Hormonal and Neural Mechanisms of Sodium Appetite

Physiology ◽  
1986 ◽  
Vol 1 (2) ◽  
pp. 51-54 ◽  
Author(s):  
MJ Fregly ◽  
NE Rowland
Keyword(s):  
Sodium Content ◽  
Neural Mechanisms ◽  
Sodium Balance ◽  
Salt Appetite ◽  
Sodium Appetite ◽  
Complex Mechanisms

A strong appetite for salt seems to be a normal link in the complex mechanisms that serve to maintain a normal sodium content of the organism. Experiments with rats have helped to unravel many aspects of the endocrine mechanisms that are involved in regulating sodium balance and salt appetite, but more work is needed to understand the mechanisms that induce salt appetite in different species.

scholarly journals Sodium Imbalance in Mice Results Primarily in Compensatory Gene Regulatory Responses in Kidney and Colon, but Not in Taste Tissue

Nutrients ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 995 ◽  
Author(s):  
Kristina Lossow ◽  
Wolfgang Meyerhof ◽  
Maik Behrens
Keyword(s):  
Prolonged Exposure ◽  
Bitter Taste ◽  
Sodium Content ◽  
Dietary Sodium ◽  
Salt Appetite ◽  
Dietary Salt ◽  
Sodium Homeostasis ◽  
Salt Taste ◽  
Sodium Appetite

Renal excretion and sodium appetite provide the basis for sodium homeostasis. In both the kidney and tongue, the epithelial sodium channel (ENaC) is involved in sodium uptake and sensing. The diuretic drug amiloride is known to block ENaC, producing a mild natriuresis. However, amiloride is further reported to induce salt appetite in rodents after prolonged exposure as well as bitter taste impressions in humans. To examine how dietary sodium content and amiloride impact on sodium appetite, mice were subjected to dietary salt and amiloride intervention and subsequently analyzed for ENaC expression and taste reactivity. We observed substantial changes of ENaC expression in the colon and kidney confirming the role of these tissues for sodium homeostasis, whereas effects on lingual ENaC expression and taste preferences were negligible. In comparison, prolonged exposure to amiloride-containing drinking water affected β- and αENaC expression in fungiform and posterior taste papillae, respectively, next to changes in salt taste. However, amiloride did not only change salt taste sensation but also perception of sucrose, glutamate, and citric acid, which might be explained by the fact that amiloride itself activates bitter taste receptors in mice. Accordingly, exposure to amiloride generally affects taste impression and should be evaluated with care.

Angiotensin and salt appetite of BALB/c mice

1990 ◽  
Vol 259 (4) ◽  
pp. R729-R735 ◽  
Author(s):  
D. A. Denton ◽  
J. R. Blair-West ◽  
M. McBurnie ◽  
P. G. Osborne ◽  
E. Tarjan ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Sodium Content ◽  
Neural Systems ◽  
Salt Appetite ◽  
Nacl Solution ◽  
Sodium Appetite ◽  
Daily Water Intake ◽  
Body Sodium ◽  
Daily Water ◽  
Ingestive Behaviors

The influence of systemic or intracerebroventricular (icv) administration of angiotensin II on the intakes of NaCl solution, water, and food was investigated in BALB/c mice. Systemic administration of angiotensin II had little, if any, influence on these ingestive behaviors. On the other hand, icv infusion of angiotensin II at 70 ng/day increased (P less than 0.05) intakes of NaCl solution and water by the third day of infusion. The amount of NaCl ingested daily during the infusion was two to three times body sodium content. The mean daily water intake increased to 40-60% of body weight. The vast increase in NaCl intake was not secondary to a natriuresis caused by the icv infusion of angiotensin II. The results suggest that angiotensin II has a direct effect on neural systems involved in sodium appetite in this species.

