scholarly journals Despite increasing aldosterone, elevated potassium is not necessary for activating aldosterone‐sensitive HSD2 neurons or sodium appetite

2021 ◽  
Vol 9 (2) ◽  
Author(s):  
Frederico S. Fazan ◽  
Eduardo Colombari ◽  
Arthur D. Loewy ◽  
Joel C. Geerling
Keyword(s):  
Sodium Appetite

scholarly journals The Role of the Hypothalamic Paraventricular Nucleus and the Organum Vasculosum Lateral Terminalis in the Control of Sodium Appetite in Male Rats

2014 ◽  
Vol 34 (28) ◽  
pp. 9249-9260 ◽  
Author(s):  
L. A. Grafe ◽  
A. E. Takacs ◽  
D. K. Yee ◽  
L. M. Flanagan-Cato
Keyword(s):  
Paraventricular Nucleus ◽  
Hypothalamic Paraventricular Nucleus ◽  
Male Rats ◽  
Sodium Appetite ◽  
Organum Vasculosum

Sodium appetite in lactating rats.

1990 ◽  
Vol 104 (5) ◽  
pp. 742-750 ◽  
Author(s):  
Edda Thiels ◽  
Joseph G. Verbalis ◽  
Edward M. Stricker
Keyword(s):  
Sodium Appetite

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.

Sodium Appetite During Captopril Blockade of Endogenous Angiotensin Formation

1986 ◽  
pp. 431-439
Author(s):  
Karen Moe ◽  
Alan N. Epstein
Keyword(s):  
Sodium Appetite

Influence of Sodium Load on Angiotensin-Induced Sodium Appetite

1986 ◽  
pp. 419-424
Author(s):  
Louise M. Fuller ◽  
J. T. Fitzsimons
Keyword(s):  
Sodium Appetite ◽  
Sodium Load

Angiotensin II-induced thirst, but not sodium appetite, via AT1 receptors in organum cavum prelamina terminalis

1995 ◽  
Vol 268 (6) ◽  
pp. R1401-R1405 ◽  
Author(s):  
M. el Ghissassi ◽  
S. N. Thornton ◽  
S. Nicolaidis
Keyword(s):  
Angiotensin Ii ◽  
Salt Intake ◽  
High Sensitivity ◽  
Ang Ii ◽  
Nacl Solution ◽  
At1 Receptors ◽  
Sodium Appetite ◽  
Specific Antagonist

The angiotensin receptor specificity, with respect to fluid intake, of the organum cavum prelamina terminalis (OCPLT), a recently discovered discrete forebrain structure with high sensitivity to angiotensin II (ANG II), was investigated. ANG II (10 ng) microinjected into the OCPLT significantly increased water consumption but did not induce intake of a hypertonic (3%) NaCl solution. Losartan, an ANG II type 1 (AT1) receptor-specific antagonist, produced dose-related (1-100 ng) inhibition of ANG II-induced drinking. The ANG II type 2 receptor-specific antagonist CGP-42112A was ineffective. Intake of the 3% NaCl solution in response to microinjection of either of the antagonists into the OCPLT was never observed. These findings suggest that water intake produced by microinjection of ANG II into the OCPLT is mediated by AT1 receptors uniquely and that, in contrast to other regions of the brain, these receptors do not induce salt intake when stimulated by ANG II.

BEHAVIORAL CONTROL OF INTRAVASCULAR FLUID VOLUME: THIRST AND SODIUM APPETITE

1969 ◽  
Vol 157 (2 Neural Regula) ◽  
pp. 553-568 ◽  
Author(s):  
Edward M. Stricker ◽  
George Wolf
Keyword(s):  
Behavioral Control ◽  
Fluid Volume ◽  
Sodium Appetite

Thirst and Sodium Appetite

1990 ◽  
pp. 23-44 ◽  
Author(s):  
J. T. Fitzsimons
Keyword(s):  
Sodium Appetite

scholarly journals Effect of sex chromosome complement on sodium appetite and Fos-immunoreactivity induced by sodium depletion

2014 ◽  
Vol 306 (3) ◽  
pp. R175-R184 ◽  
Author(s):  
Florencia M. Dadam ◽  
Ximena E. Caeiro ◽  
Carla D. Cisternas ◽  
Ana F. Macchione ◽  
María J. Cambiasso ◽  
...  
Keyword(s):  
Sex Chromosome ◽  
Area Postrema ◽  
Brain Activity ◽  
Chromosome Complement ◽  
Circumventricular Organs ◽  
Sexually Dimorphic ◽  
Sodium Depletion ◽  
Sodium Diet ◽  
Sodium Appetite ◽  
Low Sodium Diet

Previous studies indicate a sex chromosome complement (SCC) effect on the angiotensin II-sexually dimorphic hypertensive and bradycardic baroreflex responses. We sought to evaluate whether SCC may differentially modulate sexually dimorphic-induced sodium appetite and specific brain activity due to physiological stimulation of the rennin angiotensin system. For this purpose, we used the “four core genotype” mouse model, in which the effect of gonadal sex and SCC is dissociated, allowing comparisons of sexually dimorphic traits between XX and XY females as well as in XX and XY males. Gonadectomized mice were sodium depleted by furosemide (50 mg/kg) and low-sodium diet treatment; control groups were administered with vehicle and maintained on normal sodium diet. Twenty-one hours later, the mice were divided into two groups: one group was submitted to the water-2% NaCl choice intake test, while the other group was perfused and their brains subjected to the Fos-immunoreactivity (FOS-ir) procedure. Sodium depletion, regardless of SCC (XX or XY), induced a significantly lower sodium and water intake in females than in males, confirming the existence in mice of sexual dimorphism in sodium appetite and the organizational involvement of gonadal steroids. Moreover, our results demonstrate a SCC effect on induced brain FOS-ir, showing increased brain activity in XX-SCC mice at the paraventricular nucleus, nucleus of the solitary tract, and lateral parabrachial nucleus, as well as an XX-SCC augmented effect on sodium depletion-induced brain activity at two circumventricular organs, the subfornical organ and area postrema, nuclei closely involved in fluid and blood pressure homeostasis.

Methodologic aspects of sodium appetite: An addendum

1977 ◽  
Vol 20 (1) ◽  
pp. 96-103 ◽  
Author(s):  
Carlos E. Cruz ◽  
Ira B. Perelle ◽  
George Wolf
Keyword(s):  
Sodium Appetite
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