scholarly journals The effects of a 50-Hz magnetic field on the cardiovascular system in rats

2016 ◽  
Vol 57 (6) ◽  
pp. 627-636 ◽  
Author(s):  
Ling Zhou ◽  
Baoquan Wan ◽  
Xingfa Liu ◽  
Yemao Zhang ◽  
Jinsheng Lai ◽  
...  

Abstract A 50-Hz magnetic field (MF) is a potential health-risk factor. Its effects on the cardiovascular system have not been fully investigated. This study was conducted to explore the effects of long-term exposure to a 50-Hz MF on the cardiovascular system. In the study, an exposure system was constructed, and the distribution of the 50-Hz MF was determined. Sixty-four Sprague-Dawley (SD) rats were exposed to a 50-Hz MF at 100 μT for 24 weeks, 20 h per day, while another 64 rats were sham exposed. During the exposure, blood pressure was measured every 4 weeks. After 24 weeks, echocardiography, cardiac catheterization and electrocardiography were performed. Moreover, heart and body weight were recorded, and haematoxylin–eosin staining and real-time PCR were conducted. The results showed that compared with the sham group, exposure to a 50-Hz MF did not exert any effects on blood pressure, pulse rate, heart rate or cardiac rhythm. Furthermore, echocardiography and cardiac catheterization showed that there were no significant differences in the cardiac morphology or haemodynamics. In addition, histopathological examination showed that exposure to a 50-Hz MF had no effects on the structure of the heart. Finally, expression of the cardiac hypertrophy–related genes did not show any significant differences between the 50-Hz MF exposure group and the sham group. Taken together, in SD rats, exposure to a 50-Hz/100 μT MF for 24 weeks did not show any obvious effects on the cardiovascular system.

Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Daria Golosova ◽  
Adrian Zietara ◽  
Ruslan Bohovyk ◽  
Vladislav Levchenko ◽  
Alexander Staruschenko

The extensive use of opioid-based pain management strongly correlates with poor cardiovascular and cardiorenal outcomes. Our recent studies suggest that treatment with kappa opioid receptor (KOR) agonist BRL 52537 leads to the progression of chronic kidney disease (CKD) and aggravation of salt-sensitive hypertension. We hypothesize that stimulation of KORs leads to blood pressure elevation, albuminuria, and kidney damage in healthy Sprague-Dawley (SD) rats. To characterize the effect of the KOR agonist BRL 52537 on the development of blood pressure and kidney function in vivo , SD rats were treated with a daily i.v. bolus infusion of BRL 52537 or a corresponding vehicle. To test the contribution of KOR stimulation on calcium homeostasis in podocytes, BRL 52537 was used on freshly isolated glomeruli from SD rats. Single-channel analysis was applied to assess the effect of KORs stimulation on TRPC6 channel activity in the human immortalized podocytes. Chronic treatment with BRL 52537 leads to increased mean arterial pressure (88±1 vs 101±4 mmHg, vehicle vs treated, p<0.05), podocyte basal calcium (90±12 vs 216±16 a.u., vehicle vs treated, p<0.05), and GFB impairment in SD rats which is reflected by a transient increase in albumin excretion (Alb/cre ratio 0.35±0.1 vs 0.72±0.2, vehicle vs treated, p<0.05). Cumulative probability distribution analysis of the glomerular injury score revealed a rightward shift toward a high glomerular injury score in the group treated with BRL 52537 (p<0.05). Angiotensin II level was higher in a BRL-treated group (156±17 vs 232±59 pmol, vehicle vs treated, p=0.065); however, it did not reach a statistical difference. Acute application of BRL 52537 resulted in sustained calcium response (0.23±0.01 a.u., Fluo4/FuraRed, maximum calcium response) in freshly isolated glomeruli from SD rats. Furthermore, patch-clamp experiments in human immortalized podocytes (cell-attached configuration) revealed that BRL 52537 activated TRPC6 channels. Taken together, these data support the hypothesis that administration of opioids in SD rats leads to activation of the KOR/TRPC6 pathway, which in turn led to glomerular filtration barrier impairment, increased glomerular damage, and blood pressure elevation.


Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Kayla M Nist ◽  
Jesse Moreira ◽  
Richard D Wainford

AIM: We hypothesized paraventricular nucleus (PVN)-specific blood-brain barrier (BBB) dysfunction and neuroinflammation contribute to hypertension and sympathoexcitation that can be attenuated by an Angiotensin II Type 1 Receptor (AT 1 R)-dependent mechanism in the aging Sprague-Dawley (SD) rat. Methods: Naïve male SD rats aged 3-, 8- and 16-months-old (MO) (N=4-6/gp) were used in the following studies. Separate groups of 16 MO rats were administered losartan (21 days; s.c. 3 mg/kg/day) or hydrochlorothiazide (14 days; s.c. 4 mg/kg/day). Blood pressure (femoral cannulation) and plasma NE (ELISA) were assessed at end of study. In separate groups, BBB dysfunction was assessed via PVN FITC extravasation using intravascular co-infusion of FITC-Dextran (10 kDa) and rhodamine B isothiocyanate-Dextran (70 kDa). IHC/IF was performed in naive and losartan-treated rats for microglia (CD11b/c) and astrocytes (GFAP) in the PVN and subfornical organ (SFO). Results: Male SD rats develop HTN and sympathoexcitation with age. At 8 and 16 MO, rats exhibit PVN BBB dysfunction (increased FITC extravasation). However, only 16 MO rats exhibit significant PVN neuroinflammation (increased microglial activation and astrocyte reactivity). In the SFO, there is no evidence of age-dependent neuroinflammation. Losartan and HCTZ both significantly lower blood pressure to similar levels, however, only losartan significantly attenuates PVN BBB dysfunction and neuroinflammation. Conclusions: Within the PVN, a known neural control center, there are AT 1 R-dependent increases in PVN BBB disruption and neuroinflammation that we speculate contribute to hypertension in aging SD rats.


Hypertension ◽  
2020 ◽  
Vol 76 (Suppl_1) ◽  
Author(s):  
Fatima Ryalat ◽  
N Cruz-Diaz ◽  
W Graham ◽  
T Gwathmey-Williams ◽  
P E Gallagher ◽  
...  

Aldosterone plays a significant role in hypertension and target organ damage. Aldosterone antagonists are used in the management of heart failure. However, neither the influence of age nor sex on aldosterone pathophysiology is well understood. We investigated the changes in circulating aldosterone with age and its association with cardiovascular function, using male and female hypertensive renin transgenic (mRen2)27 rats and SD rats at 20 and 50 weeks of age. Both male (22 ± 3 vs. 12 ± 2 ng/dL, n = 9 - 12, p < 0.05) and female (59 ± 10 vs. 23 ± 8 ng/dL, n = 6 - 10, p < 0.05) hypertensive rats had higher serum aldosterone compared with SD rats at 20 weeks of age. At 50 weeks of age, the difference persisted in the hypertensive female rats (63 ± 8 vs. SD: 33 ± 7 ng/dL, n = 6 - 7, p < 0.05), but not in the males. SD male rats have higher systolic blood pressure (SBP) as they age, and consequently develop cardiac diastolic dysfunction associated with higher aldosterone at 50 weeks compared to 20 weeks (28 ± 3 vs. 12 ± 2 ng/dL, n = 7 - 9, p < 0.05). This aging effect on aldosterone was not significant in the other groups. We showed previously that SD males treated with polyphenol rich muscadine grape extract (MGE) have lower aldosterone, less aortic stiffness and better cardiac diastolic function (E/e’) than controls at the older age; the MGE effect was not seen in (mRen2)27 males. Sex differences in aldosterone were not significant in the SD rats at either time point. However, (mRen2)27 female rats had higher aldosterone than (mRen2)27 males at both 20 weeks (59 ± 10 vs. 22 ± 3 ng/dL, n = 10 - 12, p < 0.05) and 50 weeks (63 ± 8 vs. 31 ± 7 ng/dL, n = 6 - 7, p < 0.05), despite the lack of significant differences in SBP. (mRen2)27 female rats preserve cardiac function better than males throughout their life span, while males develop indices of heart failure. Our data suggest that lower aldosterone levels in hypertensive males compared with females do not protect against the higher lifetime burden of elevated SBP and also may reflect different mechanisms controlling circulating aldosterone between sexes. In addition, data suggest a potential therapeutic effect of MGE in the management of age-associated moderate hypertension.


