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BackgroundMethodsResultsConclusionsIn patients with diabetes mellitus (DM), vascular endothelial dysfunction (VED) is the main reason for impaired life expectancy. Melatonin (MEL) demonstrates wide-ranging effects across various organs and exhibits pleiotropic characteristics. The current study aims to investigate the modulatory roles of MEL vascular response to angiotensin II (Ang II) and its receptors including angiotensin type 1 receptor (AT-1 R) and angiotensin type 2 receptor (AT-2 R) in isolated thoracic aorta of non-diabetes (non-DM) and diabetes (DM) rats.The thoracic aortae were isolated in order to investigate the influence of MEL on AT-1 R, using valsartan (VAL) and MT-2Rusing luzindole (LUZ) via dose–response curve (DRC) measurement of Ang II reactivity. In addition, AT-1 R was involved in this study, under PD123319 with ADInstrument organ bath (Panlab apparatus, Harvard University, USA).The maximum response of Ang II was increased significantly in DM condition. In addition, AT-1 R was completely blocked under VAL, while AT-2 R was upregulated in the DM group. The combination of VAL and PD123319 led to abolishing the Ang II effect dramatically as well. Melatonin alone reduced Ang II in the DM group dramatically. This effect was also observed with MEL, PD1213319, and VAL combination, as well as, with MEL, LUZ, and PD1213319 combination.Melatonin has been demonstrated to modulate both AT-1 R and AT-2 R and has influenced the reactivity of Ang II in the aortas of diabetic rats through highly complex mechanisms. [ABSTRACT FROM AUTHOR]

Diabetes mellitus (DM) is considered as the main complication of the cardiovascular system leading to vascular endothelial dysfunction (VED). Besides, melatonin (MEL) has been known to improve the vascular tone directly or indirectly with MEL receptors (MT1R and MT2R) and antioxidant properties, respectively. The rings were extracted from three groups including non-diabetes (non-DM), streptozotocin induced diabetes (STZ-induced DM) and STZ-induced DM treated with MEL (DM+MEL) in male albino rats. The experimental procedure includes thoracic aortic vascular reactivity of angiotensin 1-7 (Ang 1-7) and histological examination. The vascular reactivity was conducted across eight distinct groups, encompassing RO-31-8220 (5 µM), protein kinase C (PKC) inhibitor, Apocyanin [(APO, 10 micromolar (µM)], the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor, rotenone (ROT 50 µM), mitochondrial complex I electron transport chain inhibitor, oxypurinol (OXY, 100 µM), xanthine oxidase inhibitor, PI-3065 (1 µM), phosphoinositide 3-kinases (PI3K) inhibitor, Ipatasertib (1 µM), protein kinase B (AKT) inhibitor, A779 (1 µM), the Mas receptor blocker and N(?)-nitro-L-arginine methyl ester (L-NAME 200 µM), the nitric oxide (NO) inhibitor pre-incubation. However, it is worth noting that the pre-incubation with OXY resulted in a notably significant rightward shift in this response. Conversely, in the STZ-induced DM group, there was a notable significant rightward shift observed in response to each of APO, ROT, and OXY. MEL appeared to regulate the vascular tone within Ang 1-7 modulation in STZ-induced DM rats. Therefore, MEL could offer many vascular benefits within Ang 1-7 under diabetic condition. [ABSTRACT FROM AUTHOR]

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Urotensin-II (UII), a pluripotent vasoactive cyclic peptide, exhibits the progression of cardiovascular diseases and the glucose metabolic disorder of insulin resistance. Type 2 Diabetes Mellitus (T2DM) is entirely associated with insulin resistance. This study aimed to demonstrate the association of UII with insulin resistance in diabetic and non-diabetic subjects. A total of 73 male and female subjects aged 40-60 years were recruited in this case-control study. They included 35 non- diabetic subjects with a body mass index of (BMI) ≤ 25 and 38 patients with Diabetes Mellitus and BMI ≥ 25. UII levels were assessed beside other vasoactive and clinical parameters. The results revealed that patients with T2DM had elevated UII and Endothelin-I (ET-I) levels, along with positive correlations with the insulin-resistance marker of Homeostatic Model Assessment for Insulin Resistance (HOMA-IR), blood pressure (BP), fasting blood glucose (FBG), hemoglobin A1c (HbA1C), and asymmetric dimethylarginine (ADMA). Results from stepwise multiple regressions indicated that UII correlated positively with the increases in the levels of serum cholesterol, ET-I, urea, ADMA, and FBG. This study concludes that the increase in UII level has a positive relation with insulin-resistance and the increase in ET-I level. However, UII could inhibit glucose-induced insulin secretion and, hence, can be utilized as a marker for T2DM and its complications through inflammatory microangiopathy. [ABSTRACT FROM AUTHOR]

Administration of L-arginine analogues, such as N-nitro-L-arginine methyl ester (L-NAME) is related with cardiovascular and renal functional alteration. The present experiment was planned to study the possible hemodynamic, renal and liver effects of cyclooxygenase (COX)-1(Aspirin) and COX-2 (Celecoxib) inhibitors in L-NAME induce hypertensive rats. The experimental rats were divided into four groups, each with six animals and the treatments were continued for 2 weeks as the following: Group 1: Control. The rats were given standard rat chow and tap water ad libitum. Group 2: L-NAME. The rats were given standard rat chow and L-NAME (20mg/kg body weight). Group 3: COX-1 inhibitor. The rats were supplied with standard rat chow with aspirin (1000 mg /kg diet) and L-NAME Group 4: COX-2 inhibitor . The rats were supplied with standard rat chow with celecoxib (1000 mg /kg diet) and L-NAME. Results showed that the systolic blood pressure (SBP) was elevated in control rats in comparison with L-NAME group. In the group of receiving COX-1 inhibitor, SBP significantly reduced, while COX-2 inhibitor reduced it but not significantly. Heart rate (H.R) was also changed after COX-2 inhibitor administration ,while COX-1 inhibitor did not change it significantly. COX-1 administration increased serum Na+ levels ,while serum K+ levels was significantly increased in COX-2 group rats compared with the L-NAME group. Supplementation of L-NAME for 15 days produced a significant increase in serum aspartate transaminase (AST) activity compared with the control group. Statistical analysis revealed that a significant reduction in alanine transaminase (ALT) activity was observed by COX-2 administration compared with the L-NAME. COX-2 inhibitor markedly elevated serum creatinine level compared with the L-NAME group. In conclusions, the results suggested that aspirin rather than celecoxib reduces SBP and in contrast to aspirin, celecoxib alter kidney functions through elevation of serum creatinine level, but it may attenuate liver functions through reduction of elevated serum ALT activity by L-NAME administration. [ABSTRACT FROM AUTHOR]