Dietary sodium intake: Influence on calcium channels and urinary calcium excretion in spontaneously hypertensive rats

1991 ◽  
Vol 41 (6-7) ◽  
pp. 893-896 ◽  
Author(s):  
Ferruccio Galletti ◽  
Aleta Rutledge ◽  
David J. Triggle
Keyword(s):  
Calcium Channels ◽  
Spontaneously Hypertensive Rats ◽  
Sodium Intake ◽  
Urinary Calcium ◽  
Urinary Calcium Excretion ◽  
Dietary Sodium ◽  
Calcium Excretion ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

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.

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)

Change in Blood Pressure during Altered Sodium Intake is not Associated with Calciotropic Hormone Level

1997 ◽  
Vol 93 (2) ◽  
pp. 153-157 ◽  
Author(s):  
Ryoji Ozono ◽  
Tetsuya Oshima ◽  
Hideo Matsuura ◽  
Katsuhiko Ishibashi ◽  
Mitsuaki Watanabe ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Calcium Metabolism ◽  
Sodium Intake ◽  
Urinary Calcium ◽  
Urinary Calcium Excretion ◽  
Mean Blood Pressure ◽  
Calcium Excretion ◽  
Sodium Restriction ◽  
Sodium Diet ◽  
Change In Mean

1. We evaluated the effects of the dietary restriction of sodium chloride on blood pressure and systemic calcium metabolism in 19 in-patients with essential hypertension (11 men and 8 women, mean age 49.9 ± 12.1 years). 2. All patients received a high-sodium diet (250 mmol/day) for 1 week, followed by a low-sodium diet (10 mmol/day) for another week. Intake of potassium (100 mmol/day) and of calcium (15 mmol/day) were kept constant throughout the study. 3. Sodium restriction significantly reduced the mean blood pressure (from 114.0 ± 1.9 to 105.0 ± 13.7 mmHg, P < 0.01). Urinary calcium excretion was significantly reduced (from 5.1 ± 2.4 to 2.2 ± 1.0 mmol/day, P < 0.01). 4. The change in mean blood pressure after sodium restriction was not correlated with a change in any parameter of calcium metabolism [whole blood ionized calcium, plasma intact parathyroid hormone, or 1,25-(OH)2 vitamin D3]. 5. Plasma renin activity during a regular sodium diet, an index of renin status, was significantly and inversely correlated with the change in blood pressure during sodium restriction, but not with any change in the parameters of calcium metabolism. 6. We conclude that sodium restriction reduces blood pressure and decreases urinary calcium excretion. However, we observed no significant role of extracellular calcium concentration or of calciotropic hormone concentration in the mechanism of sodium sensitivity.

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