Sodium—Potassium Pump Activity in Mineralocorticoid- and Glucocorticoid-Induced Hypertension

1982 ◽  
Vol 63 (s8) ◽  
pp. 69s-72s ◽  
Author(s):  
G. Wambach ◽  
A. Helber ◽  
W. Kaufmann
Keyword(s):  
Blood Pressure ◽  
Atpase Activity ◽  
Systolic Blood Pressure ◽  
Heart Tissue ◽  
Control Group ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Induced Hypertension ◽  
Pump Activity ◽  
Kidney Liver

1. The activity of ouabain-sensitive Na+,K+-dependent ATPase and ouabain-sensitive ATPase was measured in the microsomal fractions of kidney, liver and heart tissue of Sprague-Dawley rats treated with DOCA (10 mg day−1 kg−1 for 6 days, systolic blood pressure 143 ± 13 mmHg, n = 9) or 6 α-methylprednisolone (100 mg day−1 kg−1 for 6 days, systolic blood pressure 140 ± 19 mmHg, n = 9) and of a control group (systolic blood pressure 124 ± 12 mmHg, n = 9). 2. In the kidney, the ouabain-sensitive Na+,K+-ATPase activity (μmol of phosphate h−1 mg−1 of protein) was increased in the DOCA-treated (33.0 ± 6.9) and in the prednisolone-treated groups (30.8 ± 6.9) compared with that in the control group (26.4 ± 3.4) (P < 0.05). In the liver, the ouabain-sensitive Na+,K+-ATPase activity was elevated in the prednisolone-treated animals only (4.8 ± 1.3 vs 3.1 ± 0.8 in the controls, P < 0.025). The ouabain-sensitive Na+,K+-ATPase activity in heart tissue was similar in all three groups. The ouabain-insensitive ATPase activity was not altered by DOCA or prednisolone in the tissues studied. 3. In a separate study, the activity of the ouabain-sensitive Na+,K+-ATPase in erythrocyte ghosts was found to be elevated in 10 patients with Cushing's syndrome (0.91 ± 0.35 μmol of phosphate h−1 mg−1 of protein) compared with five patients with primary aldosteronism and compared with 12 normotensive control subjects (0.38 ± 0.08) (P < 0.005). 4. These data demonstrate an increased Na-K pump activity in the kidney in mineralocorticoid-induced hypertension. Glucocorticoids in addition activate the Na-K pump in a variety of other tissues. This could partially explain the redistribution of volume from the intracellular to the extracellular space.

scholarly journals Increased superoxide levels in ganglia and sympathoexcitation are involved in sarafotoxin 6c-induced hypertension

2008 ◽  
Vol 295 (5) ◽  
pp. R1546-R1554 ◽  
Author(s):  
Melissa Li ◽  
Xiaoling Dai ◽  
Stephanie Watts ◽  
David Kreulen ◽  
Gregory Fink
Keyword(s):  
Blood Pressure ◽  
Sympathetic Innervation ◽  
Sympathetic Ganglia ◽  
Plasma Norepinephrine ◽  
Sprague Dawley ◽  
Surgical Ablation ◽  
Arterial Blood ◽  
Sprague Dawley Rats ◽  
Induced Hypertension ◽  
Hypertension Development

Endothelin (ET) type B receptors (ETBR) are expressed in multiple tissues and perform different functions depending on their location. ETBR mediate endothelium-dependent vasodilation, clearance of circulating ET, and diuretic effects; all of these should produce a fall in arterial blood pressure. However, we recently showed that chronic activation of ETBR in rats with the selective agonist sarafotoxin 6c (S6c) causes sustained hypertension. We have proposed that one mechanism of this effect is constriction of capacitance vessels. The current study was performed to determine whether S6c hypertension is caused by increased generation of reactive oxygen species (ROS) and/or activation of the sympathetic nervous system. The model used was continuous 5-day infusion of S6c into male Sprague-Dawley rats. No changes in superoxide anion levels in arteries and veins were found in hypertensive S6c-treated rats. However, superoxide levels were increased in sympathetic ganglia from S6c-treated rats. In addition, superoxide levels in ganglia increased progressively the longer the animals received S6c. Treatment with the antioxidant tempol impaired S6c-induced hypertension and decreased superoxide levels in ganglia. Acute ganglion blockade lowered blood pressure more in S6c-treated rats than in vehicle-treated rats. Although plasma norepinephrine levels were not increased in S6c hypertension, surgical ablation of the celiac ganglion plexus, which provides most of the sympathetic innervation to the splanchnic organs, significantly attenuated hypertension development. The results suggest that S6c-induced hypertension is partially mediated by sympathoexcitation to the splanchnic organs driven by increased oxidative stress in prevertebral sympathetic ganglia.

