Blunted Blood Pressure Response and Elevated Plasma Adiponectin Levels in Female Sprague Dawley Rats

Kamari, Yehuda; Peleg, Edna; Leibowitz, Avshalom; Grossman, Ehud

doi:10.1038/ajh.2011.260

Cited by 14 publications

(8 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…There is little consensus in the literature regarding the impact of sex on BP responses to NOS inhibition. In contrast to our findings in SHR, male Sprague-Dawley and Wistar-Kyoto rats exhibited larger increases in BP to L-NAME and N -nitro-L-arginine (L-NNA) than females (19,30,35). However, these studies were all of longer duration (up to 24 wk) than the current study.…”

Section: L-name-induced Increases In Renal T Cells Were Dependent On contrasting

confidence: 99%

See 1 more Smart Citation

Female SHR have greater blood pressure sensitivity and renal T cell infiltration following chronic NOS inhibition than males

Brinson

Elmarakby

Tipton

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

Nitric oxide is a critical regulator of blood pressure (BP) and inflammation, and female spontaneously hypertensive rats (SHR) have higher renal nitric oxide bioavailability than males. We hypothesize that female SHR will have a greater rise in BP and renal T cell infiltration in response to nitric oxide synthase (NOS) inhibition than males. Both male and female SHR displayed a dose-dependent increase in BP to the nonspecific NOS inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME: 2, 5, and 7 mg·kg(-1)·day(-1) for 4 days each); however, females exhibited a greater increase in BP than males. Treatment of male and female SHR with 7 mg·kg(-1)·day(-1) L-NAME for 2 wk significantly increased BP in both sexes; however, prior exposure to L-NAME only increased BP sensitivity to chronic NOS inhibition in females. L-NAME-induced hypertension increased renal T cell infiltration and indices of renal injury in both sexes, yet female SHR exhibited greater increases in Th17 cells and greater decreases in regulatory T cells than males. Chronic L-NAME was also associated with larger increases in renal cortical adhesion molecule expression in female SHR. The use of triple therapy to block L-NAME-mediated increases in BP attenuated L-NAME-induced increases in renal T cell counts and normalized adhesion molecule expression in SHR, suggesting that L-NAME-induced increases in renal T cells were dependent on both increases in BP and NOS inhibition. Our data suggest that NOS is critical in the ability of SHR, females in particular, to maintain BP and limit a pro-inflammatory renal T cell profile.

show abstract

Section: L-name-induced Increases In Renal T Cells Were Dependent On contrasting

confidence: 99%

“…There are conflicting reports in the literature regarding the impact of sex on the response to chronic NOS inhibition. Normotensive female rats have been reported to be more sensitive (36), less sensitive (19,30,35), or equally sensitive (38) to NOS inhibition-induced hypertension compared with age-matched males.…”

mentioning

confidence: 99%

Female SHR have greater blood pressure sensitivity and renal T cell infiltration following chronic NOS inhibition than males

Brinson

Elmarakby

Tipton

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

show abstract

“…16,21,22 The lack of body weight gain in high-fructose diet-fed rats was not attributable to increases in activity as determined by telemetry. The development of features of the metabolic [25][26][27] and in the development of metabolic-like syndrome induced by a high-fructose diet.…”

Section: Discussionmentioning

confidence: 93%

Role of T Regulatory Lymphocytes in the Pathogenesis of High-Fructose Diet–Induced Metabolic Syndrome