Basal Activity of the Natriuretic Factor Extracted from the Rat Kidney as a Function of the Diet and its Role in the Regulation of the Acute Sodium Balance

1980 ◽  
Vol 58 (5) ◽  
pp. 385-391 ◽  
Author(s):  
F. Louis ◽  
H. Favre
Keyword(s):  
Sodium Intake ◽  
Rat Kidney ◽  
Extracellular Volume ◽  
Gel Filtration ◽  
Kidney Tissue ◽  
Weight Fraction ◽  
Sodium Content ◽  
Sodium Balance ◽  
Low Molecular Weight ◽  
Extracellular Volume Expansion

1. The effect of the sodium content of the diet on the natriuretic activity of an extract from the kidneys was studied in non-expanded and volume-expanded rats. 2. The kidney tissue was homogenized and the supernatant fractionated by gel filtration on Sephadex G-25. A single low-molecular-weight fraction eluted after the salt possessed the natriuretic activity and was tested on a rat bioassay. 3. The natriuretic activity of the fraction obtained from the kidneys of non-expanded rats was related to the sodium intake. 4. After an acute extracellular volume expansion, the natriuretic activity obtained from the fraction extracted from the kidneys was much greater than before expansion and was related to the dietary intake of sodium.

scholarly journals Parabrachial and hypothalamic interaction in sodium appetite

2011 ◽  
Vol 300 (5) ◽  
pp. R1091-R1099 ◽  
Author(s):  
S. Dayawansa ◽  
S. Peckins ◽  
S. Ruch ◽  
R. Norgren
Keyword(s):  
Weight Loss ◽  
Lateral Hypothalamus ◽  
Ibotenic Acid ◽  
The Other ◽  
Salt Appetite ◽  
Sodium Depletion ◽  
Sodium Appetite ◽  
Parabrachial Nuclei ◽  
Bilateral Lesions

Rats with bilateral lesions of the lateral hypothalamus (LH) fail to exhibit sodium appetite. Lesions of the parabrachial nuclei (PBN) also block salt appetite. The PBN projection to the LH is largely ipsilateral. If these deficits are functionally dependent, damaging the PBN on one side and the LH on the other should also block Na appetite. First, bilateral ibotenic acid lesions of the LH were needed because the electrolytic damage used previously destroyed both cells and axons. The ibotenic LH lesions produced substantial weight loss and eliminated Na appetite. Controls with ipsilateral PBN and LH lesions gained weight and displayed robust sodium appetite. The rats with asymmetric PBN-LH lesions also gained weight, but after sodium depletion consistently failed to increase intake of 0.5 M NaCl. These results dissociate loss of sodium appetite from the classic weight loss after LH damage and prove that Na appetite requires communication between neurons in the LH and the PBN.

scholarly journals Neuronal (pro)renin receptor regulates deoxycorticosterone-induced sodium intake

2018 ◽  
Vol 50 (10) ◽  
pp. 904-912 ◽  
Author(s):  
Fatima Trebak ◽  
Wencheng Li ◽  
Yumei Feng
Keyword(s):  
Sodium Intake ◽  
Renin Angiotensin System ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Sodium Balance ◽  
Total Fluid Intake ◽  
Sodium Deficiency ◽  
Sodium Appetite ◽  
The Central Nervous System ◽  
Salt Sensitive Hypertension

Increased sodium appetite is a physiological response to sodium deficiency; however, it has also been implicated in disease conditions such as congestive heart failure, kidney failure, and salt-sensitive hypertension. The central nervous system is the major regulator of sodium appetite and intake behavior; however, the neural mechanisms underlying this behavior remain incompletely understood. Here, we investigated the involvement of the (pro)renin receptor (PRR), a component of the brain renin-angiotensin system, in the regulation of sodium intake in a neuron-specific PRR knockout (PRRKO) mouse model generated previously in our laboratory. Sodium intake following deoxycorticosterone (DOCA) stimulation was tested by assessing the preference of mice for 0.9% saline or regular water in single-animal metabolic cages. Blood pressure was monitored in conscious, freely moving mice by a telemetry system. We found that saline intake and total fluid intake were significantly reduced in PRRKO mice following DOCA treatment compared with that in wild-type (WT) mice, whereas regular water intake was similar between the genotypes. Sodium preference and total sodium intake were significantly reduced in PRRKO mice compared with WT mice. PRRKO mice also excreted less urine and urinary sodium compared with WT mice following DOCA treatment, whereas potassium excretion was similar between the two groups. Finally, we found that the sodium balance, calculated by subtracting urinary sodium excretion from sodium intake, was greater in WT mice than in PRRKO mice. Collectively, these findings suggest that the neuronal PRR plays a regulatory role in DOCA-induced sodium intake.

