Increased sensitivity to norepinephrine cardiac arrhythmias in the deoxycorticosterone acetate high salt rat before the onset of hypertension

1984 ◽  
Vol 62 (6) ◽  
pp. 605-609 ◽  
Author(s):  
S. W. Rabkin ◽  
A. Y. M. Fung
Keyword(s):  
Blood Pressure ◽  
Drinking Water ◽  
Cardiac Arrhythmias ◽  
Tap Water ◽  
High Salt ◽  
Dietary Sodium ◽  
Control Group ◽  
Deoxycorticosterone Acetate ◽  
Salt Loading ◽  
Group I

To determine whether salt loading increases the sensitivity of the myocardium to fatal arrhythmias induced by norepinephrine, four groups of Sprague–Dawley rats were studied. Group I received both saline (0.9%) as drinking water and deoxycorticosterone acetate (DOCA) (0.5 mg/kg, 3 times) for 14 days (DOCA high salt group); group II received only 0.9% saline as drinking water (high salt group); group III received DOCA in the same dose regime, but tap water to drink (DOCA group); and group IV received tap water (control). Under pentobarbital anesthesia, norepinephrine was infused and electrocardiogram and blood pressure were monitored. The DOCA high salt group developed arrhythmias significantly (p < 0.05) earlier than at lower norepinephrine doses. The dose at which 50% mortality occurred was 20 μg∙kg−1∙min−1 in DOCA high salt group, 37 μg∙kg−1∙min−1 in high salt group, 40 μg∙kg−1∙min−1 in the control, and 44 μg∙kg−1∙min−1 in the DOCA group. The cumulative dose of norepinephrine associated with 50% mortality was 160 μg/kg in the DOCA high salt group, 370 μg/kg in the high salt group, 530 μg/kg in the control group, and 600 μg/kg in the DOCA group. The blood pressure after sodium loading before norepinephrine infusion was similar in all three groups. The blood pressure response to norepinephrine was not significantly different between the four groups. Myocardial content of the electrolytes Na+, K+, Mg2+, and Ca2+, were not significantly different between three of the groups, namely those receiving DOCA plus high salt, high salt or neither DOCA nor high salt as ascertained in other animals who were treated according the the three protocols. These data suggest that excess dietary sodium enhances the sensitivity to norepinephrine-induced cardiac arrhythmias.

EFFECT OF DIETARY EDTA ON THE ABILITY OF CHICKS TO TOLERATE SODIUM CHLORIDE IN THE WATER

1971 ◽  
Vol 51 (3) ◽  
pp. 633-637
Author(s):  
T. K. J. COWAN ◽  
G. D. PHILLIPS ◽  
D. B. BRAGG
Keyword(s):  
Drinking Water ◽  
Weight Gain ◽  
Sodium Chloride ◽  
Salt Water ◽  
Tap Water ◽  
Block Design ◽  
High Salt ◽  
Control Group ◽  
Plasma Sodium ◽  
Broiler Chicks

Broiler chicks, allocated in a randomized block design, were fed four diets containing ethylene diamine tetraacetic acid (EDTA) at 0, 0.1, 0.2 and 0.4% of the diet and drinking water with a high salt concentration (6000 ppm). A control group received tap water and the EDTA-free diet. The addition of 6000 ppm NaCl in the drinking water had no effect on weight gain or feed conversion. Similarly, the inclusion of up to 0.4% EDTA in the feed had no adverse effect on weight gain. Analyses of packed-cell volume (PCV) and plasma sodium, chloride and calcium concentrations showed no changes as a result of treatment. Water consumption almost doubled for the chicks subjected to high salt water regimens compared with the control. Two groups of chicks received the EDTA-free diet, and significantly (P < 0.10) higher mortality was found for the group on the salt water compared with the tap water controls. The mortality in the former was also significantly (P < 0.10) higher than for the group receiving 0.2% EDTA in the diet and salt water. The chicks on the 0.4% EDTA diet had significantly (P < 0.05) higher mortality than control chicks on tap water and those chicks receiving salt water and diets containing 0.1% and 0.2% EDTA. Postmortem examination indicated that ascites and widespread edema were the causes of death in chicks that drank salt water and consumed diets containing no EDTA or 0.4% EDTA. The death of chicks on treatments that resulted in low mortality rates was not attributable to ascites. The reason for the apparent beneficial effect of feeding 0.2% EDTA in the diet in conjunction with the salt water remains open to conjecture.

