Effects of High Salt Intake and Meclofenamate on Arterial Pressure and Renal Function in the Spontaneously Hypertensive Rat

1979 ◽  
Vol 57 (s5) ◽  
pp. 251s-253s ◽  
Author(s):  
S. G. Chrysant
Keyword(s):  
Renal Function ◽  
Arterial Pressure ◽  
Sodium Intake ◽  
Left Ventricular ◽  
Spontaneously Hypertensive ◽  
High Sodium ◽  
High Sodium Intake ◽  
High Salt Intake ◽  
Group 2 ◽  
Group 1

1. The effects of prolonged high sodium intake (duration 3 months) and meclofenamate were studied in two groups of male spontaneously hypertensive (SH) rats. 2. Group 1 (eight rats) received 1% NaCl in water and served as controls, and group 2 received 1% NaCl in water plus meclofenamate (3·5–4·0 mg daily). 3. Group 2 rats developed higher arterial pressure, renal vascular resistance and left ventricular weight and greater renal histological changes, with lower effective renal plasma flow, renal blood flow and glomerular filtration rate, than group 1. No differences were observed between the two groups in heart rate, body weight, fluid intake, urine volume, UNaV, UKV and right ventricular weight. 4. The results suggest that the combination of high sodium intake and meclofenamate exerts a greater damaging effect on the arterial pressure and renal function of SH rats than salt alone.

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

Dopamine receptor-mediated activation of phospholipase C is associated with natriuresis during high salt intake

1992 ◽  
Vol 262 (3) ◽  
pp. F494-F498 ◽  
Author(s):  
S. J. Vyas ◽  
A. L. Jadhav ◽  
J. Eichberg ◽  
M. F. Lokhandwala
Keyword(s):  
Phospholipase C ◽  
Inositol Phosphates ◽  
Sodium Intake ◽  
Tap Water ◽  
Sch 23390 ◽  
Urinary Sodium ◽  
Water Excretion ◽  
High Sodium ◽  
High Sodium Intake ◽  
High Salt Intake

Activation of phospholipase C (PLC) is considered to be one of the cellular signaling events involved in dopamine (DA)-mediated natriuresis. In the present study we have examined the role of renal cortical PLC in contributing to the increase in urinary sodium excretion during high sodium intake and its relationship with intrarenal DA synthesis. Rats were given either 1% NaCl (high sodium intake) or tap water (normal sodium intake) to drink for 24 h, and urine was collected over this time period. PLC activity in the renal cortex from these rats was measured by prelabeling cortical slices with myo-[2-3H]inositol and was expressed as fractional release (FR) of inositol (mono-, bis-, and tris-) phosphates. Acute increase in sodium intake produced 93 +/- 8% increase over control in urinary DA excretion. These changes were accompanied by significant increases (30 +/- 8%) in basal FR of inositol phosphates and 243 +/- 40 and 76 +/- 14% increases in urinary sodium and water excretion, respectively. The elevated basal PLC activity in rats with high sodium intake was significantly reduced in the presence of Sch 23390, a selective DA-1 receptor antagonist. Exogenously added DA (3 mM) also produced significant increases in PLC activity, although the magnitudes of increases were different in rats with high (37 +/- 8%) and normal (66 +/- 9%) sodium intake. However, Sch 23390 alone or carbidopa pretreatment did not affect the basal PLC activity in rats maintained on normal sodium intake.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of nitric oxide in the arterial pressure and renal adaptations to long-term changes in sodium intake

1997 ◽  
Vol 272 (4) ◽  
pp. R1162-R1169 ◽  
Author(s):  
R. D. Manning ◽  
L. Hu ◽  
J. F. Reckelhoff
Keyword(s):  
Nitric Oxide ◽  
Arterial Pressure ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Urinary Sodium Excretion ◽  
Control Group ◽  
High Sodium ◽  
Sodium Sensitivity ◽  
High Sodium Intake

