Effect of Hydrogen Sulfide on Sympathoinhibition in Obese Pithed Rats and Participation of K Channel.

Elevated blood pressure is the leading metabolic risk factor in attributable deaths, and hydrogen sulfide (HS) regulates vascular tone and blood pressure. Thus, this study aims to evaluate the mechanism by which NaHS (HS donor) produces inhibition of the vasopressor sympathetic outflow in obese rats. For that purpose, animals were fed a high-fat diet (HFD) (60% calories from fat) for 12 weeks.

Hydrogen sulfide ameliorates hypertension and vascular dysfunction induced by insulin resistance in rats by reducing oxidative stress and activating eNOS.

Hydrogen sulfide (HS) is a gasotransmitter implied in metabolic diseases, insulin resistance, obesity, and type 2 Diabetes Mellitus. This study aimed to determine the effect of chronic administration of sodium hydrosulfide (NaHS; inorganic HS donor), L-Cysteine (L-Cys; substrate of HS producing enzymes) and DL-Propargylglycine (DL-PAG; cystathionine-gamma-lyase inhibitor) on the vascular dysfunction induced by insulin resistance in rat thoracic aorta. For this purpose, 72 animals were divided into two main sets that received: 1) tap water (control group; n = 12); and 2) fructose 15% w/v in drinking water [insulin resistance group (IR); n = 60] for 20 weeks.

[Diet as a source of hydrogen sulfide and its effects on health and disease].

Initially known for its deleterious health effects, hydrogen sulfide (H2S) has recently been recognized as a biologically important gas carrier, like nitric oxide and carbon monoxide. H2S is produced endogenously in mammalian cells by enzymatic and non-enzymatic pathways. When it is produced by the enzymatic pathway, its synthesis is carried out from the amino acid L-cysteine through the transsulfuration pathway.

Chronic administration of NaHS and L-Cysteine restores cardiovascular changes induced by high-fat diet in rats.

Hydrogen sulfide plays an important role in the regulation of the cardiovascular system, insulin secretion, and glucose homeostasis. The aim of the present study was to examine the effects of chronic treatment with sodium hydrosulfide (NaHS), L-Cysteine (L-Cys) and DL-Propargylglycine (DL-PAG) on the changes induced by a high-fat diet (HFD) in zoometric and metabolic variables as well as cardiovascular changes such as hypertension and sympathetic hyperactivity. For this purpose, male Wistar rats were fed a normal fat diet (NFD) or HFD for 12 weeks.

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

It has been reported that metformin reduces blood pressure although the mechanisms have not been described. Indeed, several mechanisms could be implicated including the interaction with α-adrenoceptors or inhibition of sympathetic outflow. Therefore, this study was designed to determine the capability of metformin to block the vasopressor responses induced by α-adrenoceptor agonists or selective electrical stimulation of sympathetic outflow.