Effects of altered NaCl intake on renal hemodynamic and renin release responses to RNS

1987 ◽  
Vol 253 (5) ◽  
pp. F976-F981 ◽  
Author(s):  
J. L. Osborn ◽  
D. D. Kinstetter
Keyword(s):  
Sodium Chloride ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Renin Release ◽  
Renal Vasculature ◽  
Renal Nerve ◽  
High Sodium ◽  
Low Sodium ◽  
Anesthetized Dogs ◽  
Neurogenic Vasoconstriction

Relationships between frequency of renal nerve stimulation (RNS) and renal blood flow (RBF), glomerular filtration rate (GFR), and plasma renin activities (PRA) were evaluated in anesthetized dogs placed on low (5 meq/day)-, normal (40 meq/day)-, and high (200 meq/day)-sodium chloride diets. Arterial pressure, RBF, GFR, and renal venous and arterial PRA were determined before and during direct electrical RNS at 0.5, 1.0, and 2.0 Hz (15 V, 1.0 ms). Dogs on low sodium intakes increased renal venous PRA at 0.5, 1.0-, and 2.0-Hz RNS, whereas dogs on normal sodium intakes did not increase renal venous PRA until RNS reached 2.0 Hz. High sodium dogs did not increase PRA at any frequency of RNS tested. RNS at 0.5 Hz was not associated with any changes in GFR or RBF in any of the groups. Dogs on normal sodium and high sodium intakes decreased both GFR and RBF during 1.0- and 2.0-Hz RNS. Low-sodium dogs, however, only decreased GFR and RBF during 2.0-Hz RNS, and these hemodynamic responses were significantly less than 2.0-Hz GFR and RBF responses of high sodium dogs. These data indicate that renal vasoconstrictor responses to RNS are potentiated, and renin release responses to RNS are reduced by elevation of sodium chloride intake. We suggest that during low sodium intake, activation of sympathetic nerve activity elicits an enhanced renin release response, whereas the renal vasculature may be protected against neurogenic vasoconstriction.

EFFECT OF SODIUM CHLORIDE INTAKE AND MINERALOCORTICOID LEVEL ON THE GRANULARITY OF JUXTAGLOMERULAR CELLS

1958 ◽  
Vol 17 (3) ◽  
pp. 261-264 ◽  
Author(s):  
M. L. WIEDMAN ◽  
F. W. DUNIHUE ◽  
W. VAN B. ROBERTSON
Keyword(s):  
Sodium Chloride ◽  
Sodium Intake ◽  
Granular Cell ◽  
Juxtaglomerular Apparatus ◽  
High Sodium ◽  
Low Sodium ◽  
Similar Series ◽  
Adrenal Response ◽  
Reported Data ◽  
Sodium Chloride Intake

SUMMARY The effect of combinations of normal, low and high sodium chloride intake with normal, low and high mineralocorticoid level on granularity of cells in the juxtaglomerular apparatus has been studied in the rat. The results have been compared with previously reported data from a similar series in the cat. With one exception, low sodium intake by normal rats, the granular cell index in both rat and cat was inversely related to the mineralocorticoid level and unrelated to the sodium intake. Data are presented which suggest that this exception is only apparent and may be explained on the basis of a different adrenal response by the rat.

scholarly journals Dietary sodium modulates the interaction between efferent and afferent renal nerve activity by altering activation of α2-adrenoceptors on renal sensory nerves

2011 ◽  
Vol 300 (2) ◽  
pp. R298-R310 ◽  
Author(s):  
Ulla C. Kopp ◽  
Michael Z. Cicha ◽  
Lori A. Smith ◽  
Saku Ruohonen ◽  
Mika Scheinin ◽  
...  
Keyword(s):  
Substance P ◽  
Sodium Intake ◽  
Sensory Nerves ◽  
Nerve Activity ◽  
Renal Nerve ◽  
High Sodium ◽  
Sodium Diet ◽  
Low Sodium ◽  
Renal Nerve Activity ◽  
High Sodium Diet