Amiloride-sensitive sodium channels and expression of sodium appetite in rats

1987 ◽  
Vol 253 (2) ◽  
pp. R371-R374 ◽  
Author(s):  
I. L. Bernstein ◽  
C. J. Hennessy
Keyword(s):  
Sodium Channels ◽  
Transport System ◽  
Sodium Transport ◽  
Taste Bud ◽  
Sodium Balance ◽  
Gustatory System ◽  
Sodium Appetite ◽  
Amiloride Hydrochloride

Lingual application of amiloride hydrochloride blocks a sodium transport system in the mammalian gustatory system. Effects of exposure to amiloride on subsequent licking for 3% NaCl by rats were found to differ as a function of the animal's sodium balance. Licking for 3% NaCl was significantly increased in sodium-replete rats and significantly decreased in sodium-deplete rats by amiloride pretreatment. In fact, expression of sodium appetite was virtually eliminated by pretreatment with amiloride. This suggests that the recognition of sodium solutions in animals with a sodium deficit is dependent on amiloride-sensitive sodium transport at the taste bud.

Role of renal nerves in sodium depletion-induced salt appetite

1996 ◽  
Vol 271 (3) ◽  
pp. R806-R812 ◽  
Author(s):  
R. L. Thunhorst ◽  
R. F. Kirby ◽  
A. K. Johnson
Keyword(s):  
Enzyme Inhibitor ◽  
Sodium Intake ◽  
Extracellular Fluid ◽  
Sodium Balance ◽  
Renal Nerves ◽  
Salt Appetite ◽  
Subcutaneous Injections ◽  
Intact Control ◽  
Water And Sodium Excretion

The ingestion of water and 0.3 M NaCl solution and the secretion of key hormones were studied in groups of intact and bilaterally renal-denervated rats after extracellular fluid depletion. Hypovolemia with mild hypotension was produced by subcutaneous injections of the diuretic furosemide (10 mg/kg) followed by injections of the angiotensin-converting enzyme inhibitor captopril (5 mg/kg s.c.). Denervated rats drank significantly less of a concentrated saline solution in response to depletion than intact control rats did, but drank similar amounts of water. Denervated rats finished testing in significantly greater negative water and sodium balance compared with controls. Renal denervation did not impair the secretion of renin and aldosterone or the formation of angiotensin I. The diminished sodium intake of denervated rats is not attributable to reduced water and sodium excretion in response to the hypovolemic protocol. These results indicate that the integrity of the renal nerves is important for the normal elaboration of salt appetite in response to hypovolemia/hypotension.

Brain vasopressin and sodium appetite

2002 ◽  
Vol 282 (4) ◽  
pp. R1236-R1244 ◽  
Author(s):  
Francis W. Flynn ◽  
Thomas R. Kirchner ◽  
Margaret E. Clinton
Keyword(s):  
Receptor Antagonist ◽  
Salt Intake ◽  
Antagonistic Activity ◽  
Intraventricular Injection ◽  
Salt Appetite ◽  
Sucrose Intake ◽  
Dramatic Decrease ◽  
Sodium Appetite ◽  
Arterial Blood ◽  
Intraventricular Injections