Proximal tubule microvilli remodeling and albuminuria in the Ren2 transgenic rat

2007 ◽  
Vol 292 (2) ◽  
pp. F861-F867 ◽  
Author(s):  
Melvin R. Hayden ◽  
Nazif A. Chowdhury ◽  
Shawna A. Cooper ◽  
Adam Whaley-Connell ◽  
Javad Habibi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Proximal Tubule ◽  
Structural Damage ◽  
Kidney Tissue ◽  
Proximal Tubule Cell ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

TG(mRen2)27 (Ren2) transgenic rats overexpress the mouse renin gene, with subsequent elevated tissue ANG II, hypertension, and nephropathy. The proximal tubule cell (PTC) is responsible for the reabsorption of 5–8 g of glomerular filtered albumin each day. Excess filtered albumin may contribute to PTC damage and tubulointerstitial disease. This investigation examined the role of ANG II-induced oxidative stress in PTC structural remodeling: whether such changes could be modified with in vivo treatment with ANG type 1 receptor (AT1R) blockade (valsartan) or SOD/catalase mimetic (tempol). Male Ren2 (6–7 wk old) and age-matched Sprague-Dawley rats were treated with valsartan (30 mg/kg), tempol (1 mmol/l), or placebo for 3 wk. Systolic blood pressure, albuminuria, N-acetyl-β-d-glucosaminidase, and kidney tissue malondialdehyde (MDA) were measured, and ×60,000 transmission electron microscopy images were used to assess PTC microvilli structure. There were significant differences in systolic blood pressure, albuminuria, lipid peroxidation (MDA and nitrotyrosine staining), and PTC structure in Ren2 vs. Sprague-Dawley rats (each P < 0.05). Increased mean diameter of PTC microvilli in the placebo-treated Ren2 rats ( P < 0.05) correlated strongly with albuminuria ( r2 = 0.83) and moderately with MDA ( r2 = 0.49), and there was an increase in the ratio of abnormal forms of microvilli in placebo-treated Ren2 rats compared with Sprague-Dawley control rats ( P < 0.05). AT1R blockade, but not tempol treatment, abrogated albuminuria and N-acetyl-β-d-glucosaminidase; both therapies corrected abnormalities in oxidative stress and PTC microvilli remodeling. These data indicate that PTC structural damage in the Ren2 rat is related to the oxidative stress response to ANG II and/or albuminuria.

scholarly journals NIFEDIPINEON;

2019 ◽  
Vol 26 (02) ◽  
Author(s):  
Sidra Hamid ◽  
Qaiser Aziz ◽  
Aneela Jamil ◽  
Lubna Meraj ◽  
Shazia Muazam ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Luteinizing Hormone ◽  
Serum Testosterone ◽  
Serum Testosterone Level ◽  
Control Group ◽  
Channel Blockers ◽  
Sprague Dawley ◽  
Study Objective ◽  
Serum Luteinizing Hormone ◽  
Sprague Dawley Rats

Background: The most potent and effective drugs used for the management of blood pressure in hypertensive patients are Calcium channel blockers (CCBs). Nifedipine, a CCB, acts by blocking entry of calcium ions all the way through the voltage gated calcium channels (VGCCs) of L-type present in the smooth muscle cells of blood vesselsand reducing the blood pressure by decreasing the peripheral vascular resistance. Objectives: The study objective was to determine the effect of nifedipine on serum luteinizing hormone (LH) and serum testosterone in male Sprague Dawley rats. Study Design: Animal experimental study. Setting: All experiments were conducted at the Research laboratory of Shifa College of Medicine, Islamabad along with National Institute of Health (NIH), Islamabad. Period: October, 2012 to April, 2014. Methods: The study was done on adult male Sprague-Dawley rats (N= 60) aged 90-120 days old and their body weights varied between 200 + 50 grams. Rats were divided intotwo groups (n=30). Group A was administered0.5 ml distilled water/rat daily orally, group B was administered orally with nifedipine 50 mg/kg/rat dissolved in 1ml of DMSO. All the doses were given to rats for 8 weeks. After 8 weeks, serum luteinizing hormone and serum testosterone were measured in both groups. Results: In Nifedipine treated group, serum testosterone was significantly decreasedand serum LH was unaffected as compared to the control group. Conclusion: Nifedipine has adverse effects on male fertility as it decreases serum testosterone level.