scholarly journals The Effects of Short-Term Changes in Sodium Intake on Plasma Marinobufagenin Levels in Patients with Primary Salt-Sensitive and Salt-Insensitive Hypertension

Nutrients ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1502
Author(s):  
Katarzyna Łabno-Kirszniok ◽  
Agata Kujawa-Szewieczek ◽  
Andrzej Wiecek ◽  
Grzegorz Piecha
Keyword(s):  
Blood Pressure ◽  
Diastolic Blood Pressure ◽  
Sodium Intake ◽  
Left Ventricular ◽  
Primary Hypertension ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Short Term ◽  
Salt Loading ◽  
Dietary Sodium Restriction

Increased marinobufagenin (MBG) synthesis has been suggested in response to high dietary salt intake. The aim of this study was to determine the effects of short-term changes in sodium intake on plasma MBG levels in patients with primary salt-sensitive and salt-insensitive hypertension. In total, 51 patients with primary hypertension were evaluated during acute sodium restriction and sodium loading. Plasma or serum concentrations of MBG, natriuretic pro-peptides, aldosterone, sodium, potassium, as well as hematocrit (Hct) value, plasma renin activity (PRA) and urinary sodium and potassium excretion were measured. Ambulatory blood pressure monitoring (ABPM) and echocardiography were performed at baseline. In salt-sensitive patients with primary hypertension plasma MBG correlated positively with diastolic blood pressure (ABPM) and serum NT-proANP concentration at baseline and with serum NT-proANP concentration after dietary sodium restriction. In this subgroup plasma MBG concentration decreased during sodium restriction, and a parallel increase of PRA was observed. Acute salt loading further decreased plasma MBG concentration in salt-sensitive subjects in contrast to salt insensitive patients. No correlation was found between plasma MBG concentration and left ventricular mass index. In conclusion, in salt-sensitive hypertensive patients plasma MBG concentration correlates with 24-h diastolic blood pressure and dietary sodium restriction reduces plasma MBG levels. Decreased MBG secretion in response to acute salt loading may play an important role in the pathogenesis of salt sensitivity.

Abstract 142: A Fructose-but Not a Glucose-enriched Diet, Induces a Salt-dependent Increase in Blood Pressure and Enhances NKCC2 Phosphorylation in Normal Rats

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Keyona N King-Medina ◽  
Emily Henson ◽  
Pablo Ortiz
Keyword(s):  
Blood Pressure ◽  
Drinking Water ◽  
Salt Intake ◽  
Caloric Intake ◽  
High Salt ◽  
Human Consumption ◽  
Thick Ascending Limb ◽  
Sprague Dawley ◽  
High Fructose ◽  
High Salt Intake

