic action of H 2 S on acetylcholine release (Sha et al, 2013 ). Therefore, the inhibitory action of H 2 S donors on the vasopressor response elicited by preganglionic stimulation of the sympathetic nervous system (Centurión et al, 2016 ) most likely involves a decrease in membrane excitability caused by an activation of K ATP channels.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, blockers of these enzymes were reported to inhibit ganglionic transmission, while NaHS was found to increase the same (Sha et al, 2013 ). Such an augmentation of neurotransmission within sympathetic ganglia by H 2 S is in sharp contrast with the inhibition of vasopressor responses triggered by preganglionic stimulation (Centurión et al, 2016 ), and this discrepancy led us to investigate in detail direct actions of H 2 S and H 2 S donors onto neurons within sympathetic ganglia. In primary cultures of dissociated sympathetic ganglia one gains direct experimental access to different subcellular compartments of such neurons within one culture dish; thereby, one cannot only investigate effects occurring at the somatodendritic region that is in vivo located within the ganglia, but also actions on noradrenaline release which otherwise takes place at sympathetic varicosities situated within the innervated tissues such as arteries (Boehm and Huck, 1997 ).…”

Section: Introductionmentioning

confidence: 96%

“…Effects of H 2 S or H 2 S donors on blood pressure when injected into central nuclei involved in the control of the sympathetic tone have been investigated in detail (Meng et al, 2014 ; van Goor et al, 2016 ). Moreover, systemic administration of H 2 S or H 2 S donors does not only reduce blood pressure (Meng et al, 2014 ; van Goor et al, 2016 ), but also inhibits the vasopressor response to preganglionic stimulation of the sympathetic nervous system while leaving the vasopressor response to noradrenaline and methoxamine, an α - adrenergic agonist, unaltered (Centurión et al, 2016 ). This suggests that H 2 S may act at the level of postganglionic sympathetic neurons, but direct effects of this gasotransmitter on such neurons have not been investigated.…”

Section: Introductionmentioning

confidence: 99%

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Electrophysiological Investigation of the Subcellular Fine Tuning of Sympathetic Neurons by Hydrogen Sulfide

et al. 2017

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H2S is well-known as hypotensive agent, whether it is synthetized endogenously or administered systemically. Moreover, the H2S donor NaHS has been shown to inhibit vasopressor responses triggered by stimulation of preganglionic sympathetic fibers. In contradiction with this latter result, NaHS has been reported to facilitate transmission within sympathetic ganglia. To resolve this inconsistency, H2S and NaHS were applied to primary cultures of dissociated sympathetic ganglia to reveal how this gasotransmitter might act at different subcellular compartments of such neurons. At the somatodendritic region of ganglionic neurons, NaHS raised the frequency, but not the amplitudes, of cholinergic miniature postsynaptic currents via a presynaptic site of action. In addition, the H2S donor as well as H2S itself caused membrane hyperpolarization and decreased action potential firing in response to current injection. Submillimolar NaHS concentrations did not affect currents through Kυ7 channels, but did evoke currents through KATP channels. Similarly to NaHS, the KATP channel activator diazoxide led to hyperpolarization and decreased membrane excitability; the effects of both, NaHS and diazoxide, were prevented by the KATP channel blocker tolbutamide. At postganglionic sympathetic nerve terminals, H2S and NaHS enhanced noradrenaline release due to a direct action at the level of vesicle exocytosis. Taken together, H2S may facilitate transmitter release within sympathetic ganglia and at sympatho-effector junctions, but causes hyperpolarization and reduced membrane excitability in ganglionic neurons. As this latter action was due to KATP channel gating, this channel family is hereby established as another previously unrecognized determinant in the function of sympathetic ganglia.

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Pharmacological evidence that metformin blocks the vasopressor responses mediated by stimulation of α 1 - and α 2 -adrenoceptors in pithed rats

Cruz

Medina-Terol

Beltrán-Ornelas

et al. 2018

European Journal of Pharmacology

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Pharmacological evidence that NaHS inhibits the vasopressor responses induced by stimulation of the preganglionic sympathetic outflow in pithed rats

Cited by 17 publications

References 23 publications

Central Administration of Hydrogen Sulfide Donor NaHS Reduces Iba1-Positive Cells in the PVN and Attenuates Rodent Angiotensin II Hypertension

Central Administration of Hydrogen Sulfide Donor NaHS Reduces Iba1-Positive Cells in the PVN and Attenuates Rodent Angiotensin II Hypertension

Electrophysiological Investigation of the Subcellular Fine Tuning of Sympathetic Neurons by Hydrogen Sulfide

Pharmacological evidence that metformin blocks the vasopressor responses mediated by stimulation of α 1 - and α 2 -adrenoceptors in pithed rats

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