Gum acacia (GA) is used in pharmaceutical, cosmetic and food industries as an emulsifier and stabilizer, and in some countries in the traditional treatment of patients with chronic kidney disease (CKD). We have previously found that GA ameliorates adenine -induced chronic renal failure (CRF) in rats. Different brands of GA are commercially available, but their comparative efficacy against adenine-induced CKD is unknown. Here, we explored the effects of three different brands of GA (Sudanese GA, SupergumTM and GA from BDH) on some physiological, biochemical, and histological effects of adenine-induced CRF in rats. Adenine (0.75 %, w/w in feed, four weeks) reduced body weight, and increased urine output. It also induced significant increases in blood pressure, and in creatinine, urea, several inflammatory cytokines in plasma, and indices of oxidative stress, and caused histological damage in kidneys. Treatment of rats concomitantly with any of the three GA brands, significantly, and to a broadly similar extent, mitigated all the signs of CRF. The results suggested equivalent efficacy of these brands in antagonizing the CRF in this animal model. However, to enable standardization of different brands between laboratories, the use of the chemically well-characterized GA preparation (such as SupergumTM) is recommended., B. H. Ali, ... [et al.]., and Obsahuje seznam literatury
The endothelium contributes to the maintenance of vasodilator
tone by releasing endothelium-derived relaxing factors, including
nitric oxide (NO). In hypertension, endothelial nitric oxide
synthase (eNOS) produces less NO and could be one of the
contributing factors to the increased peripheral vascular
resistance. Agonist-induced Ca2+ entry is essential for the
activation of eNOS. The transient receptor potential vanilloid
type 4 (TRPV4) channel, a Ca2+-permeant cation channel, is
expressed in the endothelial cells and involved in the regulation
of vascular tone. The present study aimed to investigate the role
of TRPV4 channel in endothelium-dependent NO-mediated
relaxation of the resistance artery in hypertensive rats. Using
a wire myograph, relaxation response to the TRPV4 activator,
4α-phorbol-12,13-didecanoate (4αPDD) was assessed in
mesenteric arteries obtained from Wistar-Kyoto (WKY) and
spontaneously hypertensive rats (SHRs). Compared to WKY, SHR
demonstrated a significantly attenuated 4αPDD-induced
endothelium-dependent NO-mediated relaxation. Immunohistochemical analysis revealed positive staining for TRPV4 in the
endothelium of mesenteric artery sections in both WKY and SHR.
Furthermore, TRPV4 mRNA and protein expressions in SHR were
significantly lower than their expression levels in WKY rats.
We conclude that 4αPDD-induced endothelium-dependent
NO-mediated vasorelaxation is reduced in SHR and downergulation of TRPV4 could be one of the contributing mechanisms.
To investigate lisinopril effect on the contribution of nitric oxide (NO) and KCa channels to acetylcholine (ACh)-induced relaxation in isolated mesenteric arteries of spontaneously hypertensive rats (SHRs). Third branch mesenteric arteries isolated from lisinopril treated SHR rats (20 mg/kg/day for ten weeks, SHR-T) or untreated (SHR-UT) or normotensi ve WKY rats were mounted on tension myograph and ACh concentration-response curves were obtained. Westernblotting of eNOS and K Ca channels was performed. ACh-induced relaxations were similar in all groups while L-NMMA and indomethacin caused significant rightward shift only in SHR-T group. Apamin and TRAM-34 (SKCa and IKCa channels blockers, respectively) significantly attenuated ACh-induced maximal relaxation by similar magnitude in vessels from all three groups. In the presence of L-NMMA, indomethacin, apamin and TRAM-34 further attenuated ACh-induced relaxation only in SHR-T. Furthermore, lisinopril treatment increased expression of eNOS, SKCa and BKCa proteins. Lisinopril treatment increased expression of eNOS, SKCa , BKCa channel proteins and increased the contribution of NO to ACh-mediated relaxation. This increased role of NO was apparent only when EDHF component was blocked by inhibiting SKCa and IKCa channels. Such may suggest that in mesenteric arteries, non-EDHF component functions act as a reserve system to provide compensatory vasodilatation if (and when) hyperpolarization that is mediated by SKCa and IKCa channels is reduced, S. Albarwani, S. Al-Siyabi, I. Al-Husseini, A. Al-Ismail, I. Al-Lawati, I. Al-Bahrani, M. O. Tanira., and Obsahuje bibliografii