Testosterone reduces vascular relaxation by altering cyclic adenosine monophosphate pathway and potassium channel activation in male Sprague Dawley rats fed a high-salt diet

Oloyo, Ahmed Kolade; Sofola, OA; Anigbogu, C.N.; Nair, R. V.; Vijayakumar, Harikrishnan S.; Fernandez, Adelaide C.

doi:10.1177/1753944713479996

Cited by 7 publications

(11 citation statements)

References 35 publications

(51 reference statements)

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“…The increase in blood pressure in rats fed a high salt diet in this study is consistent with our previous findings [8, 9, 24] and that of others [25]. In this study, myocardial oxygen demand (MOD) was calculated as the rate pressure product (RPP) from the product of the heart rate and the systolic blood pressure.…”

Section: Discussionsupporting

confidence: 92%

“…For instance, a high salt diet has been shown to increase the left ventricular mass, thicken and stiffen the aorta while thickening and narrowing the resistance arteries such as mesenteric, coronary and renal arteries [5, 6, 7]. We have previously shown that high salt diet thickens and narrows the mesenteric artery by promoting vascular smooth muscle cells hyperplasia and extracellular matrix proteins deposition [8] and that, high salt diet also impairs both endothelium - dependent and independent relaxation response to agonist [9, 10]. Other harmful effects of a high salt diet aside BP elevation include, cardiac and vascular hypertrophy as well as renal dysfunction which, may be independent of the arterial pressure [6].…”

Section: Introductionmentioning

confidence: 99%

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Sex differences in cardiac and renal responses to a high salt diet in Sprague-Dawley rats

Oloyo

Imaga

Fatope

et al. 2019

Heliyon

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High dietary salt intake is an important risk factor for cardiovascular and renal diseases. However, sexual disparity exists in the response of target organs to high salt diet (HSD). To determine how sex affects cardiac and renal functions’ response to HSD, 20 weanling Sprague-Dawley rats (10 males and 10 females) were divided into 4 groups of 5 rats each. The rats were fed a normal diet (0.3% NaCl) or HSD (8% NaCl) for 12 weeks. Fluid balance (FB) was determined from 24 hrs water intake and voided urine. Blood pressure (BP) was measured via arterial cannulation under anesthesia (25% w/v urethane and 1% w/v α-chloralose; 5 ml/kg, i.p). Serum levels of troponin I, aminotransaminases, creatinine, urea, uric acid and electrolytes as well as urinary concentration of albumin, creatinine, and electrolytes were measured using appropriate assay kits. Values are presented as mean ± S.E.M, compared by two-way ANOVA and Bonferroni post Hoc test. In the male rat, HSD significantly increased BP, serum: Troponin I, LDH and sodium (p < 0.05), urinary: albumin, sodium, potassium and FB (p < 0.05). In the female rat, HSD increased BP, serum: troponin I, LDH, sodium and creatinine clearance (p < 0.05), urinary: albumin, sodium and potassium (p < 0.01). However, HSD increased more, the BP, serum: Troponin I, LDH, urinary albumin and FB in male rats, while HSD increased urinary sodium more in female rats. Basal values in male vs. female of serum LDH and urinary albumin were significantly different. Thus, sex plays an important role in the response of the heart and kidney to salt stress.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Sex differences in cardiac and renal responses to a high salt diet in Sprague-Dawley rats

Oloyo

Imaga

Fatope

et al. 2019

Heliyon

Self Cite

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“…As a vital ion transport determining membrane potential ( Iwamoto, 2006b ), the Na(+)/Ca(2+) exchanger (NCX) type 1 was reported to increase vascular tone by mediating Ca 2+ entry in arterial smooth muscle cells in response to excess salt intake, which could partly explain the link between dietary salt to salt-dependent hypertension ( Iwamoto et al, 2005 ; Iwamoto, 2006a ). Besides, a HSD could inhibit potassium channels ( Oloyo et al, 2013 ). In addition, recent evidence showed that several transient receptor potential channels (TRP), including TRPV1 and TRPC3, are involved in high-salt intake–induced cardiac hypertrophy by mediating mitochondrial function via regulating mitochondrial calcium uptake ( Lang et al, 2015 ; Ma et al, 2019 ).…”

Section: Discussionmentioning

confidence: 99%

Nitric Oxide Alleviated High Salt–Induced Cardiomyocyte Apoptosis and Autophagy Independent of Blood Pressure in Rats

Mao

et al. 2021

Front. Cell Dev. Biol.