The goals of this study were to determine whether long-term nitric oxide (NO) synthesis inhibition in dogs results in an increase in the sodium sensitivity of arterial pressure and whether changes in plasma renin activity or the plasma concentrations of arginine vasopressin (AVP) and aldosterone play an important role in this hypertension. Studies were conducted in a control group and groups that received NO inhibition with N(G)-nitro-L-arginine methyl ester (L-NAME) at 10 or 25 microg x kg(-1) x min(-1). Each group was challenged with normal, low, and high sodium intake for periods of 5 days each. Urinary nitrate + nitrite excretion (UNOx) more than doubled in the control group during high sodium intake. In both L-NAME groups, UNOx decreased significantly, there was a hypertensive shift in the relation between urinary sodium excretion and arterial pressure, and urinary sodium excretion remained normal even in the high-sodium intake period. L-NAME infusion did not change the sodium sensitivity of arterial pressure or plasma renin activity, plasma aldosterone, and plasma AVP. In conclusion, the data suggest that, in dogs, increases in NO synthesis are not necessary to excrete a chronic sodium load, and decreases in NO do not increase the sodium sensitivity of arterial pressure.

Relationship between dietary sodium intake, hemodynamics, and cardiac mass in SHR and WKY rats

1993 ◽  
Vol 264 (1) ◽  
pp. R30-R34 ◽  
Author(s):  
E. D. Frohlich ◽  
Y. Chien ◽  
S. Sesoko ◽  
B. L. Pegram
Keyword(s):  
Arterial Pressure ◽  
Sodium Intake ◽  
Left Ventricular ◽  
Cardiac Mass ◽  
Dietary Sodium ◽  
Shr Rats ◽  
High Sodium ◽  
Blood Flows ◽  
Wky Rats ◽  
Regional Hemodynamics

To study the effects of sodium intake on circulatory homeostasis and cardiac structure, changes in cardiac mass, systemic hemodynamics, and organ blood flows were determined in spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats after 10 wk of controlled dietary intake of low sodium (0.01%), standard sodium (0.44%), and high sodium (2 levels: 1.44 and 4%). Systemic and regional hemodynamics were measured in conscious rats using the radioactive microsphere reference method. The various dietary sodium manipulations did not cause any changes in systemic and regional hemodynamics in the WKY rats. In contrast, the high-sodium diets increased arterial pressure and total peripheral resistance progressively in the SHR rats while decreasing cardiac index, heart rate, and organ blood flows to heart, kidneys, and splanchnic area. The higher sodium intake (4%) increased total and left ventricular mass index in both the SHR and the WKY rats even though hemodynamics of the WKY rats remained unchanged. These data indicate that the high-sodium diet, in addition to producing general vasoconstriction and exacerbation of hypertension, increased cardiac mass further in SHR rats; it also increased cardiac mass in the WKY rats independent of arterial pressure changes, suggesting that high sodium intake may be an independent pathogenetic factor for the development of cardiac hypertrophy.

scholarly journals Contribution of Nitric Oxide to Arterial Pressure and Heart Rate Variability in Rats Submitted to High-Sodium Intake

Hypertension ◽  
2001 ◽  
Vol 38 (3) ◽  
pp. 326-331 ◽  
Author(s):  
Silvia Lacchini ◽  
Elton L. Ferlin ◽  
Ruy S. Moraes ◽  
Jorge P. Ribeiro ◽  
Maria Claudia Irigoyen
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Arterial Pressure ◽  
Sodium Intake ◽  
High Sodium ◽  
High Sodium Intake

Renal nerves and experimental hypertension: evidence and controversy

1987 ◽  
Vol 65 (8) ◽  
pp. 1540-1547 ◽  
Author(s):  
Robert L. Kline
Keyword(s):  
Renal Function ◽  
Arterial Pressure ◽  
Renal Denervation ◽  
Spontaneously Hypertensive Rat ◽  
Sodium Intake ◽  
Renal Nerves ◽  
Experimental Hypertension ◽  
Renal Nerve ◽  
Spontaneously Hypertensive ◽  
Hemodynamic Variables