2005 ◽  
Vol 98 (3) ◽  
pp. 772-779 ◽  
Author(s):  
Andrew D. Baines ◽  
Patrick Ho

Hypothetically either decreased nitric oxide (NO) or increased O2 could initiate 20-HETE-mediated vasoconstriction associated with hemoglobin-based blood substitutes (HBOC). To test this hypothesis, we infused Tm-Hb, an HBOC with low O2 affinity, into isoflurane-anesthetized Wistar (W) and Sprague-Dawley (SD) rats after exchanging 20% of their blood with Ringer lactate. For comparison we infused an equal amount of BSA or BSA with NG-nitro-l-arginine methyl ester (BSA+NAME). Tm-Hb increased blood pressure (BP) and renal vascular resistance (RVR) equally in W and SD rats. Renal blood flow (RBF; Doppler ultrasound) decreased. BSA decreased RVR and raised glomerular filtration rate. BSA+NAME raised BP, RVR, and GFR. HET0016, an inhibitor of 20-HETE production, blunted BP and RVR responses to Tm-Hb and BSA+NAME in SD but not W rats. Arterial O2 content with BSA was lower than with Tm-Hb but O2 delivery was 60% higher with BSA because of higher RBF. BSA raised Po2 (Oxylite) in cortex and medulla and reduced RVR. Tm-Hb decreased Po2 and increased RVR. Switching rats from breathing air to 100% O2 raised intrarenal Po2 two- to threefold and increased BP and RVR. HET0016 did not alter hyperoxic responses. In conclusion, 20-HETE contributes to vasoconstriction by Tm-Hb in SD but not in W rats, and increased 20-HETE activity results primarily from decreased NO.


1984 ◽  
Vol 247 (4) ◽  
pp. H556-H562
Author(s):  
C. H. Bennett ◽  
D. R. Richardson

The purpose of this study was to determine the effects of long-term consumption of tobacco smoke on arterial blood pressure regulation. Male Sprague-Dawley rats were administered tobacco smoke for 6-8 mo. Two groups of animals (A and B) received tobacco smoke containing different levels of nicotine (group A: high nicotine, 4 mg/cigarette; group B: low nicotine, 1 mg/cigarette), while a third group (C) served as a sham control by receiving only puffs of room air. Reflex adjustments in mean arterial blood pressure (MAP), heart rate (HR), lower body blood flow, and lower body vascular resistance were compared between the three groups. In the anesthetized control state, no significant difference existed for the cardiovascular parameters measured in the three groups. However, perturbating the cardiovascular system by reducing central blood volume via a 60 degrees head-up tilt elicited less of a fall in MAP in the two smoke groups compared with the sham group. Percent decreases in MAP follow: group A, 23%; group B, 22%; and group C, 48%. Increasing MAP with phenylephrine elicited a significantly greater (P less than 0.05) reduction in HR in groups A and B (smoke treated) compared with group C (sham treated). Finally, varying carotid sinus pressure elicited significantly greater (P less than 0.01) changes in MAP in the smoke-treated animals (A and B) compared with the sham group (C). It is concluded that chronic tobacco smoke administration to laboratory rats increases the sensitivity of the reflex control of the cardiovascular system.


2005 ◽  
Vol 23 (3) ◽  
pp. 311-317 ◽  
Author(s):  
Sherry O. Kasper ◽  
Christy S. Carter ◽  
Carlos M. Ferrario ◽  
Detlev Ganten ◽  
Leon F. Ferder ◽  
...  