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The present study aimed to explore whether high-salt diet (HSD) could cause cardiac damage independent of blood pressure, and whether nitric oxide (NO) could alleviate high-salt–induced cardiomyocyte apoptosis and autophagy in rats. The rats received 8% HSD in vivo. H9C2 cells or primary neonatal rat cardiomyocytes (NRCM) were treated with sodium chloride (NaCl) in vitro. The levels of cleaved-caspase 3/caspase 3, cleaved-caspase 8/caspase 8, Bax/Bcl2, LC3 II/LC3 I, Beclin-1 and autophagy related 7 (ATG7) were increased in the heart of HSD rats with hypertension (HTN), and in hypertension-prone (HP) and hypertension-resistant (HR) rats. Middle and high doses (50 and 100 mM) of NaCl increased the level of cleaved-caspase 3/caspase 3, cleaved-caspase 8/caspase 8, Bax/Bcl2, LC3 II/LC3 I, Beclin-1, and ATG7 in H9C2 cells and NRCM. The endothelial NO synthase (eNOS) level was increased, but p-eNOS level was reduced in the heart of HSD rats and H9C2 cells treated with 100 mM NaCl. The level of NO was reduced in the serum and heart of HSD rats. NO donor sodium nitroprusside (SNP) reversed the increases of cleaved-caspase 3/caspase 3, cleaved-caspase 8/caspase 8, Bax/Bcl2 induced by NaCl (100 mM) in H9C2 cells and NRCM. SNP treatment attenuated the increases of cleaved-caspase 3/caspase 3, Bax/Bcl2, LC3 II/LC3 I, Beclin-1, and ATG7 in the heart, but had no effect on the blood pressure of HSD rats with HR. These results demonstrated that HSD enhanced cardiac damage independently of blood pressure. Exogenous NO supplementarity could alleviate the high salt–induced apoptosis and autophagy in cardiomyocytes.

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“…Groups 1 and II contained rats that were sham-operated, groups III and IV contained rats that were bilaterally orchidectomised while groups V and VI contained rats that were given Sustanon ® injection as testosterone replacement post orchidectomy. For orchidectomy, randomly selected rats were anaesthetized with intramuscular 90 mg and 10 mg/kg/body weight of ketamine and xylazine respectively [20], [21], [24], thereafter their 2scorotums were removed surgically under an aseptic condition. Sham-operated rats of groups I and II rats only had their scrotal sacs opened and sutured back as a model of sham orchidectomy [21]; [19].…”

Section: Methodsmentioning

confidence: 99%

High Salt Diet Blunted Baroreflex Sensitivity (BRS) to Bilateral Common Carotid Artery Occlusion (BCCO) in Male Sprague –Dawley Rats – Permissive Effect of Testosterone

Oloyo

Elias

Tom

et al. 2021

EJMED

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Autonomic dysfunction is involved in the onset of salt-sensitive hypertension as baroreflex sensitivity (BRS) is blunted in salt-sensitive hypertension. However, salt sensitivity exhibits sex disparity because in salt-sensitive hypertension, blood pressure (BP) is usually higher in males when compared with females. The mechanism(s) underlying this sexual dimorphism is not clear. We, therefore, designed this study to determine BRS in weanling male Sprague – Dawley rats that were either bilaterally orchidectomized or sham-operated (under ketamine and xylazine anaesthesia (90 mg and 10 mg/kg/body weight i.m) respectively, with or without testosterone replacement (10 mg/kg sustanon 250® i.m once in 3 weeks) and were placed on normal (0.3%) or high (8%) NaCl diet for 6 weeks. Blood pressure (BP) and heart rate (HR) were measured via arterial cannulation under urethane and α-chloralose anesthesia (5 ml/kg body weight i.p). BRS was determined as change in HR per unit change in BP in response to 30 seconds bilateral common carotid artery occlusion (BCCO). Serum concentration of testosterone was measured using enzyme-linked immunosorbent assay (ELISA). High salt diet (HSD) increased both the basal BP and peak BP after BCCO when compared with control. Orchidectomy attenuated but testosterone replacement restored the elevated BP in rats fed HSD. HSD blunted BRS to BCCO. However, this effect of HSD was lost in the absence of testosterone as there was no significant difference in BRS between rat fed a normal or high salt diet. Our results suggest that blunting of the BRS may be one of the mechanisms by which testosterone promotes salt-induced hypertension and serves as one of the bases for sex disparity in salt-sensitive hypertension.

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Testosterone reduces vascular relaxation by altering cyclic adenosine monophosphate pathway and potassium channel activation in male Sprague Dawley rats fed a high-salt diet

Abstract: Inhibition of potassium channel or adenylyl cyclase activation appears to contribute to the mechanisms by which a high-salt diet increases vascular tone. These effects were counteracted by orchidectomy in male Sprague Dawley rats.

Cited by 7 publications

References 35 publications

Sex differences in cardiac and renal responses to a high salt diet in Sprague-Dawley rats

Sex differences in cardiac and renal responses to a high salt diet in Sprague-Dawley rats

Nitric Oxide Alleviated High Salt–Induced Cardiomyocyte Apoptosis and Autophagy Independent of Blood Pressure in Rats

High Salt Diet Blunted Baroreflex Sensitivity (BRS) to Bilateral Common Carotid Artery Occlusion (BCCO) in Male Sprague –Dawley Rats – Permissive Effect of Testosterone

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