The Influence of Oral Potassium Chloride on Blood Pressure in Hypertensive Men on a Low-Sodium Diet

In Sprague-Dawley rats with unilateral renal artery stenosis and an intact contralateral kidney, administration of a low-sodium diet did not prevent the development of hypertension. Despite an elevated blood pressure, hyponatremia, marked activation of the renin-angiotensin system, and increased hematocrit values, only 10% of the rats showed lesions of malignant hypertension. Systolic blood pressures of one- and two-kidney sham-operated rats fed a low-sodium diet were significantly higher than that of normotensive controls fed a normal diet. Uninephrectomy did not reduce plasma renin activity. The low-sodium diet increased plasma renin activity to about the same level in one- and two-kidney normotensive rats. However, the increase in plasma renin activity elicited by dietary sodium restriction was markedly less in one-kidney Goldblatt hypertension. Systolic blood pressure reached similar levels in one- and two-kidney Goldblatt hypertensive rats fed a low-sodium diet. These data indicate that a decrease in sodium intake does not prevent the development of two-kidney Goldblatt hypertension.

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Effectiveness of a multifactorial intervention, consisting of self-management of antihypertensive medication, self-measurement of blood pressure, hypocaloric and low sodium diet, and physical exercise, in patients with uncontrolled hypertension taking 2 or more antihypertensive drugs

Medicine ◽

10.1097/md.0000000000019769 ◽

2020 ◽

Vol 99 (17) ◽

pp. e19769

Author(s):

Fabián Unda Villafuerte ◽

Joan Llobera Cànaves ◽

Patricia Lorente Montalvo ◽

María Lucía Moreno Sancho ◽

Bartolomé Oliver Oliver ◽

...

Keyword(s):

Blood Pressure ◽

Physical Exercise ◽

Antihypertensive Medication ◽

Antihypertensive Drugs ◽

Self Management ◽

Uncontrolled Hypertension ◽

Multifactorial Intervention ◽

Sodium Diet ◽

Low Sodium Diet ◽

Low Sodium

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Effect of the low sodium diet and the rice diet on arterial blood pressure

The American Journal of Medicine ◽

10.1016/0002-9343(48)90160-0 ◽

1948 ◽

Vol 5 (6) ◽

pp. 815-820 ◽

Cited By ~ 7

Author(s):

Benjamin Rosenberg ◽

Alfred E. Rosenthal ◽

Milton B. Rosenbluth

Keyword(s):

Blood Pressure ◽

Arterial Blood Pressure ◽

Sodium Diet ◽

Low Sodium Diet ◽

Low Sodium ◽

Arterial Blood ◽

Rice Diet

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Angiotensin II utilizes Janus kinase 2 in hypertension, but not in the physiological control of blood pressure, during low-salt intake

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00071.2011 ◽

2011 ◽

Vol 301 (4) ◽

pp. R1169-R1176 ◽

Cited By ~ 15

Author(s):

Amy K. L. Banes-Berceli ◽

Hind Al-Azawi ◽

Daniel Proctor ◽

Harvey Qu ◽

Dominic Femminineo ◽

...

Keyword(s):

Blood Pressure ◽

Mean Arterial Pressure ◽

Arterial Pressure ◽

Janus Kinase ◽

Ang Ii ◽

Physiological Control ◽

Sodium Diet ◽

Low Sodium Diet ◽

Low Sodium ◽

Low Salt

Janus kinase (JAK) 2 is activated by ANG II in vitro and in vivo, and chronic blockade of JAK2 by the JAK2 inhibitor AG-490 has been shown recently to attenuate ANG II hypertension in mice. In this study, AG-490 was infused intravenously in chronically instrumented rats to determine if the blunted hypertension was linked to attenuation of the renal actions of ANG II. In male Sprague-Dawley rats, after a control period, ANG II at 10 ng·kg−1·min−1 was infused intravenously with or without AG-490 at 10 ng·kg−1·min−1 iv for 11 days. ANG II infusion (18 h/day) increased mean arterial pressure from 91 ± 3 to 168 ± 7 mmHg by day 11. That response was attenuated significantly in the ANG II + AG-490 group, with mean arterial pressure increasing only from 92 ± 5 to 127 ± 3 mmHg. ANG II infusion markedly decreased urinary sodium excretion, caused a rapid and sustained decrease in glomerular filtration rate to ∼60% of control, and increased renal JAK2 phosphorylation; all these responses were blocked by AG-490. However, chronic AG-490 treatment had no effect on the ability of a separate group of normal rats to maintain normal blood pressure when they were switched rapidly to a low-sodium diet, whereas blood pressure fell dramatically in losartan-treated rats on a low-sodium diet. These data suggest that activation of the JAK/STAT pathway is critical for the development of ANG II-induced hypertension by mediating its effects on renal sodium excretory capability, but the physiological control of blood pressure by ANG II with a low-salt diet does not require JAK2 activation.