Transgenic rats with targeted decreased glial expression of angiotensinogen (ASrAogen rats) did not show an increase in systolic pressure compared with Sprague-Dawley (SD) rats during aging (15–69 wk of age). ASrAogen animals had lower body weights throughout the study, similar to reports for animals with systemic knockout of angiotensinogen or treated long term with renin-angiotensin system (RAS) blockers. Further characterization of indexes of growth and metabolism in ASrAogen rats compared with (mRen2)27 and SD rats, which express elevated versus normal brain and tissue angiotensin II levels, respectively, revealed that serum leptin was 100–200% higher in SD and (mRen2)27 rats at 46 wk and 69 wk of age. Consistent with low serum leptin, ASrAogen rats had higher food intake (73%) compared with SD or (mRen2)27 rats. (mRen2)27 rats had higher resting insulin levels than ASrAogen rats at all ages. Insulin levels were constant during aging in ASrAogen rats, whereas an increase occurred in SD rats, leading to higher insulin levels at 46 and 69 wk of age compared with ASrAogen rats. IGF-1 was comparable among strains at all ages, but (mRen2)27 rats had longer and ASrAogen rats had shorter tail lengths versus SD rats at 15 wk of age. In conclusion, reduced expression of glial angiotensinogen blunts the age-dependent rise in insulin levels and weight gain, findings that mimic the effects of long-term systemic blockade of the RAS or systemic knockout of angiotensinogen. These data implicate glial angiotensinogen in the regulation of body metabolism as well as hormonal mechanisms regulating blood pressure.


2001 ◽  
Vol 281 (2) ◽  
pp. R635-R644 ◽  
Author(s):  
Azeez A. Aileru ◽  
Aline De Albuquerque ◽  
John M. Hamlyn ◽  
Paolo Manunta ◽  
Jui R. Shah ◽  
...  

Altered sympathetic nervous system activity has been implicated often in hypertension. We examined short-term potentiation [posttetanic potentiation (PTP)] and long-term potentiation (LTP) in the isolated superior cervical ganglia (SCG) from Sprague-Dawley (SD) rats given vehicle, digoxin, or ouabain by subcutaneous implants as well as in animals with ouabain-induced hypertension (OHR), and inbred Baltimore ouabain-resistant (BOR) and Baltimore ouabain-sensitive (BOS) strains of rats. Postganglionic compound action potentials (CAP) were used to determine PTP and LTP following a tetanic stimulus (20 Hz, 20 s). Baseline CAP magnitude was greater in ganglia from OHR than in vehicle-treated SD rats before tetanus, but the decay time constant of PTP was significantly decreased in OHR and in rats infused with digoxin that were normotensive. In hypertensive BOS and OHR, the time constants for the decay of both PTP and LTP ( t L) were increased and correlated with blood pressure (slope = 0.15 min/mmHg, r = 0.52, P < 0.047 and 6.7 min/mmHg, r = 0.906, P < 0.0001, respectively). In BOS and OHR, t L (minutes) was 492 ± 40 ( n = 7) and 539 ± 41 ( n = 5), respectively, and differed ( P < 0.05) from BOR (257 ± 48, n = 4), SD vehicle rats (240 ± 18, n = 4), and captopril-treated OHR (370 ± 52, n = 5). After the tetanus, the CAP at 90 min in BOS and OHR SCG declined less rapidly vs. SD vehicle rats or BOR. Captopril normalized blood pressure and t L in OHR. We conclude that the duration of ganglionic LTP and blood pressure are tightly linked in ouabain-dependent hypertension. Our results favor the possibility that enhanced duration of LTP in sympathetic neurons contributes to the increase in sympathetic nerve activity in ouabain-dependent hypertension and suggest that a captopril-sensitive step mediates the link of ouabain with LTP.


2004 ◽  
Vol 91 (6) ◽  
pp. 857-865 ◽  
Author(s):  
Sophie Robin ◽  
Véronique Maupoil ◽  
Pascal Laurant ◽  
Alain Jacqueson ◽  
Alain Berthelot

