The Effect of Chronic Sodium Loading and Sodium Restriction on Plasma and Renal Concentrations of Prostaglandin a in Normal Wistar and Spontaneously Hypertensive Aoki Rats

1973 ◽  
Vol 45 (s1) ◽  
pp. 325s-329s ◽  
Author(s):  
R. M. Zusman ◽  
B. H. Forman ◽  
G. Schneider ◽  
B. V. Caldwell ◽  
L. Speroff ◽  
...  
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Wistar Rats ◽  
Sodium Intake ◽  
Dietary Group ◽  
Sodium Restriction ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
High Sodium ◽  
High Sodium Intake ◽  
Low Sodium

1. In normal and hypertensive rats prostaglandin A (PGA) in plasma and kidney increased on low sodium intake and decreased on high sodium intake. 2. Plasma and renal concentrations of PGA were higher in spontaneously hypertensive rats than in normal Wistar rats in each dietary group.

Effects of high sodium intake on cardiovascular aldosterone synthesis in stroke-prone spontaneously hypertensive rats

2001 ◽  
Vol 19 (Supplement) ◽  
pp. 635-639 ◽  
Author(s):  
Yoshiyu Takeda ◽  
Takashi Yoneda ◽  
Masashi Demura ◽  
Kenji Furukawa ◽  
Isamu Miyamori ◽  
...  
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Sodium Intake ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
High Sodium ◽  
High Sodium Intake

Prevention of hypertension and maintenance of normotension in spontaneously hypertensive rats is dependent on continuous severe dietary sodium restriction

1987 ◽  
Vol 65 (4) ◽  
pp. 573-578 ◽  
Author(s):  
Esther A. Wilczynski ◽  
Frans H. H. Leenen
Keyword(s):  
Blood Pressure ◽  
Sympathetic Activity ◽  
Spontaneously Hypertensive Rats ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Ganglionic Blockade ◽  
Dietary Sodium Restriction

Spontaneously hypertensive rats were placed on a very low (9 μmol/g) or control (101 μmol/g) sodium diet at birth or 4 weeks of age. These diets were continued to 16 weeks of age, or at 10 weeks were increased from 9 to 26 or 101 μmol/g. Sodium restriction initiated up to 4 weeks of age and continued to 16 weeks of age severely retarded growth, prevented the development of hypertension, and reduced effective sympathetic activity as assessed by the response of blood pressure to ganglionic blockade. Only a small increase in sodium intake at 10 weeks of age (to 26 μmol/g or more) resulted in a marked increase in growth rate, an elevation of blood pressure, and a return of the response to ganglionic blockade towards normal. These data indicate that very severe sodium restriction must be continuous to maintain decreased sympathetic activity and normal blood pressure in spontaneously hypertensive rats. It appears that severe dietary sodium restriction suppresses one or more of the mechanisms involved in normal growth and development of hypertension in spontaneously hypertensive rats, but these mechanisms may still proceed once the sodium intake is increased.

Dietary sodium restriction and blood pressure response to sympathetic blockade in young versus adolescent spontaneously hypertensive rats

1990 ◽  
Vol 68 (1) ◽  
pp. 46-50 ◽  
Author(s):  
Frans H. H. Leenen ◽  
Giannoula Klement
Keyword(s):  
Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Sodium Intake ◽  
Blood Pressure Response ◽  
Dietary Sodium ◽  
Sympathetic Blockade ◽  
Sodium Restriction ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Dietary Sodium Restriction

The effects of dietary sodium restriction on the maintenance of blood pressure (BP) by sympathetic tone were evaluated in young versus more mature spontaneously hypertensive rats (SHR) and Wistar–Kyoto rats (WKY). Sympathetic activity was assessed by BP responses to α1-receptor blockade (prazosin), central inhibition of sympathetic outflow (clonidine), and by ganglionic blockade (hexamethonium). On regular sodium intake, SHR showed elevated BP and increased BP responses to sympathetic blockade at both 10 and 16 weeks of age. Sodium restriction to 9 or 17 μmol Na+/g food prevented or blunted development of hypertension in SHR when started at 4 weeks of age but did not affect BP when started at 10 weeks of age. Sodium restriction initiated in young SHR also prevented development of increased BP responses to sympathetic blockade. However, sodium restriction in more mature SHR did not decrease the increased BP responses to sympathetic blockade. We conclude that prevention of development of sympathetic hyperactivity in young SHR represents a major mechanism in the antihypertensive effect of sodium restriction in young SHR.Key words: dietary sodium, blood pressure, spontaneously hypertensive rats, age, sympathetic blockade.

scholarly journals Brain “ouabain,” ANG II, and sympathoexcitation by chronic central sodium loading in rats

1998 ◽  
Vol 274 (4) ◽  
pp. H1269-H1276 ◽  
Author(s):  
Bing S. Huang ◽  
Shereeni J. Veerasingham ◽  
Frans H. H. Leenen
Keyword(s):  
Wistar Rats ◽  
Sodium Intake ◽  
Renin Angiotensin System ◽  
Ang Ii ◽  
Baroreflex Control ◽  
Spontaneously Hypertensive ◽  
High Sodium ◽  
High Sodium Intake ◽  
Fab Fragments ◽  
Γ Globulins