Noradrenergic fibers innervate various parts of the nephron and can contribute to sodium and water homeostasis by influencing hemodynamic variables, tubular reabsorptive mechanisms, and renin release. As renal function is considered to be a primary determinant of arterial pressure, efferent renal nerves may be an important link between the central nervous system and the kidney in the development and maintenance of hypertension. Little is known about the relative importance of renal nerves and their interactions with other factors in influencing renal function chronically. There is disagreement about the evidence for enhanced noradrenergic drive to the kidney in hypertensive rats, as the renal nerve firing rate, neurotransmitter release and metabolism, and receptor properties are generally not studied in association with measurements of renal function. However, chronic renal denervation has been shown to significantly affect arterial pressure in diverse forms of experimental hypertension in rats, including genetic models, as well as renovascular, mineralocorticoid, neurogenic, and angiotensin II hypertension. The actual mechanisms responsible for this effect of renal denervation are not clear, but presumably reflect changes in the arterial pressure – urinary sodium output relationship. On the whole, there is reasonable correlation between neurophysiological, biochemical, and renal denervation studies in the spontaneously hypertensive rat, suggesting that renal nerves do play a role in the onset of hypertension in these animals. The effect of renal denervation in other models of hypertension seems less clear, with recent reports showing that renal denervation does not alter the hypertensive process in renovascular, mineralocorticoid, and salt-related hypertension. These contradictory findings are not easily explained, but there is some indication that elevated sodium intake may alter the response to renal denervation. Resolution of these controversies must await a better understanding of the influence of renal nerves on renal function and arterial pressure in normal and hypertensive animals.

scholarly journals MO086THE EFFECT OF HIGH SODIUM CHLORIDE INTAKE ON CARDIOVASCULAR SYSTEM AND KIDNEYS IN SPONTANEOUSLY HYPERTENSIVE RATS

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Ivan Kayukov, ◽  
Olga Beresneva ◽  
Marina Parastaeva ◽  
Galina Ivanova ◽  
Mikhail Zaraiski ◽  
...  
Keyword(s):  
Sodium Chloride ◽  
Spontaneously Hypertensive Rats ◽  
Standard Diet ◽  
Myocardial Remodeling ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
High Sodium ◽  
High Consumption ◽  
Group 2 ◽  
Group 1

Abstract Background and Aims It is believed that high consumption of sodium chloride (NaCl) leads to the development of arterial hypertension, which result in heart remodeling, however, NaCl can probably cause direct heart damage. We aimed to evaluate the effects of high and normal NaCl containing diets on blood pressure (BP), myocardial remodeling, as well as on the level of nuclear transcription factor κB (NFκB) expression in myocardium and kidneys. Method 49 spontaneously hypertensive rats (SHR) were enrolled and subdivided into 2 groups: Group 1 (n=24) received standard diet (NaCl=0,34%); Group 2 (n=25) was on high sodium diet (NaCl=8%). In 2 months, systolic BP, myocardial and renal mass indices, morphological changes, as well as NFκB expression in heart and kidneys were assessed. Results are presented as mean ± SD. Results BP in group 2 did not change significantly (190 ± 10 mm Hg, p> 0.05) compared to group 1, yet left ventricle muscle mass indices as well as, right and left kidney mass indices were higher. Hypertrophy of cardiomyocytes (CMC) was found in group2: (area of the nucleus- 43.55 ± 17.39 μm2 (p <0.001); area of CMC-21799.31 ± 579.89 μm2 (p <0.001), compared to group 1: (area of the nucleus- 36.14 ± 4.67 μm2 (p <0.001); area of CMC-19011.13 ± 571.8 μm2 (p <0.001). Also, perivascular fibrosis was found in group2 (area of perivascular connective tissue(APCT)- 4038.96 ± 28.58 μm2 (p <0.001), compared to group1 (APCT-3718.36 ± 91.8 μm2, p <0.001). An increase in arterial wall thickness was noted in group 2 (15.71 ± 6.28 μm, p<0,001), compared to group 1 (13.51 ± 8 ,68 μm, p<0,001). The expression level of NFκB in myocardial tissue (n = 7) in group 2 was 33 times higher, and in kidney tissue (n = 5) 12 times higher than in group 1 (n = 8). Conclusion High consumption of NaCl induces NFκB activation in kidneys and myocardium, and may cause myocardial remodeling, probably via NFκB - associated signaling pathways.

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