Salt appetite is suppressed by interference with angiotensin II and aldosterone

1986 ◽  
Vol 251 (4) ◽  
pp. R762-R768 ◽  
Author(s):  
R. R. Sakai ◽  
S. Nicolaidis ◽  
A. N. Epstein
Keyword(s):  
Angiotensin Ii ◽  
Food Intake ◽  
Sodium Excretion ◽  
Salt Appetite ◽  
Mineralocorticoid Receptors ◽  
Sodium Depletion ◽  
Ru 28318 ◽  
Ingestive Behaviors ◽  
Captopril Treatment

Blockade of central but not peripheral mineralocorticoid receptors, with the antimineralocorticoid RU-28318, reduces but does not suppress salt appetite aroused by sodium depletion in the rat. When central mineralocorticoid blockade is combined with captopril treatment to prevent formation of endogenous angiotensin II the appetite is completely suppressed. Suppression of the appetite occurred without changes in the animals' spontaneous ingestive behaviors, sodium excretion, or insulin-induced food intake. These results demonstrate that a synergy of angiotensin II and aldosterone is responsible for the expression of depletion-induced salt appetite in the rat.

Modulation of salt appetite by lateral ventricular infusions of angiotensin II and carbachol during sodium depletion

1985 ◽  
Vol 346 (2) ◽  
pp. 273-280 ◽  
Author(s):  
Douglas A. Fitts ◽  
Robert L. Thunhorst ◽  
John B. Simpson
Keyword(s):  
Angiotensin Ii ◽  
Salt Appetite ◽  
Sodium Depletion

scholarly journals Lateral parabrachial nucleus serotonergic mechanisms and salt appetite induced by sodium depletion

1998 ◽  
Vol 274 (2) ◽  
pp. R555-R560 ◽  
Author(s):  
José Vanderlei Menani ◽  
Laurival Antonio De Luca ◽  
Alan Kim Johnson
Keyword(s):  
Water Deprivation ◽  
Sodium Intake ◽  
Parabrachial Nucleus ◽  
Salt Appetite ◽  
Sodium Depletion ◽  
Volume Depletion ◽  
Deficient Diet ◽  
Lateral Parabrachial Nucleus ◽  
Sodium Loss ◽  
Ingestive Behaviors

This study investigated the effects of bilateral injections of a serotonin (5-HT) receptor agonist into the lateral parabrachial nucleus (LPBN) on the intake of NaCl and water induced by 24-h water deprivation or by sodium depletion followed by 24 h of sodium deprivation (injection of the diuretic furosemide plus 24 h of sodium-deficient diet). Rats had stainless steel cannulas implanted bilaterally into the LPBN. Bilateral LPBN injections of the serotonergic 5-HT1/2 receptor antagonist methysergide (4 μg/200 nl at each site) increased hypertonic NaCl intake when tested 24 h after sodium depletion and after 24 h of water deprivation. Water intake also increased after bilateral injections of methysergide into the LPBN. In contrast, the intake of a palatable solution (0.06 M sucrose) under body fluid-replete conditions was not changed after bilateral LPBN methysergide injections. The results show that serotonergic mechanisms in the LPBN modulate water and sodium intake induced by volume depletion and sodium loss. The finding that sucrose intake was not affected by LPBN serotonergic blockade suggests that the effects of the methysergide treatment on the intakes of water and NaCl are not due to a mechanism producing a nonspecific enhancement of all ingestive behaviors.

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.

THE DEPENDENCE OF URINARY CALCIUM AND OTHER ELECTROLYTES ON ADRENAL FUNCTION DURING ACUTE SODIUM DEPLETION AND LOADING

1970 ◽  
Vol 64 (1) ◽  
pp. 65-74 ◽  
Author(s):  
Lars Runeberg ◽  
B.-A. Lamberg ◽  
P. Reissell ◽  
H. Adlercreutz
Keyword(s):  
Sodium Excretion ◽  
Extracellular Volume ◽  
Normal Subjects ◽  
Urinary Calcium ◽  
Calcium Excretion ◽  
Minor Importance ◽  
Sodium Depletion ◽  
Sodium Loading ◽  
Urinary Potassium ◽  
Normal Controls

ABSTRACT The time course of the renal excretion of calcium, magnesium, sodium, and potassium during sodium depletion and the rapid correction of the extracellular volume deficit was studied in normal subjects and in patients with Addison's disease (AD). The decrease in body weight was similar in the two groups, but the haematocrit value increased more in the patients with AD. Sodium depletion suppressed sodium excretion much more efficiently in normal controls than in the AD patients. Calcium excretion was roughly equally depressed in two groups. During sodium loading there was an immediate increase in renal sodium excretion in the patients with AD, whereas the sodium-retaining state generally continued for about one day in the normal controls. Urinary potassium decreased gradually during the first day of sodium loading in the normal controls but not in the AD patients. In the normal subjects calcium excretion remained low during the first day and increased on the second day of sodium loading. In the AD patients there was a gradual increase in urinary calcium during the first day of sodium loading, which did not, however, parallel the changes in urinary sodium content in individual urine samples. Urinary magnesium did not change significantly. It is concluded that the effect of adrenal steroids on renal calcium excretion is of minor importance. They may, however, to some extent induce calcium retention.