et al. 2013

View full text Add to dashboard Cite

Abstract-We recently showed that T regulatory lymphocytes (Treg), which are immune suppressors of inflammatory responses, play a role blunting the development of hypertension-induced injury. Treg are unchanged or decreased in children with metabolic syndrome, and therefore, their role in metabolic syndrome remains unclear. We hypothesized that Treg number or function would be depressed in a high-fructose diet-induced metabolic syndrome-like model in rats. Sprague-Dawley rats were fed normal chow or a high-fructose diet for 5 weeks. The high-fructose diet-induced a 3.8-fold increase in plasma triglycerides and a 14% reduction in high-density lipoprotein cholesterol (P<0.001). The high-fructose diet increased reactive oxygen species in aorta and periaortic adipose tissue 2.8-fold (P<0.05), and reduced nicotinamide adenine dinucleotide phosphate oxidase activity 1.9-fold in aorta, and 2.5-fold in the heart (P<0.05). It also increased plasma nitric oxide metabolite levels 6.4-fold (P<0.001). Western blots showed that the high-fructose diet increased ≥2.3-fold vascular and in platelet endothelial cell adhesion molecule 1 in aorta (P<0.01). It did not affect monocyte/macrophage aortic infiltration but caused a 2.4-fold increase in collagen deposition in the aortic media (P<0. 01 FoxP3+ cells was observed in children with metabolic syndrome (2.5 versus 3.1%). 15To determine the role of Treg in the metabolic syndrome, vascular oxidative stress and inflammation and the number and function of Treg were studied in high-fructose diet-fed SpragueDawley rats, a well-established model mimicking some features of the western diet-induced metabolic syndrome. 16,17 These rats exhibit hypertension, insulin resistance, and abnormal lipid profile resembling the human metabolic syndrome better than a monogenic model. We hypothesized that vascular oxidative stress and inflammation and changes in the immune response, including Treg activity and response, participate in the mechanisms leading to the metabolic syndrome. Materials and MethodsAdditional materials and methods are described in the online-only Data Supplement. Experimental DesignEight-week-old Sprague-Dawley male rats (Harlan Laboratories, Indianapolis, IN) were fed a high-fructose diet (TD.89247, Harlan Laboratories) composed of 60% fructose, 21% protein, 5% fat, 8% cellulose, and standard vitamins and mineral mix or normal chow diet (control) for 5 weeks. Systolic BP (SBP) was measured by the tailcuff method after 4 weeks on the diet. SBP was also determined by telemetry together with heart rate and animal activity every 5 minutes for 10 seconds for 2 consecutive days at baseline and at the end of every week during the 5 weeks of treatment. Three days before the end of the protocol, blood was collected from the saphenous vein on heparin for triglycerides, and high-density lipoprotein cholesterol was determined after 5 hours of fasting. At the end of the protocol, body weight was evaluated, and rats were anesthetized with 3% isoflurane mixed with O 2 at 1 L/min (depth of ane...

show abstract

“…Moreover, testosterone treatment of fructose-fed female rats increased BP [17]. There is also information that a similar testosterone effect is seen in high-fat-fed rats [33].…”

Section: Controlmentioning

confidence: 83%

“…This effect is sex related and needs the presence of testosterone to become apparent [17]. Meanwhile, obesity is associated with an altered hormonal milieu that can affect the reproductive system, as shown by the association of increased body mass index (BMI) in men with low testosterone and sex hormone-binding globulin levels [18].…”

Section: Introductionmentioning

confidence: 99%

Melatonin and diet-induced metabolic syndrome in rats: impact on the hypophysial-testicular axis

Bernasconi¹,

Cardoso

Reynoso³

et al. 2013

Hormone Molecular Biology and Clinical Investigation

View full text Add to dashboard Cite

Combinations of fructose- and fat-rich diets in experimental animals can model the human metabolic syndrome (MS). In rats, the increase in blood pressure (BP) after diet manipulation is sex related and highly dependent on testosterone secretion. However, the extent of the impact of diet on rodent hypophysial-testicular axis remains undefined. In the present study, rats drinking a 10% fructose solution or fed a high-fat (35%) diet for 10 weeks had higher plasma levels of luteinizing hormone (LH) and lower plasma levels of testosterone, without significant changes in circulating follicle-stimulating hormone or the weight of most reproductive organs. Diet manipulation brought about a significant increase in body weight, systolic BP, area under the curve (AUC) of glycemia after an intraperitoneal glucose tolerance test (IPGTT), and plasma low-density lipoprotein cholesterol, cholesterol, triglycerides, and uric acid levels. The concomitant administration of melatonin (25 μg/mL of drinking water) normalized the abnormally high LH levels but did not affect the inhibited testosterone secretion found in fructose- or high-fat-fed rats. Rather, melatonin per se inhibited testosterone secretion. Melatonin significantly blunted the body weight and systolic BP increase, the increase in the AUC of glycemia after an IPGTT, and the changes in circulating lipid profile and uric acid found in both MS models. The results are compatible with a primary inhibition of testicular function in diet-induced MS in rats and with the partial effectiveness of melatonin to counteract the metabolic but not the testicular sequelae of rodent MS.

show abstract

Blunted Blood Pressure Response and Elevated Plasma Adiponectin Levels in Female Sprague Dawley Rats

Abstract: Elevated plasma adiponectin levels, perhaps due to lack of suppression by testosterone, are associated with a blunting of BP response in female compared to male SD rats.

Cited by 14 publications

References 43 publications

Female SHR have greater blood pressure sensitivity and renal T cell infiltration following chronic NOS inhibition than males

Female SHR have greater blood pressure sensitivity and renal T cell infiltration following chronic NOS inhibition than males

Role of T Regulatory Lymphocytes in the Pathogenesis of High-Fructose Diet–Induced Metabolic Syndrome

Melatonin and diet-induced metabolic syndrome in rats: impact on the hypophysial-testicular axis

Contact Info

Product

Resources

About