Obesity-Induced Hypertension Develops in Young Rats Independently of the Renin-Angiotensin-Aldosterone System

2006 ◽  
Vol 231 (3) ◽  
pp. 282-287 ◽  
Author(s):  
Anita D. Smith ◽  
Michael W. Brands ◽  
Mong-Heng Wang ◽  
Anne M. Dorrance
Keyword(s):  
Blood Pressure ◽  
Blood Glucose ◽  
Vascular Reactivity ◽  
Fasting Blood Glucose ◽  
Plasma Renin ◽  
Diet Group ◽  
Sprague Dawley ◽  
Diet Induced Obesity ◽  
Sprague Dawley Rats ◽  
Induced Hypertension

A correlation exists between obesity and hypertension. In the currently available models of diet-induced obesity, the treatment of rats with a high fat (HF) diet does not begin until adulthood. Our aim was to develop and characterize a model of pre-pubescent obesity-induced hypertension. Male Sprague-Dawley rats were fed a HF diet (35% fat) for 10 weeks, beginning at age 3 weeks. Blood pressure was measured by tail-cuff, and a terminal blood sample was obtained to measure fasting blood glucose, insulin, plasma renin, aldosterone, thiobarbitutic acid reactive substances (TBARS), and free 8-isoprostanes levels. The vascular reactivity in the aorta was assessed using a myograph. Blood pressure was increased in rats fed the HF diet (HF, 161 ± 2 mm Hg vs. control, 137 ± 2 mm Hg, P < 0.05). Blood glucose (HF, 155 ± 4 mg/dL vs. control, 123 ± 5 mg/dL, P < 0.05), insulin (HF, 232 ± 63 pM vs. control, 60 ± 11 pM, P < 0.05), TBARS (expressed as nM of malondialdehyde [MDA]/ml [HF, 1.8 ± 0.37 nM MDA/ml vs. control 1.05 ± 0.09 nM MDA/ml, P < 0.05]), and free 8-isoprostanes (HF, 229 ± 68 pg/ml vs. control, 112 ± 9 pg/ml, P < 0.05) levels were elevated in the HF diet group. Interestingly, plasma renin and aldosterone levels were not different between the groups. The maximum vasoconstriction to phenylephrine (10−4 M) was increased in the HF diet group (HF, 26.1 ± 1.5 mN vs. control 22.3 ± 1.2 mN, P < 0.05). In conclusion, pre-pubescent rats become hypertensive and have increased oxidative stress and enhanced vasoconstriction when fed a HF diet. Surprisingly, this occurs without the increase in renin or aldosterone levels seen in the adult models of diet-induced obesity.

Parathyroidectomy significantly decreases hypertension in spontaneously hypertensive and deoxycorticosterone plus saline treated rats

1982 ◽  
Vol 60 (2) ◽  
pp. 208-212 ◽  
Author(s):  
Alexis Gairard ◽  
Alain Berthelot ◽  
René Schleiffer ◽  
Fanny Pernot
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Systolic Blood Pressure ◽  
Normal Serum ◽  
Male Rats ◽  
Shr Rats ◽  
Sprague Dawley ◽  
Spontaneously Hypertensive ◽  
Sprague Dawley Rats ◽  
Normal Serum Calcium