Human consumption of fructose as a sweetener has increased in the past 30 years. High fructose intake has been implicated in the development of hypertension, diabetes, and obesity. In the US, the upper 10th percentile of the population consumes up to 40% of their caloric intake from added sugars, in which fructose represents half of these. Fructose metabolism is strikingly different from that of glucose. Yet, the effect of a fructose or glucose-enriched diet in salt handling by the kidney, affecting blood pressure, and its interaction with high salt intake has been poorly studied. In genetic models of salt-sensitive hypertension, the activity of the Na + /K + /2Cl - cotransporter (NKCC2) in the thick ascending limb (TAL) is abnormally enhanced. We hypothesized that chronic fructose in drinking water induces a salt-dependent increase in blood pressure and stimulates NKCC2 during high salt intake in normal rats. Sprague-Dawley rats were given 20% fructose or 20% glucose in drinking water for 1 week after which a high salt (HS) diet (4% Na + in chow) was started for 3 weeks. When we measured systolic blood pressure (SBP) by tail cuff plethysmography in fructose-fed and glucose-fed rats on a HS diet, only the fructose-fed rats had an increased SBP from 120±10 to 132±6 mmHg on day 7 of HS (p<0.01). SBP continued to increase up to 144±18 mmHg after 3 weeks (p<0.01 vs glucose). Fructose or glucose alone did not increase SBP after 4 weeks. We then repeated the protocol using radiotelemetry to monitor the blood pressure (BP). In rats fed fructose, by day 5 of HS the SBP increased by 12±3 mmHg (p<0.02) and SBP remained elevated for 3 weeks (delta: 10±2.5 mmHg, n=3). In rats fed glucose, a HS diet did not significantly change SBP for 3 weeks (n=5). Moreover, NKCC2 activity in the TAL is enhanced by phosphorylation at Thr96, 101. We found that NKCC2 phosphorylation was higher in rats fed fructose plus HS (p<0.02) but not in rats fed glucose plus HS for 3 weeks (HS: 100, fructose+HS: 250±40%, glucose+HS: 95±10%). Therefore, we conclude that a high fructose (but not a glucose) diet in normal rats induces a salt-dependent increase in BP independently from caloric intake. Thus, the increase in BP may in part be due to the stimulation of NKCC2 phosphorylation in the TAL by fructose.

Abstract 099: Functional Remodeling of the Renal Vasculature Precedes the Establishment of Salt-sensitive Hypertension in Eln-deficient Mice

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Elizabeth A Owens ◽  
Li Jie ◽  
Beverly Reyes ◽  
Elisabeth J Van Bockstaele ◽  
Patrick Osei-Owusu
Keyword(s):  
Blood Pressure ◽  
Structural Damage ◽  
Vascular Dysfunction ◽  
Renal Perfusion ◽  
Dietary Sodium ◽  
Intraluminal Pressure ◽  
Renal Vasculature ◽  
Salt Loading ◽  
Vascular Stiffening ◽  
Renal Vascular

Vascular stiffening due to elastin deficiency is a leading risk for hypertension and chronic kidney disease (CKD). However, the mechanisms by which elastin deficiency is involved in the pathogenesis of hypertension and/or CKD are poorly understood. Here, we used elastin heterozygous mice ( Eln+/- ), an animal model of elastin insufficiency, to test the hypothesis that renal dysfunction due to elastin deficiency occurs independently of and precedes the development of hypertension in this mouse model. We assessed blood pressure (BP) and renal hemodynamics in 30-day (P30) and 12-week old anesthetized male and female mice. At P30, mean blood pressure of Eln+/- was similar to wild type (WT) controls ( Eln+/- , 79 ± 5 vs. WT, 69±3 mmHg, P = 0.06); however, renal blood flow was lower ( Eln+/- 2.9 ± 0.2 vs. WT 4.0 ± 0.5 mL/min/g KW, P = 0.03) whereas renal vascular resistance (RVR; Eln+/- 29 ± 3 vs. WT 18 ± 3 mmHg/mL/min/g KW, P = 0.03) was augmented at baseline in Eln+/- mice. At 12 wks old, RVR remained elevated while filtration fraction was higher in male Eln+/- relative to WT mice ( Eln+/- 44 ± 3 vs. WT 38±5 % P = 0.07). Eln+/- mice showed isolated systolic hypertension that was evident only at nighttime ( Eln+/- 136 ± 2 vs. WT 112 ± 6 mmHg, P <0.01). Acute salt loading with 6% dietary sodium increased daytime systolic blood pressure only in male Eln+/- mice ( Eln+/- 118 ± 5 vs. WT 102 ± 6 mmHg, P = 0.03), causing a rightward shift and blunted slope of the pressure-natriuresis curve. Renal interlobar artery basal tone and myogenic response to increasing intraluminal pressure at P10 were similar ( Eln+/- 78 ± 3 vs. WT 67 ± 6 % P = 0.06) whereas they were augmented at P30 ( Eln+/- 63 ± 4 vs. WT 49 ± 6 % P = 0.05) and at 12 wks old in Eln+/- mice ( Eln+/- 50 ± 2 vs. WT 33 ± 3 % P < 0.01), and normalized by the AT1R blocker, candesartan ( Eln+/- 22 ± 9 vs. WT 8 ± 5 % P = 0.10). We conclude that AT1R mediates augmented mechanotransduction and renal vascular dysfunction due to Eln insufficiency that in turn contribute to altered renal sodium handling and increased BP. Such prolonged systemic BP elevation leads to glomerular structural damage due to high renal perfusion pressure. Therefore, therapies that target the AT1R to control BP in patients with elastin deficiency may be beneficial in preventing hypertension-evoked kidney damage.

