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.

The antihypertensive action of C-phycocyanin is related to the prevention of angiotensin II-caused vascular dysfunction in chronic kidney disease.

C-phycocyanin (CPC) is a photosynthetic protein found in Arthrospira maxima with a nephroprotective and antihypertensive activity that can prevent the development of hemodynamic alterations caused by chronic kidney disease (CKD). However, the complete nutraceutical activities are still unknown. This study aims to determine if the antihypertensive effect of CPC is associated with preventing the impairment of hemodynamic variables through delaying vascular dysfunction.

Sodium Hydrosulfide Reverts Chronic Stress-Induced Cardiovascular Alterations by Reducing Oxidative Stress.

Chronic stress induces a group of unrecognized cardiovascular impairments, including elevated hemodynamic variables and vascular dysfunction. Moreover, hydrogen sulfide (H 2 S), a gasotransmitter that regulates the cardiovascular system decreases under chronic stress. Thus, this study assessed the impact of sodium hydrosulfide (NaHS) (H 2 S donor) on chronic restraint stress (CRS)-induced cardiovascular changes.

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.

NaHS restores the vascular alterations in the renin-angiotensin system induced by hyperglycemia in rats.

Hyperglycemia (HG) impairs the renin-angiotensin system (RAS), which may contribute to vascular dysfunction. Besides, hydrogen sulfide (HS) exerts beneficial cardiovascular effects in metabolic diseases. Therefore, our study aimed to determine the effects of chronic administration of sodium hydrosulfide (NaHS; inorganic HS donor) and DL-Propargylglycine [DL-PAG; cystathionine-ץ-lyase (CSE) inhibitor] on the RAS-mediated vascular responses impairments observed in thoracic aortas from male diabetic Wistar rats.

Hydrogen sulfide as a neuromodulator of the vascular tone.

Hydrogen sulfide (HS) is a unique signaling molecule that, along with carbon monoxide and nitric oxide, belongs to the gasotransmitters family. HS is endogenously synthesized by enzymatic and non-enzymatic pathways. Three enzymatic pathways involving cystathionine-γ-lyase, cystathionine-β-synthetase, and 3-mercaptopyruvate sulfurtransferase are known as endogenous sources of HS.

Hydrogen sulfide prevents the vascular dysfunction induced by severe traumatic brain injury in rats by reducing reactive oxygen species and modulating eNOS and HS-synthesizing enzyme expression.

Aim: To assess the effects of subchronic administration with NaHS, an exogenous HS donor, on TBI-induced hypertension and vascular impairments.

Main Methods: Animals underweministration does not prevent the body weight loss but slightly imnt a lateral fluid percussion injury, and the hemodynamic variables were measured in vivo by plethysmograph method. The vascular function in vitro, the ROS levels by the DCFH-DA method and the expression of HS-synthesizing enzymes and eNOS by Western blot were measured in isolated thoracic aortas at day 7 post-TBI.

Targeting hydrogen sulfide and nitric oxide to repair cardiovascular injury after trauma.

The systemic cardiovascular effects of major trauma, especially neurotrauma, contribute to death and permanent disability in trauma patients and treatments are needed to improve outcomes. In some trauma patients, dysfunction of the autonomic nervous system produces a state of adrenergic overstimulation, causing either a sustained elevation in catecholamines (sympathetic storm) or oscillating bursts of paroxysmal sympathetic hyperactivity. Trauma can also activate innate immune responses that release cytokines and damage-associated molecular patterns into the circulation.

Effect of chronic administration of 17β-estradiol on the vasopressor responses induced by the sympathetic nervous system in insulin resistance rats.

Several studies have demonstrated that the underlying mechanism of insulin resistance (IR) is linked with developing diseases like diabetes mellitus, hypertension, metabolic syndrome, and polycystic ovary syndrome. In turn, the dysfunction of female gonadal hormones (especially 17β-estradiol) may be related to the development of IR complications since different studies have shown that 17β-estradiol has a cardioprotector and vasorelaxant effect. This study aimed was to determine the effect of the 17β-estradiol administration in insulin-resistant rats and its effects on cardiovascular responses in pithed rats.

TRPA1, but not TRPV1, is involved in the increase of the non-adrenergic non-cholinergic outflow induced by hydrogen sulfide in pithed rats.

Hydrogen sulfide (HS) is a gasotransmitter that modulates the peripheral transmission regulating the vascular tone. In vitro studies have suggested that HS induces vasodilation by stimulating capsaicin-sensitive sensory neurons. This study was designed to determine the effects of HS on the non-adrenergic/non-cholinergic (NANC) outflow in the pithed rat, and the underlying mechanisms.

Pharmacological evidence that potassium channels mediate hydrogen sulfide-induced inhibition of the vasopressor sympathetic outflow in pithed rats.

Hydrogen sulfide (HS) is a gasotransmitter that modulates neurotransmission. Indeed, it has been recently demonstrated that HS inhibits the sympathetic outflow in male rats, although the mechanisms remain elusive. Thus, this study evaluated the role of potassium channels on NaHS-induced sympathoinhibition.

Exogenous hydrogen sulfide restores CSE and CBS but no 3-MST protein expression in the hypothalamus and brainstem after severe traumatic brain injury.