In male Sprague–Dawley rats, hypertensive development was diminished for 10 weeks when parathyroidectomy (PTX) was performed 1 week before deoxycorticosterone plus saline (DOCA + NaCl) treatment. In young spontaneously hypertensive male rats (SHR, Okamoto strain) parathyroidectomy performed after weaning lessened hypertensive levels and lowered heart rate for 24 weeks. When mineralocorticoid or genetic hypertension was established, parathyroidectomy did not significantly change blood pressure levels. High dietary calcium in PTX–SHR rats reestablished normal serum calcium but not systolic blood pressure to the level of sham SHR. From our present and previously reported results, it appears that the parathyroid gland is necessary for the total development of hypertension in both models.

scholarly journals Comparation of Antihypertensive Effect of Goldenberry, Cucumber, and Combination Juice Against Systolic Blood Pressure on Rats Induced 8% NaCl

2019 ◽  
Vol 3 (1) ◽  
pp. 43
Author(s):  
Fiki Husna ◽  
Amilia Yuni Damayanti ◽  
Dianti Desita Sari
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Mean Difference ◽  
Group Method ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Before And After ◽  
Post Test ◽  
The Mean ◽  
Post Hoc

<p><em>This study was</em><em> a</em><em> </em><em>true e</em><em>xperimental study </em><em>using the </em><em>randomized controlled group method with a </em><em>pre</em><em>-</em><em>post test</em><em> design</em><em>. </em><em>The </em><em>Sprague-Dawley rats </em><em>were </em><em>divided into 4 groups (5</em><em> rats/</em><em>group</em><em>):</em><em> K (+) Captopril 0</em><em>,</em><em>45 mg/200 g BW, goldenberry juice 1</em><em>,</em><em>8 ml/200 g BW</em><em> (P1)</em><em>, cucumber juice 1</em><em>,</em><em>8 ml/200 g BW</em><em> (P2)</em><em>, and 1</em><em>,</em><em>8 ml/200 g BW (</em><em>P3, </em><em>combination juice 50%:50%). Systolic blood pressure measured by blood pressure analyzer with the tail-cuff method. The result of systolic blood pressure analyzed by Paired t-Test to determine the mean difference of systolic blood pressure before and after 8% NaCl induction. One Way ANOVA test followed by Post Hoc Duncan to determine the mean difference of systolic blood pressure between groups.</em><em> Goldenberry, cucumber, and combination juice have a significant effect of reducing systolic blood pressure in hypertension with p = 0</em><em>,</em><em>000 (&lt;0</em><em>,</em><em>05). Goldenberry juice was </em><em>the </em><em>most effectively on reducing systolic blood pressure in hypertension with 42.21%.</em><em></em></p>

Orchidectomy attenuates impaired endothelial effects of a high-salt diet in Sprague–Dawley rats

2011 ◽  
Vol 89 (4) ◽  
pp. 295-304 ◽  
Author(s):  
A.K. Oloyo ◽  
O.A. Sofola ◽  
C.N. Anigbogu
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
High Salt ◽  
Sprague Dawley ◽  
High Salt Diet ◽  
Salt Diet ◽  
Arterial Blood ◽  
Sprague Dawley Rats ◽  
Induced Hypertension

The effect of sex hormones on vascular reactivity is considered one of the underlying factors contributing to gender differences in cardiovascular functions and diseases. Experiments were designed to investigate the role of androgens in salt-induced hypertension by assessing the relaxation response of isolated aortic rings to acetylcholine and sodium nitroprusside in the presence or absence of l-nitroarginine methyl ester in Sprague–Dawley rats. The rats were either orchidectomized or sham-operated, with or without testosterone replacement, and were placed on a normal or high-salt diet for 6 weeks. The results indicate a significant increase (p < 0.001) in the mean arterial blood pressure of rats on the high-salt diet, when compared with control or orchidectomized rats. Orchidectomy elicited a reduction in mean arterial blood pressure (p < 0.01), while testosterone replacement normalized mean arterial blood pressure to values seen in intact rats on the high-salt diet. The high-salt diet reduced the relaxation response to acetylcholine both in the presence and absence of inhibition of endothelial nitric oxide synthase with l-nitroarginine methyl ester. Bilateral orchidectomy attenuated the impaired endothelial function induced by the high-salt diet in rats, but this was reversed by concomitant administration of testosterone, suggesting a role for androgens in enhancing long-term vascular smooth muscle tone and hence maintenance of high blood pressure in salt-induced hypertension.