scholarly journals INTERVENSI PROGRESSIVE MUSCLE RELAXATION LEBIH MENURUNKAN TEKANAN DARAH DARI PADA SLOW STROKE BACK MASSAGE PADA PASIEN HIPERTENSI DERAJAT I YANG MENGONSUMSI OBAT ANTI HIPERTENSI DI BADUNG

2019 ◽  
Author(s):  
Ni Komang Ayu Juni Antari ◽  
Alex Pangkahila ◽  
Muh. Ali Imron ◽  
I Putu Adiartha Griadhi ◽  
Luh Made Indah Sri Handari Adiputra ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Physical Exercise ◽  
Muscle Relaxation ◽  
Progressive Muscle Relaxation ◽  
Control Group ◽  
Relaxation Techniques ◽  
Group I ◽  
Significant Difference ◽  
Group 2 ◽  
Back Massage

ABTSRACT Introduction: Physical exercise as anticipate of hypertension along with nutrition and medicines. One of physical exercise that can be applicated here is relaxation techniques which is showed positive impact in decreased blood pressure. Objective: Determine the difference between PMR intervention with SSBM intervention to reduce blood pressure for grade I hypertension patients whose consumed anti-hypertension medicine in badung regency. Methods: Experimental method Pre and post-test control group design and used 24 subjects, divided in to 2 groups, in which the experimental group I (n=12) received progressive muscle relaxation (PMR) while the treatment group 2 (n=12) received slow stroke back massage (SSBM). Intervention is given 3 times a week for 4 weeks. This study was using simple random sampling. Blood pressure was measured by sphygmomanometer and stethoscope. Result: Independent Sample T-test showed there was significant difference between Group 1 and Group 2 which (p<0.05) for systolic and diastolic blood pressure. Conclusion: Progressive muscle relaxation intervention decrease blood pressure more than slow stroke back massage intervention in patients grade I hypertension whose consumed anti-hypertension medicine in Badung Regency.Keywords: progressive muscle relaxation, slow stroke back massage, grade I hypertension, blood pressure

Prolonged NOS inhibition in the brain elevates blood pressure in normotensive rats

1998 ◽  
Vol 275 (2) ◽  
pp. R410-R417 ◽  
Author(s):  
Atsushi Sakima ◽  
Hiroshi Teruya ◽  
Masanobu Yamazato ◽  
Rijiko Matayoshi ◽  
Hiromi Muratani ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Salt Intake ◽  
High Salt ◽  
Salt Loading ◽  
Salt Diet ◽  
Intracerebroventricular Infusion ◽  
Air Jet ◽  
Sd Rats ◽  
Low Salt ◽  
The Brain