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The Effect of a Reduced Sodium Intake on Post-Renal Transplantation Hypertension in Rats

Clinical Science ◽

10.1042/cs0660269 ◽

1984 ◽

Vol 66 (3) ◽

pp. 269-276 ◽

Cited By ~ 3

Author(s):

M. H. De Keijzer ◽

A. P. Provoost ◽

E. D. Wolff ◽

W. J. Kort ◽

I. M. Weijma ◽

...

Keyword(s):

Blood Pressure ◽

Systolic Blood Pressure ◽

Sodium Intake ◽

Plasma Renin ◽

Normal Diet ◽

Transplant Recipients ◽

Plasma Renin Concentration ◽

Sodium Diet ◽

Low Sodium Diet ◽

Low Sodium

1. In an experimental model of post-renal transplantation hypertension in rats, we studied the effect of a reduction of sodium intake on the development of this type of hypertension. 2. Systolic blood pressure, plasma- renin concentration and renal function were measured regularly in recipients of an allogeneic kidney transplant that had previously undergone active immunological enhancement. 3. Transplant recipients on a normal diet showed a rise in systolic blood pressure during the second week after transplantation. The systolic blood pressure of recipients on a low sodium diet remained normotensive throughout the 15 weeks follow-up period. 4. The plasma renin concentration was low in the hypertensive recipients on a normal diet, as compared with unilaterally nephrectomized controls. Although the plasma renin concentration of recipients on a low sodium diet fell below that of unilaterally nephrectomized controls on a low sodium diet, it was higher than that of recipients on a normal diet. 5. The renal function of transplant recipients was greatly reduced compared with that of control rats. The glomerular filtration rate was reduced to a greater extent than the effective renal plasma flow. 6. In a separate experiment it was revealed that a similar reduction in the glomerular filtration rate of kidneys permanently damaged by temporary ischaemia did not result in an increase in the systolic blood pressure. 7. Survival up to 6 weeks after transplantation was the same for both groups of recipients. Recipients on a low sodium diet, however, showed a better 15 weeks survival, probably owing to the absence of hypertension in this group. 8. The prevention of the development of hypertension by means of a reduction of sodium intake, points to an involvement of sodium retention in this post-transplantation hypertension model.

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Effects of High and Low Sodium Diet on Blood Pressure and Heart Rate in Mice Lacking the Functional Grainyhead-Like 1 Gene

Physiological Research ◽

10.33549/physiolres.933298 ◽

2017 ◽

pp. 163-165 ◽

Cited By ~ 6

Author(s):

A. WALKOWSKA ◽

M. PAWLAK ◽

S. M. JANE ◽

E. KOMPANOWSKA-JEZIERSKA ◽

T. WILANOWSKI

Keyword(s):

Blood Pressure ◽

Essential Hypertension ◽

Standard Diet ◽

Wild Type ◽

Causative Gene ◽

Major Health Problem ◽

Sodium Diet ◽

Low Sodium Diet ◽

Low Sodium ◽

Increased Risk

Hypertension is a major health problem throughout the world because of its high prevalence and its association with increased risk of cardiovascular disease. Two independent studies discovered a locus conferring susceptibility to essential hypertension on chromosome 2, in the 2p25 region, but the causative gene remains unknown. Grainyhead-like 1 (GRHL1) is one of the genes located in this region. Our experiments determined that the Grhl1-null mice, when fed standard diet, have the same blood pressure as their wild type littermate controls. However, we discovered that blood pressure of these mice increases following high sodium diet and decreases when they are fed low sodium diet, and similar effects were not observed in the control wild type littermates. This suggests that the Grhl1-null mice are sensitive to the development of salt-sensitive hypertension. Thus it is possible that the GRHL1 gene is involved in the regulation of blood pressure, and it may be the causative gene for the locus of susceptibility to essential hypertension in the 2p25 region.

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