Activation of efferent renal sympathetic nerve activity (ERSNA) increases afferent renal nerve activity (ARNA), which then reflexively decreases ERSNA via activation of the renorenal reflexes to maintain low ERSNA. The ERSNA-ARNA interaction is mediated by norepinephrine (NE) that increases and decreases ARNA by activation of renal α1-and α2-adrenoceptors (AR), respectively. The ERSNA-induced increases in ARNA are suppressed during a low-sodium (2,470 ± 770% s) and enhanced during a high-sodium diet (5,670 ± 1,260% s). We examined the role of α2-AR in modulating the responsiveness of renal sensory nerves during low- and high-sodium diets. Immunohistochemical analysis suggested the presence of α2A-AR and α2C-AR subtypes on renal sensory nerves. During the low-sodium diet, renal pelvic administration of the α2-AR antagonist rauwolscine or the AT1 receptor antagonist losartan alone failed to alter the ARNA responses to reflex increases in ERSNA. Likewise, renal pelvic release of substance P produced by 250 pM NE (from 8.0 ± 1.3 to 8.5 ± 1.6 pg/min) was not affected by rauwolscine or losartan alone. However, rauwolscine+losartan enhanced the ARNA responses to reflex increases in ERSNA (4,680 ± 1,240%·s), and renal pelvic release of substance P by 250 pM NE, from 8.3 ± 0.6 to 14.2 ± 0.8 pg/min. During a high-sodium diet, rauwolscine had no effect on the ARNA response to reflex increases in ERSNA or renal pelvic release of substance P produced by NE. Losartan was not examined because of low endogenous ANG II levels in renal pelvic tissue during a high-sodium diet. Increased activation of α2-AR contributes to the reduced interaction between ERSNA and ARNA during low-sodium intake, whereas no/minimal activation of α2-AR contributes to the enhanced ERSNA-ARNA interaction under conditions of high sodium intake.

Renal nerve effects on renal adaptation to changes in sodium intake during ovine pregnancy

1992 ◽  
Vol 262 (5) ◽  
pp. F823-F829
Author(s):  
G. W. Aberdeen ◽  
S. C. Cha ◽  
S. Mukaddam-Daher ◽  
B. S. Nuwayhid ◽  
E. W. Quillen
Keyword(s):  
Steady State ◽  
Sodium Intake ◽  
Urinary Sodium Excretion ◽  
Renal Nerves ◽  
Renal Nerve ◽  
High Sodium ◽  
Low Sodium ◽  
Pregnant Sheep ◽  
Urinary Potassium ◽  
Renal Nerve Activity

To assess the possibility of an enhanced role of renal nerves in the control of urinary sodium excretion (UNaV) and fluid homeostasis during pregnancy, urine output, UNaV, and urinary potassium excretion were assessed hourly for 3 days before and for 6 days after a step reduction in total daily sodium intake from 400 to 40 mmol. Studies were performed in normal conscious sheep (4 nonpregnant and 4 pregnant). Each animal was prepared with a divided bladder so that urine could be collected simultaneously from one normally innervated and one denervated kidney. In nonpregnant ewes, ratios of the rates of excretion by denervated vs. innervated kidneys for UNaV averaged 1.00 +/- 0.07 under steady-state conditions at high levels of sodium intake. This ratio was not different at the low-sodium-intake state. In contrast, this ratio was 1.15 +/- 0.07 at high sodium intake and 1.13 +/- 0.03 at low sodium intake in pregnant ewes. The ratios at both steady-state intake levels were different (P less than 0.05) between nonpregnant and pregnant sheep. During the transition between sodium intake states, these ratios were unchanged in nonpregnant animals, whereas pregnant animals exhibited peak ratios of 2.20 +/- 0.39 (P less than 0.05), indicating sodium wasting by the denervated kidneys. In summary, the data suggest that renal nerve activity may not be completely suppressed by high sodium intakes in pregnant sheep. Furthermore, the renal nerves have an enhanced influence on sodium conservation during and after the transition from high- to low-sodium-intake states during pregnancy.(ABSTRACT TRUNCATED AT 250 WORDS)

Decreased Plasma Renin Activity and Renin Release in Rats with Phaeochromocytoma

1977 ◽  
Vol 53 (5) ◽  
pp. 447-452
Author(s):  
J. C. S. Fray ◽  
P. V. H. Mayer
Keyword(s):  
Sodium Chloride ◽  
Plasma Renin Activity ◽  
Perfusion Pressure ◽  
Plasma Renin ◽  
Renin Activity ◽  
Renin Release ◽  
High Sodium ◽  
Sodium Chloride Loading ◽  
And Control ◽  
Renin Content