Systemic inhibition of nitric oxide synthase (NOS) evokes hypertension, which is enhanced by salt loading, partly via augmented sympathetic activity. We investigated whether inhibition of brain NOS elevates blood pressure (BP) in normotensive rats and, if so, whether the BP elevation is enhanced by salt loading. After a 2-wk low-salt (0.3%) diet, male Sprague-Dawley (SD) rats were divided into four groups. Groups 1 and 2 received a chronic intracerebroventricular infusion of 0.5 mg ⋅ kg−1 ⋅ day−1of N G-monomethyl-l-arginine (l-NMMA), and groups 3 and 4 were given artificial cerebrospinal fluid (aCSF). Groups 1 and 3 were placed on a high-salt (8%) diet, whereas groups 2 and 4 were on a low-salt diet. On day 9or 10, group 1 showed significantly higher mean arterial pressure (MAP) in a conscious unrestrained state (129 ± 3 mmHg vs. 114 ± 3, 113 ± 1, and 108 ± 3 mmHg in groups 2, 3, and 4, respectively, P < 0.05). On a high-salt diet, response of renal sympathetic nerve activity but not of BP to air-jet stress was significantly larger in rats givenl-NMMA than in rats given aCSF (29 ± 4% vs. 19 ± 3%, P < 0.05). When the intracerebroventricular infusions were continued for 3 wk, MAP was significantly higher in rats givenl-NMMA than in rats given aCSF irrespective of salt intake, although the difference was ∼7 mmHg. Thus chronic inhibition of NOS in the brain only slightly elevates BP in SD rats. Salt loading causes a more rapid rise in BP. The mechanisms of the BP elevation and its acceleration by salt loading remain to be elucidated.

Protective effect of L-carnitine against oxidative damage caused by experimental chronic aflatoxicosis in quail (Coturnix coturnix)

2005 ◽  
Vol 53 (3) ◽  
pp. 319-324 ◽  
Author(s):  
M. Citil ◽  
V. Gunes ◽  
O. Atakisi ◽  
Ayla Ozcan ◽  
M. Tuzcu ◽  
...  
Keyword(s):  
Drinking Water ◽  
Whole Blood ◽  
Reduced Glutathione ◽  
Group Iv ◽  
Control Group ◽  
Total Aflatoxin ◽  
Group Iii ◽  
Coturnix Coturnix ◽  
Group I ◽  
Plasma Malondialdehyde

This study was designed to evaluate the effect of L-carnitine supplementation on the plasma malondialdehyde (MDA) and whole blood reduced glutathione (GSH) concentrations in experimentally-induced chronic aflatoxicosis in quails. For this purpose, a total of 80 quails up to 8 weeks old were divided into four equal groups. Group I served as control, Group II was given L-carnitine at the dose of 200 mg/litre in the drinking water for 60 days, Group III was given 60 µg total aflatoxin/kg diet for 60 days, and Group IV was given both 60 µg total aflatoxin/kg diet and 200 mg L-carnitine/litre in the drinking water for 60 days. Aflatoxin treatment caused a significant increase in plasma MDA and a significant decrease in blood GSH concentrations. On the other hand, there was a significant decrease in plasma MDA and a significant increase in whole blood GSH in the L-carnitine-supplemented group. The present study demonstrated that L-carnitine brought about the inhibition of lipid peroxidation by enhancing antioxidant capacity in quails with chronic aflatoxicosis.

Effect of chlorothiazide on serial measurements of exchangeable sodium and blood pressure in spontaneously hypertensive rats

1985 ◽  
Vol 69 (5) ◽  
pp. 511-515 ◽  
Author(s):  
P. J. O. Manhem ◽  
S. A. Clark ◽  
W. B. Brown ◽  
G. D. Murray ◽  
J. I. S. Robertson
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
Spontaneously Hypertensive Rats ◽  
Tap Water ◽  
Treated Group ◽  
Temporal Association ◽  
Control Group ◽  
Exchangeable Sodium ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

1. Chlorothiazide (100 mg/kg body weight) was given by gavage daily to spontaneously hypertensive rats for 4 weeks. Another group of spontaneously hypertensive rats was given only tap water and served as control. 2. Measurements of total exchangeable sodium, blood pressure and weight were performed for 2 weeks before and for 4 weeks during treatment. 3. Before treatment, exchangeable sodium, blood pressure and weight were similar in the two groups of rats. 4. Chlorothiazide significantly attenuated the blood pressure increase in spontaneously hypertensive rats, the effect being most marked during the first 2 1/2 weeks of treatment and less thereafter. 5. Rats in the chlorothiazide-treated group gained weight more slowly than did those of the control group. 6. Exchangeable sodium, expressed as mmol/kg body weight, did not differ significantly between the two groups at any stage. 7. When exchangeable sodium was expressed as mmol/rat, there was a more gradual rise in the chlorothiazide-treated animals, in accordance with their slower gain in weight. 8. There was no temporal association between the antihypertensive effect of chlorothiazide and changes in exchangeable sodium. 9. Thus whereas chlorothiazide treatment of spontaneously hypertensive rats slows the increase of both weight and exchangeable sodium, other mechanisms are apparently responsible for the antihypertensive action of the drug.