The objectives of the present study were to evaluate the effects of a methionine-supplemented diet on systolic blood pressure (BP) and vasomotor functions in Sprague–Dawley (SD) and deoxycorticosterone acetate (DOCA)–salt hypertensive rats. SD and DOCA rats were fed a normal or a methionine (8 g/kg)-supplemented diet for 10 weeks. Systolic BP was monitored and plasma homocysteine, methionine and cysteine levels were determined at the end of the experiment. Vasoconstriction and vasodilatation of aortic rings were measured. The methionine-supplemented diet induced a greater increase in homocysteinaemia concentration in DOCA rats than in SD rats and an increase in plasma cysteine concentration in DOCA rats. This diet was associated with an increase in systolic BP in SD rats and with a lesser development of DOCA–salt hypertension. An enhanced aortic constriction and a decreased responsiveness to acetylcholine, bradykinin and sodium nitroprusside in the SD rats fed the methionine-rich diet were consistent with the elevated systolic BP. In DOCA rats the increased responsiveness to bradykinin was in accordance with the systolic BP-lowering effect. In conclusion, the methionine-enriched diet cannot simply be considered as model of hyperhomocysteinaemia, since other metabolites and mechanisms seemed to be implicated in these complex interactions. The differential vasopressive effect of the methionine supplementation in SD and DOCA rats, and in particular the lowering of systolic BP obtained with a greater degree of hyperhomocysteinaemia in DOCA rats, suggest that more complex interactions exist between hyperhomocysteinaemia and BP than the simple positive association described previously.


1999 ◽  
Vol 276 (6) ◽  
pp. H1918-H1926 ◽  
Author(s):  
Piotr Paczwa ◽  
Ewa Szczepańska-Sadowska ◽  
Slawomir Łoń, Ursula Ganten ◽  
Detlev Ganten

In acute experiments, intracranially applied angiotensin II and vasopressin elicit significant cardiovascular effects. The purpose of the present study was to find out whether chronic intrabrain elevation of these peptides, occurring in the renin transgenic TGR(mRen2)27 (TGR) rats, results in an alteration of the cardiovascular control. Mean arterial blood pressure (MAP) and heart rate responses to hypovolemia were examined in hypertensive TGR and normotensive Sprague-Dawley (SD) rats under control conditions and during blockade of central AT1 or V1 receptors. Both groups received cerebroventricular infusions of either 1) cerebrospinal fluid ( series 1), 2) AT1 receptors antagonist (AT1ANT, series 2), or 3) V1 receptors antagonist (V1ANT, series 3). Blockade of AT1 and V1 receptors decreased MAP in TGR but not in SD rats. In SD rats, bleeding elicited a similar decrease of MAP in each series and a transient increase of heart rate in series 3. In TGR, hemorrhage caused bradycardia and decrease of MAP, which was greater than in SD rats. Hemorrhagic hypotension in TGR was abolished by V1ANT and bradycardia by V1ANT or AT1ANT. The results demonstrate remarkable differences in cardiovascular adjustment to hemorrhage in SD and TGR rats and provide evidence for enhanced involvement of central V1 and AT1 receptors in the regulation of blood pressure during hypovolemia in TGR. Central V1 vasopressin receptors play a crucial role in eliciting posthemorrhagic hypotension and bradycardia in this strain.


2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Yanqing Chen ◽  
Liyan Miao ◽  
Yusheng Yao ◽  
Weilan Wu ◽  
Xiaodan Wu ◽  
...  

The aim was to verify that dexmedetomidine (DEX) can attenuate CLP-induced intestinal injury via inhibition of inflammation. Male Sprague-Dawley (SD) rats were randomly allocated into Sham group and the other three CLP model groups, in terms of different treatments: placebo, DEX, and yohimbine plus DEX (DEX + YOH) groups. Pathology examination was conducted with HE stain. To identify differences among groups, the levels of DAO, and D-lactate in serum were measured by spectrophotometry, and the levels of TNF-α, IL-1β, and IL-6 in serum and organ were measured by ELISA. The expressions of occludin and TLR4 in tissue were detected by Western blot. The survival rate of an additional group of animals within 7 d was recorded. In DEX group, mortality was lower, histology change was minor, DAO, and D-lactate levels were reduced, and occludin expression was increased; the expressions of TNF-α, IL-1β, IL-6, and TLR4 were also decreased in DEX group. These results indicated that acute intestinal injury induced by CLP was mitigated by DEX treatment. However, these effects of DEX were significantly attenuated by yohimbine in DEX + YOH group. Our study indicated the protective effects of DEX on CLP-induced injury, which may be associated with the inhibition of inflammation via modulating TLR4 pathway and can be blocked by yohimbine.


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