Intraventricular injections of vasopressin (VP) and antagonists with varying degrees of specificity for the VP receptors were used to identify the action of endogenous brain VP on 0.3 M NaCl intake by sodium-deficient rats. Lateral ventricular injections of 100 ng and 1 μg VP caused barrel rotations and a dramatic decrease in NaCl intake by sodium-deficient rats and suppressed sucrose intake. Intraventricular injection of the V1/V2 receptor antagonist [d(CH2)5 1,O-Et-Tyr2,Val4, Arg8]VP and the V1 receptor antagonist [d(CH2)5 1,O-Me-Tyr2,Arg8]VP (MeT-AVP) significantly suppressed NaCl intake by sodium-deficient rats without causing motor disturbances. MeT-AVP had no effect on sucrose intake (0.1 M). In contrast, the selective V2 receptor antagonist had no significant effect on NaCl intake. Last, injections of 100 ng MeT-AVP decreased mean arterial blood pressure (MAP), whereas 100 ng VP elevated MAP and pretreatment with MeT-AVP blocked the pressor effect of VP. These results indicate that the effects produced by 100 ng MeT-AVP represent receptor antagonistic activity. These findings suggest that the effect of exogenous VP on salt intake is secondary to motor disruptions and that endogenous brain VP neurotransmission acting at V1 receptors plays a role in the arousal of salt appetite.

scholarly journals Distinct neural mechanisms for the control of thirst and salt appetite in the subfornical organ

2016 ◽  
Vol 20 (2) ◽  
pp. 230-241 ◽  
Author(s):  
Takashi Matsuda ◽  
Takeshi Y Hiyama ◽  
Fumio Niimura ◽  
Taiji Matsusaka ◽  
Akiyoshi Fukamizu ◽  
...  
Keyword(s):  
Subfornical Organ ◽  
Neural Mechanisms ◽  
Salt Appetite

Role of renal nerves in renal sodium retention of nephrotic syndrome

1989 ◽  
Vol 256 (5) ◽  
pp. F823-F829 ◽  
Author(s):  
P. J. Herman ◽  
L. L. Sawin ◽  
G. F. DiBona
Keyword(s):  
Nephrotic Syndrome ◽  
Renal Denervation ◽  
Sodium Content ◽  
Vehicle Control ◽  
Dietary Sodium ◽  
Sodium Balance ◽  
Renal Nerves ◽  
Sodium Retention ◽  
Edema Formation

To define the role of the renal nerves in the renal sodium retention of the nephrotic syndrome, experiments were conducted in rats given adriamycin to produce nephrotic syndrome. All rats developed proteinuria and hypoalbuminemia and exhibited edema formation. Adriamycin-injected nephrotic rats were subjected to bilateral renal denervation (ADRIADNX) or sham renal denervation (ADRIASHAM). Rats injected with adriamycin vehicle were subjected to bilateral renal denervation (DNX) or sham renal denervation (SHAM). Metabolic balance studies were carried out in all rats beginning on the 8th day after bilateral or sham renal denervation. Dietary sodium content was 210 meq/kg Na on days 8-12 and days 24-26 and was 10 meq/kg Na on days 13-23. Nephrotic rats demonstrated significantly greater overall (19 days) cumulative sodium balance than vehicle control rats, ADRIASHAM 8.47 +/- 0.81 vs. SHAM 5.74 +/- 0.34 meq Na, P less than 0.01. Bilateral renal denervation did not significantly affect overall cumulative sodium balance in the vehicle control rats, DNX 6.15 +/- 0.71 vs. SHAM 5.74 +/- 0.34 meq Na. However, bilateral renal denervation significantly decreased overall cumulative sodium balance in the nephrotic rats, ADRIADNX 6.59 +/- 0.56 vs. ADRIASHAM 8.47 +/- 0.81 meq Na, P less than 0.01. Results indicated that the increased renal sodium retention characteristic of nephrotic syndrome is dependent, in large part, on increased efferent renal sympathetic nerve activity.

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