Both brain ouabain-like activity (“ouabain”) and brain angiotensin II (ANG II) contribute to the sympathoexcitatory and pressor responses to high sodium intake in spontaneously hypertensive (SHR) and Dahl salt-sensitive (Dahl S) rats. To assess whether increases in cerebrospinal fluid (CSF) sodium can mimic this pattern of changes, Wistar rats were chronically infused with artificial CSF (aCSF) or sodium-rich aCSF (0.8 or 1.2 M sodium) intracerebroventricularly through osmotic minipumps for 14 days. Sodium-rich aCSF (0.8 M) was also infused intracerebroventricularly for 2 wk concomitantly with either antibody Fab fragments that bind ouabain and related steroids with high affinity, γ-globulins as control (200 μg/day for both), or the AT1blocker losartan (1 mg ⋅ kg−1 ⋅ day−1). Sodium-rich aCSF increased CSF sodium from 146 ± 2 to 152 ± 2 (0.8 M) and 160 ± 3 (1.2 M) mmol/l, and increased brain “ouabain” in the hypothalamus, pituitary, and pons. In conscious rats, sodium-rich aCSF increased baseline mean arterial pressure (MAP), enhanced MAP, heart rate (HR), and renal sympathetic nerve activity (RSNA) responses to intracerebroventricular α2-adrenoceptor agonist guanabenz and air stress, and desensitized arterial and cardiopulmonary baroreflex control of HR and RSNA. These effects were largely prevented by intracerebroventricular Fab fragments or losartan. Thus, in Wistar rats, both brain “ouabain” and the brain renin-angiotensin system contribute to sympathoexcitation, impairment of baroreflexes, and hypertension caused by chronically increased CSF sodium. The similar patterns of changes caused by CSF sodium in Wistar rats and by high sodium intake in SHR and Dahl S rats indicate that if high sodium intake increases central sodium, such changes may contribute to sympathoexcitation and hypertension.

Dietary Na and baroreflex modulation of blood pressure and RSNA in normotensive vs. spontaneously hypertensive rats

1994 ◽  
Vol 266 (2) ◽  
pp. H496-H502 ◽  
Author(s):  
B. S. Huang ◽  
F. H. Leenen
Keyword(s):  
Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Sodium Intake ◽  
Marked Change ◽  
Dietary Sodium ◽  
Hypertensive Rats ◽  
Baroreflex Control ◽  
Spontaneously Hypertensive ◽  
High Sodium ◽  
Wistar Kyoto

Different changes in baroreflex control of the circulation have been postulated to play a role in the different blood pressure (BP) effects of dietary sodium in normotensive vs. genetically hypertensive rats. We therefore evaluated in young Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR), with or without chronic sinoaortic denervation (SAD), the effects of low, regular, and high dietary sodium intake from 4 to 8 wk of age on BP and baroreflex function. The latter was assessed by changes in renal sympathetic nerve activity (RSNA) and heart rate in response to (de)pressor agents. In SHR, the above range of sodium caused a marked change in resting BP, somewhat more in intact (48 mmHg) vs. SAD (36 mmHg) rats. In contrast, in WKY this range of sodium intake caused only a minor (7 mmHg) change in resting BP of intact WKY but a significant (16 mmHg) change in WKY with SAD, mainly due to an increase in BP on high sodium. In intact WKY increasing dietary sodium from low to regular to high caused stepwise increases in the gain of the RSNA-BP reflex, whereas in intact SHR only an increase from low to regular sodium intake increased the gain. After SAD, the gain of the RSNA-BP reflex was very low, and no longer affected by dietary sodium in either strain. These data suggest that in WKY a sensitization in arterial baroreflex control of RSNA prevents a sodium-induced increase in BP.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of atrial natriuretic peptide in sodium balance in conscious spontaneously hypertensive rats

1990 ◽  
Vol 258 (4) ◽  
pp. F916-F926 ◽  
Author(s):  
A. A. Seymour ◽  
J. N. Swerdel ◽  
S. A. Fennell ◽  
V. J. Kratunis ◽  
M. M. Asaad
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Spontaneously Hypertensive Rats ◽  
Sodium Intake ◽  
Sodium Balance ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
High Sodium ◽  
Renal Responses ◽  
Atrial Natriuretic

Sodium and fluid intake were precisely regulated by 3 days of infusion of 0.07, 0.35, or 3.5 mu eq Na/min at rates of 25, 50, or 100 microliters/min in nine groups of conscious spontaneously hypertensive rats (SHR). At each level of sodium and volume intake, the acute depressor and renal responses to three doses of exogenous atrial natriuretic peptide (ANP)-(99-126) were determined in conscious, unrestrained SHR. The natriuretic responses to the highest dose of ANP-(99-126) (150 pmol/min) were independent of the rate of fluid infusion but were highly dependent on the sodium intake. The maximal increases in sodium excretion averaged 0.9 +/- 0.5 (253%), 2.6 +/- 0.5 (302%), and 15.4 +/- 2.1 mu eq.kg-1.min-1 (577%) in SHR maintained on 0.07, 0.35, and 3.5 mu eq Na/min, respectively. In addition, the diuretic but not the depressor responses to ANP-(99-126) were dependent on the sodium intake and were unrelated to the rate of fluid delivery. In separate groups of SHR, 3 days of infusions of 3.5 mu eq Na/min at 25 and 100 microliters/min significantly elevated plasma ANP from 89 +/- 16 to 200 +/- 60 and 159 +/- 24 fmol/ml, respectively. In conclusion, high sodium intake enhanced the renal responses to exogenous ANP-(99-126) despite increases in endogenous peptide concentrations in conscious SHR.

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