Portal Venous Flow Is Increased by Jejunal but Not Colonic Hydrogen Sulfide in a Nitric Oxide-Dependent Fashion in Rats
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ORIGINAL ARTICLE
Portal Venous Flow Is Increased by Jejunal but Not Colonic Hydrogen Sulfide in a Nitric Oxide‑Dependent Fashion in Rats Aleksandr Birg1 · Henry C. Lin1,2 · Nancy Kanagy3 Received: 8 June 2020 / Accepted: 29 August 2020 © Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Hydrogen sulfide ( H2S) is a recently discerned endogenous signaling molecule that modulates the vascular system. Endogenous hydrogen sulfide has been shown to dilate both the mesenteric and portal vasculature. Gut microbiome, via sulfur reducing bacteria, is another source of H2S production within the gut lumen; this source of H2S is primarily produced and detoxified in the colon under physiologic conditions. Nitric oxide (NO), a major endogenous vasodilator in the portal circulation, participates in H 2S-induced vasodilation in some vascular beds. We hypothesize that jejunal but not colonic H 2S increases portal vein flow in a NO-dependent fashion. To evaluate the effects of luminal H 2S, venous blood flow, portal venous pressure, and systemic venous pressure were measured in rats after administration of either vehicle or an H2S donor (NaHS) into the jejunum or the colon. We found that portal venous pressure and systemic pressure did not change and were similar between the three study groups. However, portal venous blood flow significantly increased following jejunal administration of NaHS but not in response to colonic NaHS or vehicle administration. To test the contribution of NO production to this response, another group of animals was treated with either an NO synthase inhibitor (N-Ω-nitro-l-arginine, L-NNA) or saline prior to jejunal NaHS infusion. After L-NNA pretreatment, NaHS caused a significant fall rather than increase in portal venous flow compared to saline pretreatment. These data demonstrate that H 2S within the small intestine significantly increases portal venous blood flow in a NO-dependent fashion. Keywords Hydrogen sulfide · Microbiome · Portal venous blood flow · Nitric oxide · Portal hypertension
Introduction H2S is a recently described gaseous signaling molecule that plays an important role in the physiology of many organs including those of the cardiovascular system where it has a significant impact on health and disease [1]. Endogenously produced H2S has been shown to regulate both mesenteric [2] and portal [3] hemodynamics. Conflicting reports have shown H2S causing either vasodilation [2] or vasoconstriction [4] of the mesenteric vasculature. Other studies also * Aleksandr Birg [email protected] 1
Division of Gastroenterology and Hepatology, Department of Internal Medicine, MSC10-5550, 1 University of New Mexico, Albuquerque, NM 87131, USA
2
New Mexico VA Health Care System, Albuquerque, NM 87108, USA
3
Department of Cell Biology and Physiology, University of New Mexico, Albuquerque, NM 87131, USA
showed that H2S can either increase [4] or decrease [5] systemic blood pressure in subjects with liver disease. Thus, the mechanism of action of H
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