Hydrogen sulfide (HS) is a gasotransmitter endogenously synthesized by cystathionine-γ-lyase (CSE), cystathionine-β-synthase (CBS), and 3-mercaptopiruvate sulfurtransferase (3-MST) enzymes. HS exogenous administration prevents the development of hemodynamic impairments after traumatic brain injury (TBI). Since the hypothalamus and the brainstem highly regulate the cardiovascular system, this study aimed to evaluate the effect of NaHS subchronic treatment on the changes of HS-sythesizing enzymes in those brain areas after TBI and in physiological conditions.

Sex-dependent antiallodynic effect of α adrenergic receptor agonist tizanidine in rats with experimental neuropathic pain.

The purpose of this study was to investigate the mechanism of antiallodynic effect of tizanidine in neuropathic rats. Spinal nerve ligation reduced withdrawal threshold which was interpreted as tactile allodynia. Increasing doses of tizanidine induced a dose-dependent antiallodynic effect in nerve injured rats.

Hydrogen Sulfide Subchronic Treatment Improves Hypertension Induced by Traumatic Brain Injury in Rats through Vasopressor Sympathetic Outflow Inhibition.

Traumatic brain injury (TBI) represents a critical public health problem around the world. To date, there are no accurate therapeutic approaches for the management of cardiovascular impairments induce by TBI. In this regard, hydrogen sulfide (HS), a novel gasotransmitter, has been proposed as a neuro- and cardioprotective molecule.

Fenofibrate Protects Cardiomyocytes from Hypoxia/Reperfusion- and High Glucose-Induced Detrimental Effects.

Lesions caused by high glucose (HG), hypoxia/reperfusion (H/R), and the coexistence of both conditions in cardiomyocytes are linked to an overproduction of reactive oxygen species (ROS), causing irreversible damage to macromolecules in the cardiomyocyte as well as its ultrastructure. Fenofibrate, a peroxisome proliferator-activated receptor alpha (PPAR) agonist, promotes beneficial activities counteracting cardiac injury. Therefore, the objective of this work was to determine the potential protective effect of fenofibrate in cardiomyocytes exposed to HG, H/R, and HG+H/R.

Activation of 5-HT and 5-HT receptors enhanced a positively reinforced long-term memory.

Memory is one of the most important capabilities of our mind since it determines our individuality. Memory formation involves different stages: acquisition, consolidation and retrieval. There are many studies about early stages, however little is known about memory retrieval.

Cardiovascular Responses to 5-hydroxytryptamine in Methimazole-induced Hypothyroid Pithed Rats.

Background: Patients suffering from hypothyroidism tend to develop diastolic hypertension. 5-Hydroxytryptamine (5-HT) is an amine that contributes to the maintenance of the blood pressure through central and peripheral 5-HT receptors. Curiously, the hypothyroidism alters the density of the 5-HT receptors in rodent brains.

Blocking properties of terguride at the 5-HT receptor subtypes mediating cardiovascular responses in the rat.

In vitro studies have suggested that terguride blocks the contractile and relaxant responses produced by 5-hydroxytryptamine (5-HT) via 5-HT receptors. This study has now investigated terguride's blocking properties on central/peripheral 5-HT receptors in anaesthetized or pithed rats. Male Wistar anaesthetized/pithed rats were cannulated for recording blood pressure and heart rate and for i.

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.

Therapeutic effect of treatment with metformin and/or 4-hydroxychalcone in male Wistar rats with nonalcoholic fatty liver disease.

Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease in the world. Despite the impact of this pathology in the population, nowadays there is no specific treatment for this disease, focusing its treatment on risks factors. However, it is imperative the existence of a specific treatment, due to this, the aim of this study was to determine the therapeutic effect of treatment with metformin, 4-hydroxychalcone or co-treatment on male Wistar rats with NAFLD.

Potential vascular α-adrenoceptor blocking properties of metformin in rat aorta and tail artery.

Metformin is a widely used drug for the treatment of type 2 Diabetes Mellitus. Several studies have also suggested that metformin decreases blood pressure; although an interaction with α-adrenoceptors has been proposed, this mechanism needs to be further investigated. Since α-adrenoceptors play a significant role to regulate vascular tone, this study has analysed the potential ability of metformin to block α-adrenoceptors in rat aorta and tail artery.

Fructose-Induced Insulin Resistance as a Model of Neuropathic Pain in Rats.

Peripheral neuropathy is one of the main complications of diabetes. The pathogenesis of this affectation is not completely understood. Several studies refer to hyperglycemia as the principal cause of diabetic neuropathy.

Histopathological and biochemical changes in the development of nonalcoholic fatty liver disease induced by high-sucrose diet at different times.

The high intake of sweetened drinks is associated with obesity and insulin resistance. These pathologies are directly related to the development of nonalcoholic fatty liver disease (NAFLD), considered a condition of metabolic syndrome (MS). Due to their increasing worldwide prevalence, experimental animal models have been developed to gain a better understanding of its physiopathology; notwithstanding, few studies have evaluated its progression in association with MS and ingestion of sweetened drinks.

NaHS prejunctionally inhibits the cardioaccelerator sympathetic outflow in pithed rats.

Hydrogen sulfide is a gasotransmitter that mediates cardiovascular responses and could protect the heart from ischemia-reperfusion damage. Furthermore, this gas mediates bradycardia although the mechanisms involved remain elusive. In this regard, the inhibition of the cardiac sympathetic outflow may be partially involved.