Antagonistic effect of theophylline on the adenosine-induced decreased in renin release

1984 ◽  
Vol 247 (2) ◽  
pp. F246-F251 ◽  
Author(s):  
W. S. Spielman
Keyword(s):  
Angiotensin Ii ◽  
Sodium Excretion ◽  
Renal Cortex ◽  
Fractional Excretion ◽  
Antagonistic Effect ◽  
Renin Release ◽  
Detectable Effect ◽  
Fractional Sodium Excretion ◽  
Fractional Excretion Of Sodium ◽  
Anesthetized Dogs

The action of theophylline on the adenosine-induced decrease in renin release was studied in anesthetized dogs. Adenosine inhibited renin release, decreased GFR and fractional sodium excretion, and decreased the concentration of angiotensin II in the renal lymph. Theophylline (5 mumol/min intrarenally) had no significant effect on GFR or RBF yet produced a significant increase in the release of renin and the fractional excretion of sodium. The intrarenal infusion of adenosine (3 X 10(-7) mol/min) during theophylline infusion produced no effect on GFR or RBF, but fractional sodium excretion and renin release were significantly decreased. Adenosine was infused at a lower dose (3 X 10(-8) mol/min) during theophylline (5 X 10(-6) mol/min) infusion in a second group of dogs. With the exception of fractional sodium excretion, all effects of adenosine were effectively antagonized by theophylline. Theophylline at 5 X 10(-6) mol/min, which stimulates renin release and effectively antagonizes the renal effects of adenosine, had no detectable effect on cAMP measured in renal cortex. Furthermore, no change in cortical cAMP was observed until theophylline was increased 50-fold over the dose effective in antagonizing adenosine. These findings demonstrate that theophylline, at concentrations having no effect on cortical cAMP, antagonizes the effect of adenosine on renin release. The results are also consistent with the view that theophylline stimulates renin release by a mechanism other than its action on cAMP.

scholarly journals Networking Between Systemic Angiotensin II and Cardiac Mineralocorticoid Receptors

Hypertension ◽  
2008 ◽  
Vol 52 (6) ◽  
pp. 1016-1018 ◽  
Author(s):  
Augusto C. Montezano ◽  
Rhian M. Touyz
Keyword(s):  
Angiotensin Ii ◽  
Mineralocorticoid Receptors

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.

Effect of Changes in Sodium Balance on Potassium/Aldosterone Dose-Response Curves in the Dog

1982 ◽  
Vol 62 (4) ◽  
pp. 373-380 ◽  
Author(s):  
M. G. Nicholls ◽  
M. Tree ◽  
J. H. Livesey ◽  
R. Fraser ◽  
J. J. Morton ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Dose Response ◽  
Plasma Potassium ◽  
Plasma Aldosterone ◽  
Dietary Sodium ◽  
Sodium Balance ◽  
Sodium Depletion ◽  
Beagle Dogs ◽  
Response Curves ◽  
Dose Response Curves

1. Potassium was infused intravenously in an incremental fashion and the plasma aldosterone responses were measured in conscious beagle dogs at five different intakes of dietary sodium. 2. Potassium/aldosterone dose—response curves were constructed for each dietary sodium regimen. 3. The rate of increase of plasma potassium during graded potassium infusion became progressively greater with increasing sodium depletion. 4. Regression lines of plasma aldosterone on plasma potassium were progressively elevated and steepened with increasing sodium depletion. 5. The alteration of these dose-response curves could in part have been the result of chronic elevation of plasma potassium and angiotensin II, and depression of plasma sodium, with sodium deprivation. 6. By contrast, acute changes in plasma angiotensin II or sodium concentrations across incremental infusions of potassium did not explain the progressive changes in the potassium/aldosterone dose—response curves. 7. The steepest part of the plasma aldosterone response curve was in the plasma potassium range 4–6 mmol/l. 8. Maximum achieved aldosterone levels were similar to or greater than those attained during angiotensin II infusion in previous studies in beagle dogs. 9. Potassium, like angiotensin II and adrenocorticotropic hormone, becomes a more effective stimulus to aldosterone with sodium depletion, thereby facilitating the preservation of sodium homoeostasis.

scholarly journals Vascular Type 1A Angiotensin II Receptors Control BP by Regulating Renal Blood Flow and Urinary Sodium Excretion

2015 ◽  
Vol 26 (12) ◽  
pp. 2953-2962 ◽  
Author(s):  
Matthew A. Sparks ◽  
Johannes Stegbauer ◽  
Daian Chen ◽  
Jose A. Gomez ◽  
Robert C. Griffiths ◽  
...  
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Angiotensin Ii Receptors ◽  
Vascular Type
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