Effects of hydrogen sulphide donor, sodium hydrosulphide treatment on the erectile dysfunction in L‐NAME‐induced hypertensive rats

Abstract

Men with hypertension often develop erectile dysfunction (ED). The present study aimed to examine the effects of sodium hydrosulphide (NaHS), a hydrogen (H2S) donor, treatment on ED in nitric oxide synthase (NOS) inhibitor (L‐NAME)‐induced hypertensive rats. Forty adult Sprague‐Dawley rats were divided into four groups: control, NaHS (0.037 mg kg day−1)‐treated control, L‐NAME‐induced hypertension (40 mg kg day−1) and NaHS‐treated L‐NAME‐induced hypertension. The ratio of intracavernosal pressure to mean arterial pressure and isometric tension of corpus cavernosum (CC) were measured. The penile expression of endothelial and neuronal NOS (eNOS and nNOS), inflammation markers [nuclear factor kappa B (NF‐κB) and inhibitor kappa B alpha (IκBα)], H2S‐producing enzymes[cystathionine β‐synthase (CBS) and cystathionine γ‐lyase (CSE)], the smooth muscle/collagen ratio and H2S concentrations were determined. The blood pressure was significantly increased in the hypertensive group, but not reversed by NaHS. The erectile response in hypertensive rats was partially prevented by NaHS. The relaxation response to electrical field stimulation was increased in CC from NaHS‐treated hypertensive rats. NaHS treatment restored decreased protein expression of eNOS, nNOS and CSE as well as smooth muscle/collagen ratio and H2S levels and increased NF‐κB and IκBα protein expression in the penile tissue of hypertensive rats. NaHS promoted the recovery of erectile responses in hypertensive rats by improvement of neuronal function and downregulation of fibrosis and NF‐κB signalling.

Hepatic and cardiac implications of increased toxic amyloid-beta serum level in lipopolysaccharide-induced neuroinflammation in rats: new insights into alleviating therapeutic interventions

“…Hydrogen sulfide (H 2 S) is a type of novel gaseous endogenous signaling molecule mainly synthesized from L-cysteine by the action of both cystathionine γ-lyase (CSE) and cystathionine β-synthase (CBS) mammalian enzymes tissue types (Yilmaz et al 2019 ; Jeddi et al 2020 ; Anwar et al 2019a , b ). H 2 S was found to exert potent effects on different types of cells and organs such as smooth muscle cells, endothelial cells, inflammatory cells, brain, heart, liver, and kidney.…”

Comparison of critical biomarkers in 2 erectile dysfunction models based on GEO and NOS-cGMP-PDE5 pathway

“…[ 6 ] Vascular and psychological ED animal models were also established according to different etiology. [ 7 , 8 ] Many bioinformatics technologies have been used to compare the above ED models from the point of genetics, [ 9 – 11 ] such as differentially expressed genes (DEGs) analysis between CNIED and DMED rat models. [ 11 ] By utilizing Gene Expression Omnibus (GEO), we further compared the enriched functions and pathways with Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and the protein-protein interaction (PPI) networks based on down-regulated and up-regulated DEGs respectively in DMED and CNIED.…”

“…The commonly used method to create CNIED model is to squeeze, freeze, or cut off unilateral or bilateral cavernous nerves [6] . Vascular and psychological ED animal models were also established according to different etiology [7,8] . Many bioinformatics technologies have been used to compare the above ED models from the point of genetics, [9–11] such as differentially expressed genes (DEGs) analysis between CNIED and DMED rat models [11] .…”

Preclinical Evaluation of the Antihypertensive Effect of an Aqueous Extract of Anogeissus leiocarpa (DC) Guill et Perr. Bark of Trunk in L-NAME-Induced Hypertensive Rat

“…2–5 Taken the specific case of the vascular system, endothelial dysfunction and hyperactive adrenergic-mediated vasoconstriction were known to contribute to peripheral vascular resistance increases, which results in blood pressure elevation. 6 , 7 …”

“…[2][3][4][5] Taken the specific case of the vascular system, endothelial dysfunction and hyperactive adrenergic-mediated vasoconstriction were known to contribute to peripheral vascular resistance increases, which results in blood pressure elevation. 6,7 Moreover, vascular oxidative stress has been associated with impaired endothelial-dependent vasorelaxation and enhanced agonist-induced vasoconstriction in oxidative stress-related hypertension. 8 Therefore, improving vasorelaxation and inhibiting oxidative stress are valuable strategies to combat hypertension.…”