1. We have examined the response of renin to chronic low and high sodium chloride intake in rats with transplanted phaeochromocytoma. 2. Phaeochromocytoma suppressed the usual elevated plasma renin activity observed during sodium deprivation. 3. Studies in isolated perfused kidneys indicated that sodium-deprived phaeochromocytoma rats released substantially less renin than sodium-deprived control rats despite an almost identical renal renin content in both sets of animals. In addition, low perfusion pressure (50 mmHg) failed to stimulate renin release in kidneys from these phaeochromocytoma rats. 4. Additional experiments demonstrated that chronic sodium chloride loading suppressed plasma renin activity, renin content and renin release in both phaeochromocytoma and control rats. Both sodium-loaded phaeochromocytoma and sodium-loaded control rats were unresponsive to low perfusion pressure. 5. We conclude that noradrenaline-secreting phaeochromocytoma impairs the response of plasma renin activity in the rat by inhibiting renin release. We also conclude that chronic sodium chloride loading has a similar effect, but the mechanisms remain to be determined.

Influence of dietary sodium on renin activity and arterial pressure during anesthesia

1976 ◽  
Vol 231 (4) ◽  
pp. 1185-1190 ◽  
Author(s):  
JC Fray ◽  
LG Siwek ◽  
WM Strull ◽  
RN Steller ◽  
JM Wilson
Keyword(s):  
Arterial Pressure ◽  
Enzyme Inhibitor ◽  
Surgical Stress ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Renin Activity ◽  
Dietary Sodium ◽  
Control Value ◽  
Low Sodium ◽  
Anesthetized Dogs

The effect of pentobarbital anesthesia on plasma renin activity (PRA) and mean arterial pressure (MAP) was studied in chronically catheterized dogs maintained on normal or low-sodium intake. Within 1 min of administration, pentobarbital caused a rapid fall in MAP which was followed by a restoration of MAP toward control within 5 min. Thirty minutes after induction of anesthesia, PRA was unchanged in sodium-replete dogs and elevated two-fold in sodium-depleted dogs. MAP was significantly lowered (20 mmHg) in normal salt dogs and only slightly decreased in low-salt dogs 30 min after pentobarbital. MAP returned to preanesthetic control value in dogs given converting enzyme inhibitor before anesthesia. Surgical stress or cutaneous electrical stimulation causey hexamethonium. These results indicate that change in PRA and MAP of pentobarbital-anesthetized dogs is significantly influenced by the sodium intake of the animal and by the degree of surgical stress.

scholarly journals Role of the renin-angiotensin system during alterations of sodium intake in conscious mice

2001 ◽  
Vol 281 (3) ◽  
pp. R987-R993 ◽  
Author(s):  
Brian C. Cholewa ◽  
David L. Mattson
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sodium Level ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Ang Ii ◽  
Plasma Renin Concentration ◽  
Renin Angiotensin ◽  
High Sodium ◽  
Low Sodium

The present studies were performed to quantify circulating components of the renin-angiotensin-aldosterone axis and to determine the functional importance of this system during alterations in sodium intake in conscious mice. Increasing sodium intake from ∼200 to 1,000 μeq/day significantly decreased plasma renin concentration from 472 ± 96 to 304 ± 83 ng ANG I · ml−1 · h−1( n = 5) but did not alter plasma renin activity from the low-sodium level of 7.7 ± 1.1 ng ANG I · ml−1 · h−1. Despite the elevated plasma renin concentration, plasma ANG II in mice on low-sodium level averaged 14 ± 3 pg/ml and was significantly suppressed to 6 ± 1 pg/ml by high-sodium intake ( n = 7). Consistent with the modulation of ANG II, plasma aldosterone significantly decreased from 41 ± 8 to 8 ± 3 ng/dl when sodium intake was elevated ( n = 6). In a final set of experiments, the continuous infusion of ANG II (20 ng · kg−1 · min−1) led to a mild salt-sensitive increase in mean arterial pressure from 108 ± 2 to 131 ± 2 mmHg as sodium intake was varied from low to high ( n = 7). In vehicle-infused mice, mean arterial pressure was unaltered from 109 ± 2 mmHg when sodium intake was increased ( n = 6). These studies indicate that the physiological suppression of circulating ANG II may be required to maintain a constancy of arterial pressure during alterations in sodium intake in normal mice.