scholarly journals Vascular Response to Graded Angiotensin II Infusion in Offspring Subjected to High-Salt Drinking Water during Pregnancy: The Effect of Blood Pressure, Heart Rate, Urine Output, Endothelial Permeability, and Gender

2014 ◽  
Vol 2014 ◽  
pp. 1-8
Author(s):  
Zahra Pezeshki ◽  
Fatemeh Eshraghi-Jazi ◽  
Mehdi Nematbakhsh
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Drinking Water ◽  
Angiotensin Ii ◽  
Urine Output ◽  
The Body ◽  
High Salt ◽  
Female Rats ◽  
Kidney Weight ◽  
Group 3

Introduction.Rennin-angiotensin system and salt diet play important roles in blood pressure control. We hypothesized that the high-salt intake during pregnancy influences the degree of angiotensin-dependent control of the blood pressure in adult offspring.Methods.Female Wistar rats in two groups (A and B) were subjected to drink tap and salt water, respectively, during pregnancy. The offspring were divided into four groups as male and female offspring from group A (groups 1 and 2) and from group B (groups 3 and 4). In anesthetized matured offspring mean arterial pressure (MAP), heart rate and urine output were measured in response to angiotensin II (AngII) (0-1000 ng/kg/min, iv) infusion.Results.An increase in MAP was detected in mothers with salt drinking water (P<0.05). The body weight increased and kidney weight decreased significantly in male offspring from group 3 in comparison to group 1 (P<0.05). MAP and urine volume in response to AngII infusion increased in group 3 (P<0.05). These findings were not observed in female rats.Conclusion.Salt overloading during pregnancy had long-term effects on kidney weight and increased sex-dependent response to AngII infusion in offspring (adult) that may reveal the important role of diet during pregnancy in AngII receptors.

scholarly journals Omega-3 Oil Ameliorate Histological and Ultrastructural Alterations Induced by Cadmium Chloride in Rats Testis

2020 ◽  
Vol 4 (1) ◽  
pp. 62-69
Author(s):  
Treefa F. Ismail ◽  
Falah M. Aziz
Keyword(s):  
Drinking Water ◽  
Tap Water ◽  
Occupational Exposures ◽  
Testicular Tissue ◽  
Male Rats ◽  
Control Group ◽  
Albino Rats ◽  
Omega 3 ◽  
Potential Threat ◽  
Ultrastructural Alterations

Cadmium (Cd) is considered to be one of the major environmental pollutants which have potential threat to human health. Reports of declining male fertility have renewed interest in the role of environmental and occupational exposures in the etiology of human infertility. Cd exposure led to obvious degenerative changes in testicular tissue. This study was performed to investigate the Cd-induced structural effects on the testes and to evaluate the possible protective effect of omega-3 oil in adult albino rats. Thirty adult male rats were used in the present work, divided randomly into five groups, six rats in each group; the first group was considered as a control group and left without treatment except the standard rat chow and tap water. The second group was given 40 mg/L of CdCl2 in drinking water while the third group was given 60 mg/L of CdCl2 in drinking water. The fourth group was given 40 mg/L of CdCl2 in drinking water plus omega-3 oil (4 g/kg diet), while the fifth group was given 60 mg/L of CdCl2 in drinking water plus omega-3 oil (4 g/kg diet), the Cd-treated rats showed dose-dependent histological and ultrastructural alterations which have been ameliorated after exposure to omega-3 oil. The present investigation concluded that omega-3 played a protective role against Cd-induced histopathological changes in rat testis.

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