scholarly journals Therapeutic Effect of Long-Term Epidural Block in Rats with Pregnancy Induced Hypertension

2018 ◽  
Vol 2018 ◽  
pp. 1-6 ◽  
Author(s):  
Nianjiao Han ◽  
Yang Li ◽  
Youjing Dong
Keyword(s):  
Blood Pressure ◽  
Therapeutic Effect ◽  
Normal Saline ◽  
Epidural Block ◽  
Control Group ◽  
Pregnancy Induced Hypertension ◽  
Serum Concentrations ◽  
Sprague Dawley ◽  
Induced Hypertension

Background. Pregnancy induced hypertension (PIH) causes a variety of systemic disorders that negatively affect the maternal placenta and fetal growth. Epidural sympathetic block elicits symptoms of decreased blood pressure. This study was designed to determine the therapeutic effect of long-term epidural block in rats with PIH. Methods. Forty healthy pregnant Sprague Dawley rats were randomized into four groups with each group consisting of 10 rats. On gestation day (GD) 14, rats in control group underwent a sham procedure; rats in RUPP group were operated on to obtain reduced uterine perfusion pressure (RUPP); rats in RUPP plus normal saline (NS) group were also subjected to the RUPP procedure and underwent epidural block with 25 μl normal saline twice daily until delivery; rats in RUPP plus epidural block (EB) group were treated as those in RUPP plus NS group except that an epidural block with 25 μl of 0.125% bupivacaine was administered two times per day until delivery. On GD 20, blood pressure was measured in all groups before delivery, and blood samples were collected in order to quantify the serum concentrations of vascular endothelial growth factor (VEGF) and soluble fms-like tyrosine kinase 1 (sFlt-1). Results. The mean arterial pressure (MAP) of rats in RUPP group (147.6±6.0 mmHg) was markedly increased when compared with control group (80.8±4.6 mmHg) (p<0.05). The MAP of rats in RUPP plus EB group (114.4±7.2 mmHg) was clearly decreased in contrast with RUPP group but was still higher than in control group (p<0.05). The variation of fetal weight in all groups followed a similar trend to that of MAP. However, there were no significant differences between control group and RUPP plus EB group with respect to placental weight (p=0.186). Variation in MAP was positively correlated with the expression of sFlt-1 in each group but was negatively correlated with VEGF. Conclusion. This study demonstrates that long-term epidural block decreases blood pressure in PIH rats and improves the serum concentrations of VEGF and sFlt-1. Taken together, long-term epidural block may have a potential role in PIH treatment.

Sexual dimorphism in angiotensin II-induced hypertension and vascular alterations

2005 ◽  
Vol 83 (5) ◽  
pp. 413-422 ◽  
Author(s):  
R Tatchum-Talom ◽  
K M Eyster ◽  
D S Martin
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Vascular Function ◽  
Vascular Dysfunction ◽  
Female Rats ◽  
Sprague Dawley ◽  
Arterial Blood ◽  
Male And Female Rats ◽  
Sprague Dawley Rats ◽  
Induced Hypertension

Sex differences in the degree of high blood pressure have been described in several forms of experimental animal models of hypertension. However, the influence of sex on angiotensin II-induced hypertension has not been studied. In the present study, we investigated and compared the effects of chronic angiotensin II treatment on blood pressure and vascular function in male and female rats. Chronic treatment with angiotensin II (0.7 mg/kg daily for 10 d) significantly raised arterial blood pressure in male but not female Sprague–Dawley rats; it upregulated the NAD(P)H oxidase gp67 phox subunit in the aorta of male but not female rats; and it exaggerated the vasoconstrictor responses to norepinephrine and serotonin in the mesenteric vascular bed (MVB) of male but not female rats. Vasodilator responses to acetylcholine (ACh) but not papaverine (PPV) or isoprenaline (ISO) were reduced in the MVB of angiotensin II-treated male but not female rats. ACh, but not PPV or ISO dilatory responses were potentiated in the MVB of angiotensin II-treated female rats. The present findings demonstrate that exogenous angiotensin II upregulates aortic NAD(P)H oxidase gp67 phox subunit, and induces hypertension and mesenteric vascular dysfunction only in male rats.Key words: gender, blood pressure, vascular endothelium, angiotensin II hypertension.

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