Abstract P252: The Effects of Sodium Reduction on Metabolism and Thirst

Circulation ◽  
2018 ◽  
Vol 137 (suppl_1) ◽  
Author(s):  
Stephen P Juraschek ◽  
Edgar R Miller ◽  
Alexander Chang ◽  
Cheryl Anderson ◽  
John E Hall ◽  
...  
Keyword(s):  
Energy Intake ◽  
Sodium Excretion ◽  
Sodium Intake ◽  
Control Diet ◽  
Urine Volume ◽  
Plasma Renin ◽  
Urine Osmolality ◽  
High Sodium ◽  
Low Sodium ◽  
Serum Aldosterone

Background: Recent studies challenge the traditional understanding of sodium physiology. Some animal studies suggest that high sodium intake may induce catabolism, leading to weight loss. Other studies suggest that high sodium intake might reduce, rather than increase, thirst. Hypothesis: Higher sodium intake increases thirst, fluid intake, and sodium excretion without altering energy intake or lowering weight. Methods: In the DASH-Sodium feeding study, adults with pre- or stage 1 hypertension without antihypertensive medications, were randomly assigned to the DASH diet or a control diet. On their assigned diet, participants consumed each of three sodium levels for 4 weeks (randomized crossover design). Participants were provided all meals, but could drink water freely. Throughout the trial, calorie intake was adjusted to keep weight constant. The three sodium levels (at 2100 kcal/d) were: low (1150 mg), medium (2300 mg), and high (3450 mg). Weight, energy intake, self-reported thirst, urine volume, plasma renin, serum aldosterone, urine osmolality, and urine sodium excretion were assessed at the end of each period. Results: Among 412 participants (57% women, 57% black, mean age 48 yrs), weight increased slightly with higher sodium on the control diet, but not the DASH diet; energy intake did not vary across sodium levels in both diets ( P -trends > 0.34) ( Table ). In contrast, participants reported more thirst with high vs low sodium (both diets P -trends < 0.001) and potentially higher fluid intake (urine volume) during the control diet (1,566 vs 1,491 ml on high vs low sodium; P -trend = 0.07). On both diets, plasma renin and serum aldosterone were lower with higher sodium (each P -trend < 0.001). Likewise, both urine osmolality and sodium excretion were higher with higher sodium intake (all P -trends < 0.001). Conclusions: Higher sodium intake did not alter energy intake, but did increase thirst and sodium excretion. These findings are consistent with the traditional understanding of the physiology of excess dietary sodium intake.

Pressure-dependent renin release: effects of sodium intake and changes of total body sodium

1999 ◽  
Vol 277 (2) ◽  
pp. R548-R555 ◽  
Author(s):  
Erdmann Seeliger ◽  
Katrin Lohmann ◽  
Benno Nafz ◽  
Pontus B. Persson ◽  
H. Wolfgang Reinhardt
Keyword(s):  
Sodium Intake ◽  
Plasma Renin ◽  
Renal Perfusion ◽  
Renin Release ◽  
Response Curves ◽  
Exponential Relationship ◽  
High Sodium ◽  
Body Sodium ◽  
Total Body ◽  
The Impact

The impact of sodium intake and changes in total body sodium (TBS) for the setting of pressure-dependent renin release (PDRR) was studied in freely moving dogs. An aortic cuff allowed servo control of renal perfusion pressure (RPP) at preset values. Protocols were 1) high sodium intake (HSI), 2) low sodium intake (LSI), 3) TBS moderately increased (+3.1 mmol Na/kg body wt) by 20% reduction of RPP for 2–4 days, 4) large increase of TBS (+8.2) by combining protocol 3 with aldosterone infusion, and 5) TBS reduced (−3.1) by peritoneal dialyses. Twenty-four-hour time courses of arterial plasma renin activity (PRA) revealed that LSI increased PRA for the first 10 h only; afterward PRA did not differ between LSI and HSI. Reduced TBS increased PRA constantly, and the large increase of TBS constantly reduced PRA. PDRR stimulus-response curves (assessed 20 h after last sodium intake) revealed an exponential relationship in each protocol. PDRR was not changed by different sodium intake. Conversely, reduced TBS increased PDRR markedly, whereas the large increase of TBS suppressed it. Thus an inverse relationship between TBS and PRA, i.e., a TBS-dependent renin release, was found. This relationship was enhanced by decreasing RPP. This interplay between TBS-dependent renin release and PDRR allows the organism a differentiated reaction to changes in TBS and arterial pressure.

