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.

Amiloride sensitivity of chorda tympani response to NaCl in Fischer 344 and Wistar rats

1991 ◽  
Vol 261 (2) ◽  
pp. R329-R333 ◽  
Author(s):  
I. L. Bernstein ◽  
A. Longley ◽  
E. M. Taylor
Keyword(s):  
Sodium Transport ◽  
Wistar Rats ◽  
Strain Differences ◽  
Chorda Tympani ◽  
Gustatory System ◽  
Electrophysiological Response ◽  
Fischer 344 ◽  
Electrophysiological Responses ◽  
Before And After ◽  
Amiloride Hydrochloride

Fischer 344 (F-344) rats fail to prefer NaCl solutions to water at any concentration and avoid NaCl solutions preferred by other strains, including Wistar rats. Behavioral and electrophysiological responses of the mammalian gustatory system to NaCl have been shown to depend on a sodium transport system that is specifically blocked by lingual application of the sodium-transport blocker amiloride. The present study examined whether strain differences exist between F-344 and Wistar rats in the amiloride sensitivity of the chorda tympani (CT) electrophysiological response to NaCl. Whole nerve CT recordings were obtained from adult F-344 and Wistar rats during chemical stimulation of the anterior tongue. Responses to NaCl solutions ranging from 0.01 to 1.0 M were examined both before and after pretreatment with amiloride hydrochloride. Integrated whole nerve responses to NaCl solutions were expressed relative to the response to 0.5 M NH4Cl. Strain differences in the response to NaCl solutions emerged, with F-344 animals showing a significantly larger amplitude of the tonic response to NaCl, relative to NH4Cl, than Wistars. F-344 rats were also more sensitive to the sodium-channel blocker amiloride. These results suggest that strain differences in amiloride sensitive signals mediated by the CT nerve may contribute to the NaCl aversion displayed by F-344 rats.

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.

Disorders of Water and Sodium Balance: Hyponatremia

2019 ◽  
Author(s):  
Danilea M. Carmona Matos ◽  
Herbert Chen
Keyword(s):  
Antidiuretic Hormone ◽  
Sodium Transport ◽  
Clinical Manifestations ◽  
Electrolyte Imbalance ◽  
Renal Physiology ◽  
Sodium Balance ◽  
Electrolyte Balance ◽  
Clear Understanding ◽  
Drug Induced ◽  
Clinical Scenarios

Disorders of water and sodium balance are common in clinical practice. To better assess them, we must have a clear understanding of water-electrolyte homeostasis and renal function. The following review goes over practical equations necessary for electrolyte balance analysis as well as the foundations of renal physiology. Emphasis is placed on the understanding of sodium transport and its physiologic and pharmacologic regulation. In addition, we explore the most common electrolyte imbalance affecting up to 28% of hospitalized patients: hyponatremia (ie, low sodium concentration). Hyponatremia has been found in several acute and chronic clinical scenarios including postoperative, drug-induced, and exercise-associated hyponatremia. However, it is not uncommon to find this disorder coexisting with other diseases such as syndrome of inappropriate secretion of antidiuretic hormone (SIADH), acquired immunodeficiency syndrome (AIDS), cancer, and in rare cases, hypothyroidism. To better understand this disorder, the etiology, diagnosis with clinical manifestations and laboratory values, and treatment options are explored. This review contains 9 figures, 6 tables, and 52 references. Key Words: aldosterone, antidiuretic hormone, body fluids, electrolyte balance, hyponatremia, hypovolemia, osmolality, sodium transport, vasopressin

Disorders of Water and Sodium Balance: Hyponatremia

2019 ◽  
Author(s):  
Danilea M. Carmona Matos ◽  
Herbert Chen
Keyword(s):  
Antidiuretic Hormone ◽  
Sodium Transport ◽  
Clinical Manifestations ◽  
Electrolyte Imbalance ◽  
Renal Physiology ◽  
Sodium Balance ◽  
Electrolyte Balance ◽  
Clear Understanding ◽  
Drug Induced ◽  
Clinical Scenarios

Disorders of water and sodium balance are common in clinical practice. To better assess them, we must have a clear understanding of water-electrolyte homeostasis and renal function. The following review goes over practical equations necessary for electrolyte balance analysis as well as the foundations of renal physiology. Emphasis is placed on the understanding of sodium transport and its physiologic and pharmacologic regulation. In addition, we explore the most common electrolyte imbalance affecting up to 28% of hospitalized patients: hyponatremia (ie, low sodium concentration). Hyponatremia has been found in several acute and chronic clinical scenarios including postoperative, drug-induced, and exercise-associated hyponatremia. However, it is not uncommon to find this disorder coexisting with other diseases such as syndrome of inappropriate secretion of antidiuretic hormone (SIADH), acquired immunodeficiency syndrome (AIDS), cancer, and in rare cases, hypothyroidism. To better understand this disorder, the etiology, diagnosis with clinical manifestations and laboratory values, and treatment options are explored. This review contains 9 figures, 6 tables, and 52 references. Key Words: aldosterone, antidiuretic hormone, body fluids, electrolyte balance, hyponatremia, hypovolemia, osmolality, sodium transport, vasopressin

