High NaCl intake of rat dams alters maternal behavior and elevates blood pressure of adult offspring

1993 ◽  
Vol 264 (2) ◽  
pp. R296-R304 ◽  
Author(s):  
R. J. Contreras
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Blood Pressure Level ◽  
Adult Offspring ◽  
Sprague Dawley ◽  
Sweetened Condensed Milk ◽  
Sprague Dawley Rats ◽  
Dietary Obesity ◽  
Solution Intake ◽  
Pelleted Food

The present study investigated whether differences in maternal NaCl intake altered 1) maternal-pup behavior and 2) the development of dietary obesity and blood pressure level of adult Sprague-Dawley rats maintained on a palatable high-fat/milk (HF/M) diet. Thirteen dams fed high (3%) NaCl and 12 dams fed basal (0.12%) NaCl were observed on postnatal days 2-21 for differences in the number of times spent 1) nursing, 2) in contact with or licking, sniffing, and carrying pups, and 3) in nest building. The offspring were continued on their respective NaCl diets to 30 days postpartum, and then both NaCl groups were fed an intermediate (1%) NaCl diet thereafter. Beginning at 60 days of age, the offspring from each maternal NaCl condition were fed either Agway R-M-H 1000 pelleted food or a HF/M diet for 14 wk. Dams fed 3% NaCl spent significantly more time licking their pups than did dams fed 0.12% NaCl. The adult offspring of dams fed 3% NaCl had a significantly higher level of systolic blood pressure and consumed more calories of sweetened condensed milk on the HF/M diet than did rats raised on 0.12% NaCl. Dietary-induced obesity did not magnify the increase in systolic blood pressure from high maternal NaCl intake. The present results raise the possibility that increased maternal licking may contribute to the increased blood pressure and solution intake that follows from high maternal NaCl intake.

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.

Dietary obesity and weight cycling in rats: a model of stress-induced hypertension?

1991 ◽  
Vol 261 (4) ◽  
pp. R848-R857 ◽  
Author(s):  
R. J. Contreras ◽  
S. King ◽  
L. Rives ◽  
A. Williams ◽  
T. Wattleton
Keyword(s):  
Heart Rate ◽  
Sodium Excretion ◽  
Mild Hypertension ◽  
Weight Cycling ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Sweetened Condensed Milk ◽  
Condensed Milk ◽  
Sprague Dawley Rats ◽  
Dietary Obesity

The present study was designed to reproduce the mild hypertension seen in dietary obese weight-cycled rats [P. Ernsberger and D. O. Nelson. Am. J. Physiol. 254 (Regulatory Integrative Comp. Physiol. 23): R47-R55, 1988] and determine whether this mild hypertension was associated with changes in sodium excretion and pressor responsiveness to angiotensin II (ANG II). Male Sprague-Dawley rats were fed pelleted chow (Pellet group) or chow plus sweetened condensed milk (Milk group) or were exposed to four cycles of a 4-day fast alternated with 2 wk of refeeding of pelleted chow and sweetened condensed milk (Cycled group). Blood pressure and heart rate were measured by tail cuff at the onset and last day of each fast and after 3 days of refeeding. During fasting, urine sodium excretion was measured. Mean arterial pressure and heart rate responses to intravenous administration of ANG II (40, 80, and 120 ng/kg), metoprolol (1 mg/kg), and methyl scopolamine (2 mg/kg) were obtained from the femoral artery in awake unrestrained rats. Weight cycling did not lead to mild hypertension or increased bradycardic response to sympathetic blockade with metoprolol. ANG II-elicited pressor responses were similar for Pellet, Milk, and Cycled groups. Sodium excretion did not change with fasting. Mild hypertension developed when obese weight-cycled rats were housed together in groups and not when housed individually. Our preliminary data are consistent with the notion that stress associated with group housing may be a factor in the mild hypertension of obese weight-cycled rats.

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>

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.

Abstract 114: K+ Rich Diet During Angiotensin II Hypertension Reduces Renal Na-Cl Cotransporter and Phosphorylation, but Not Blood Pressure

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Luciana C Veiras ◽  
Jiyang Han ◽  
Donna L Ralph ◽  
Alicia A McDonough
Keyword(s):  
Blood Pressure ◽  
Urine Volume ◽  
Weight Ratio ◽  
Distal Tubule ◽  
Reduce Blood Pressure ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
K Secretion ◽  
Pressure Natriuresis

During Ang II hypertension distal tubule Na-Cl Cotransporter (NCC) abundance and its activating phosphorylation (NCCp), as well as Epithelial Na+ channels (ENaC) abundance and activating cleavage are increased 1.5-3 fold. Fasting plasma [K+] is significantly lower in Ang II hypertension (3.3 ± 0.1 mM) versus controls (4.0 ± 0.1 mM), likely secondary to ENaC stimulation driving K+ secretion. The aim of this study was to test the hypothesis that doubling dietary K+ intake during Ang II infusion will lower NCC and NCCp abundance to increase Na+ delivery to ENaC to drive K+ excretion and reduce blood pressure. Methods: Male Sprague Dawley rats (225-250 g; n= 7-9/group) were treated over 2 weeks: 1) Control 1% K diet fed (C1K); 2) Ang II infused (400 ng/kg/min) 1% K diet fed (A1K); or 3) Ang II infused 2% K diet fed (A2K). Blood pressure (BP) was determined by tail cuff, electrolytes by flame photometry and transporters’ abundance by immunoblot of cortical homogenates. Results: As previously reported, Ang II infusion increased systolic BP (from 132 ± 5 to 197 ± 4 mmHg), urine volume (UV, 2.4 fold), urine Na+ (UNaV, 1.3 fold), heart /body weight ratio (1.23 fold) and clearance of endogenous Li+ (CLi, measures fluid volume leaving the proximal tubule, from 0.26 ± 0.02 to 0.51 ± 0.01 ml/min/kg) all evidence for pressure natriuresis. A2K rats exhibited normal plasma [K+] (4.6 ± 0.1 mM, unfasted), doubled urine K+ (UKV, from 0.20 to 0.44 mmol/hr), and increased CLi (to 0.8 ± 0.1 ml/min/kg) but UV, UNaV, cardiac hypertrophy and BP were unchanged versus the A1K group. As expected, NCC, NCCpS71 and NCCpT53 abundance increased in the A1K group to 1.5 ± 0.1, 2.9 ± 0.5 and 2.8 ± 0.4 fold versus C1K, respectively. As predicted by our hypothesis, when dietary K+ was doubled (A2K), Ang II infusion did not activate NCC, NCCpS71 nor NCCpT53 (0.91 ± 0.04, 1.3 ± 0.1 and 1.6 ± 0.2 fold versus C1K, respectively). ENaC subunit abundance and cleavage increased 1.5 to 3 fold in both A1K and A2K groups; ROMK was unaffected by Ang II or dietary K. In conclusion, evidence is presented that stimulation of NCC during Ang II hypertension is secondary to K+ deficiency driven by ENaC stimulation since doubling dietary K+ prevents the activation. The results also indicate that elevation in BP is independent of NCC activation

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