Neurogenic regulation of rate of achieving sodium balance after increasing sodium intake

1991 ◽  
Vol 261 (2) ◽  
pp. F300-F307 ◽  
Author(s):  
S. G. Greenberg ◽  
S. Tershner ◽  
J. L. Osborn
Keyword(s):  
Sodium Intake ◽  
Plasma Renin ◽  
Sympathetic Nerves ◽  
Urinary Sodium Excretion ◽  
Significant Inhibition ◽  
Sodium Balance ◽  
Renal Nerves ◽  
High Sodium ◽  
Low Sodium ◽  
Renal Tubular

Evidence that the renal sympathetic nerves have direct effects on renal tubular function suggests that neurogenic mechanisms may play an important role in the daily regulation of sodium balance. We evaluated the influence of the renal nerves on the rate of elevating urinary sodium excretion (UNaV) after a step increase in fixed sodium intake. Conscious rats with innervated (INN) or denervated (DNX) kidneys were placed on low-sodium intake (LNa = 0.3 meq/day) or a normal sodium intake (NNa = 1.0 meq/day) by intravenous infusion. Hourly changes in UNaV were determined 24 h before and 72 h after increasing sodium intake to either NNa or high-sodium intake (HNa = 5.0 meq/day). Switching from LNa to NNa, INN rats increased UNaV within 24 h; however, DNX rats did not begin to increase UNaV until hour 60. Cumulative sodium balance over 72 h was more positive in DNX rats (INN = 1.29 +/- 0.29 meq; DNX = 2.06 +/- 0.21 meq, P less than 0.05). During the LNa-to-HNa switch, both INN and DNX rats increased UNaV equally for 12 h; however, at this time INN rats continued to increase UNaV, whereas DNX rats did not. DNX rats had a net accumulation of 2.54 meq more sodium than INN rats over 72 h. Significant inhibition of plasma renin activity within the first 24 h occurred only in rats receiving the LNa-to-HNa switch in sodium intake, and this response was not different between rats with innervated and denervated kidneys. These data suggest that the renal nerves provide a rapid sodium excretory response to step increases in sodium intake.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of linoleic acid infusion on blood pressure in normotensive and hypertensive rats

1989 ◽  
Vol 257 (2) ◽  
pp. H611-H617 ◽  
Author(s):  
S. R. Reddy ◽  
R. Talwalkar ◽  
J. Downs ◽  
T. A. Kotchen
Keyword(s):  
Blood Pressure ◽  
Linoleic Acid ◽  
Sodium Chloride ◽  
Enzymatic Activity ◽  
Plasma Renin ◽  
Sprague Dawley ◽  
Acid Infusion ◽  
High Sodium ◽  
Hypotensive Response

High dietary intake of linoleic acid lowers arterial pressure, and, in vitro, linoleic acid inhibits the enzymatic activity of renin. The purpose of the present study was 1) to evaluate the effect of intravenous infusion of linoleic acid on blood pressure in normotensive and hypertensive Sprague-Dawley rats and 2) to determine whether the hypotensive response to linoleic acid infusion is caused by inhibition of circulating renin. Blood pressure was decreased (P less than 0.01) by linoleic acid infusion in normotensive sodium chloride-deprived animals and in animals with two-kidney, one-clip hypertension. In contrast, linoleic acid infusion did not affect blood pressure in normotensive rats on a "normal" or high sodium chloride intake, in rats with deoxycorticosterone acetate (DOCA)-salt hypertension, and in anephric rats. In sodium chloride-deprived rats, the reduction of blood pressure by linoleic acid infusion was associated with increased plasma renin activity (P less than 0.05); serum angiotensin-converting enzyme activity was unchanged. The in vitro enzymatic activity of exogenous renin in plasma of anephric rats was not affected by linoleic acid infusion. In two-kidney, one-clip hypertensive animals, pretreatment with indomethacin did not alter the hypotensive response to linoleic acid. Thus, although linoleic acid infusion lowered blood pressure in high renin but not in low renin states, the reduction of blood pressure was not related to inhibition of circulating renin or to alterations of endogenous prostaglandin biosynthesis.

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