Disorders of Water and Sodium Balance: Hyponatremia

2019 ◽  
Author(s):  
Danilea M. Carmona Matos ◽  
Herbert Chen
Keyword(s):  
Antidiuretic Hormone ◽  
Sodium Transport ◽  
Clinical Manifestations ◽  
Electrolyte Imbalance ◽  
Renal Physiology ◽  
Sodium Balance ◽  
Electrolyte Balance ◽  
Clear Understanding ◽  
Drug Induced ◽  
Clinical Scenarios

Disorders of water and sodium balance are common in clinical practice. To better assess them, we must have a clear understanding of water-electrolyte homeostasis and renal function. The following review goes over practical equations necessary for electrolyte balance analysis as well as the foundations of renal physiology. Emphasis is placed on the understanding of sodium transport and its physiologic and pharmacologic regulation. In addition, we explore the most common electrolyte imbalance affecting up to 28% of hospitalized patients: hyponatremia (ie, low sodium concentration). Hyponatremia has been found in several acute and chronic clinical scenarios including postoperative, drug-induced, and exercise-associated hyponatremia. However, it is not uncommon to find this disorder coexisting with other diseases such as syndrome of inappropriate secretion of antidiuretic hormone (SIADH), acquired immunodeficiency syndrome (AIDS), cancer, and in rare cases, hypothyroidism. To better understand this disorder, the etiology, diagnosis with clinical manifestations and laboratory values, and treatment options are explored. This review contains 9 figures, 6 tables, and 52 references. Key Words: aldosterone, antidiuretic hormone, body fluids, electrolyte balance, hyponatremia, hypovolemia, osmolality, sodium transport, vasopressin

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.

Activation and Supply of Channels and Pumps by Aldosterone

Physiology ◽  
1996 ◽  
Vol 11 (3) ◽  
pp. 126-133
Author(s):  
F Verrey ◽  
J Beron
Keyword(s):  
Sodium Channels ◽  
Sodium Transport ◽  
Sodium Reabsorption ◽  
Transcription Rate ◽  
Gene Products ◽  
Glucocorticoid Hormones ◽  
Early Activation ◽  
A Cell ◽  
Later Phase

Mineralocorticoid and glucocorticoid hormones stimulate sodium reabsorption across target epithelia by modulating the transcription rate of a cell-specific set of genes. Unidentified regulated gene products mediate an early activation of preexisting sodium channels and pumps. In a later phase, the supply of proteins belonging to the sodium-transport machinery is increased.

Changes in Leucocyte Sodium Transport with Alterations in Sodium balance: A Qualitative Difference in Normotensive Relatives of Hypertensives Compared to Controls

1984 ◽  
Vol 67 (s9) ◽  
pp. 39P-40P
Author(s):  
A.M. Heagerty ◽  
A. El-Ashry ◽  
R. Bradlaugh ◽  
R.F. Bing ◽  
H. Thurston ◽  
...  
Keyword(s):  
Sodium Transport ◽  
Qualitative Difference ◽  
Sodium Balance

Modulation of epithelial Na+ channel activity by long-chain n–3 fatty acids

2004 ◽  
Vol 287 (4) ◽  
pp. F850-F855 ◽  
Author(s):  
Frédérique Mies ◽  
Vadim Shlyonsky ◽  
Arnaud Goolaerts ◽  
Sarah Sariban-Sohraby
Keyword(s):  
Fatty Acids ◽  
Sodium Channels ◽  
Sodium Transport ◽  
Open Circuit ◽  
Na Channel ◽  
Open Probability ◽  
Endogenous Factors ◽  
Excised Patches ◽  
Apical Membranes

The epithelial sodium channel is found in apical membranes of a variety of native epithelial tissues, where it regulates sodium and fluid balance. In vivo, a number of hormones and other endogenous factors, including polyunsaturated fatty acids (PUFAs), regulate these channels. We tested the effects of essential n–3 and n–6 PUFAs on amiloride-sensitive sodium transport in A6 epithelial cells. Eicosapentaenoic acid [EPA; C20:5(n–3)] transiently stimulated amiloride-sensitive open-circuit current ( INa) from 4.0 ± 0.3 to 7.7 ± 0.3 μA/cm2 within 30 min ( P < 0.001). No activation was seen in the presence of 10 μM amiloride. In cell-attached but not in cell-excised patches, EPA acutely increased the open probability of sodium channels from 0.45 ± 0.08 to 0.63 ± 0.10 ( P = 0.02, paired t-test). n–6 PUFAs, including linoleic acid (C18:2), eicosatetraynoic acid (C20:4), and docosapentanoic acid (C22:5) had no effect, whereas n–3 docosahexanoic acid (C22:6) activated amiloride-sensitive INa in a manner similar to EPA. Activation of INa by EPA was prevented by H-89, a PKA inhibitor. Similarly, PKA activity was stimulated by EPA. Nonspecific stimulation of phosphodiesterase activity by CoCl2 completely prevented the effect of EPA on sodium transport. We conclude that n–3 PUFAs activate epithelial sodium channels downstream of cAMP in a cAMP-dependent pathway also involving PKA.

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