Biomedical subjects

R R Sakai

Publications and source records attributed to R R Sakai.

42 records · Page 3Linked to original sources

PubMed1990

Peripheral angiotensin II is not the cause of sodium appetite in the rat.

Activation of the renin-angiotensin system has been shown to arouse both water and sodium intake in the rat. The following experiments examine the contributions of the peripheral and central renin-angiotensin systems to the expression of sodium appetite in the adrenal-intact rat. Firstly, we find that, unlike intracerebroventricular angiotensin II, intravenous administration of the hormone at dipsogenic doses does not arouse sodium intake in the sodium replete rat when given alone or in combination with systemic mineralocorticoid pretreatment. Secondly, in the sodium depleted rat, we find that interference with central, but not peripheral, angiotensin II action suppresses sodium appetite. Together, these data confirm recent evidence which demonstrates that it is angiotensin II of cerebral origin, not angiotensin II of renal origin, that is necessary for the expression of sodium appetite.

Angiotensin II↗

PubMed1990

Dependence of adrenalectomy-induced sodium appetite on the action of angiotensin II in the brain of the rat.

Adrenalectomized rats express a robust sodium appetite that is accompanied by high levels of blood-borne angiotensin II and is caused by angiotensin II of cerebral origin. Blood-borne angiotensin II is elevated in rats consuming NaCl after adrenalectomy, and plasma angiotensin II concentrations are increased further when the animals cannot drink a NaCl solution. These phenomena are the result of the pathological removal of aldosterone, because replacement therapy returned both sodium intake and plasma angiotensin II concentrations to preadrenalectomy levels. The adrenalectomized rat's appetite for sodium is completely suppressed by interference with the central, but not the peripheral, action of angiotensin II. These data demonstrate that the mechanism of the sodium appetite of the adrenalectomized rat is a pathological instance of the angiotensin/aldosterone synergy that governs the sodium appetite of the adrenal-intact, sodium-depleted rat. Because aldosterone has been removed, angiotensin acts alone to produce the appetite. Furthermore, the data show that it is angiotensin II of central origin that is important for sodium appetite expression.

Adrenal Glands↗

PubMed1989

Prior episodes of sodium depletion increase the need-free sodium intake of the rat.

Prior episodes of sodium depletion increase the daily 3% NaCl intake of rats. They ingest large volumes and continue to do so for as long as 3 months after recovery from sodium deficit while eating sodium-rich food and while plasma sodium concentration and renal function are normal. The increased daily intake of sodium is, therefore, need-free. There is a marked sex difference in the need-free intake of 3% NaCl. Female rats drink more salt than do male rats when they are sodium replete and depletion naive. Repeated depletions raise the need-free intakes of both sexes but the effect is greater in females. Plasma concentrations of angiotensin II and aldosterone, which are markedly elevated by each episode of sodium depletion, return to basal levels between and after depletions, and are not the cause of the chronically increased need-free salt intake of the multi-depleted rat. These results suggest that the persistent increase in daily 3% NaCl intake that occurs in the rat with a history of repeated sodium depletions is a permanent, nonpathological increase in avidity for the taste of salty substances that results in life-long overconsumption of salt.

Aldosterone↗

PubMed1987

Sodium appetite and cerebrospinal fluid sodium concentration during hypovolemia.

A lowered concentration of sodium in the cerebrospinal fluid (CSF) has been suggested as a critical signal for the elicitation of sodium appetite. This was evaluated in naive male Long-Evans rats made hypovolemic by subcutaneous injection of the colloid polyethylene glycol (PEG) in a hyperoncotic concentration. At 2, 5 or 8 h after PEG or vehicle injection, under conditions of availability or non-availability of water and 0.3 M NaCl for ingestion, the rats were anesthetized and samples of CSF and blood were taken. Water intakes of the PEG treated rats were elevated at 5 and 8 h, and 0.3 M NaCl intakes were elevated at 8 h in comparison to vehicle treated rats. When fluids were not available, CSF sodium concentrations were greater in PEG than in vehicle treated rats at 2, 5 and 8 h. When fluids were available, CSF sodium concentrations were greater in PEG than in vehicle treated rats at 5 and at 8 h. There was no correlation between CSF sodium concentration and saline intake. In summary, a lowered CSF sodium concentration is not a necessary condition for sodium appetite in the hypovolemic rat.

Animals↗

PubMed1987

Salt appetite is enhanced by one prior episode of sodium depletion in the rat.

A single sodium depletion enhances the salt appetite that is expressed after a second and subsequent sodium depletions. The enhanced salt intake, as measured by a decrease in latency to drink and an increase in volume of 3% NaCl ingested, is not accounted for by an increased sodium loss. The enhanced salt intake occurs even when the interval between first and second depletion is as long as 4 months. The enhanced salt appetite does not depend on the drinking of salt after the animal's first sodium depletion and is specific for NaCl but not for KCl. Moreover, it can be produced without sodium depletion by the actions of the hormones aldosterone and angiotensin on the brain. These results suggest that angiotensin and aldosterone, which are released in response to sodium depletion, (a) increase renal sodium conservation, (b) evoke a salt appetite to restore the lost sodium, and (c) produce enduring changes in the brain that prepare it for more rapid and more vigorous expression of salt appetite in response to future sodium depletions. Thus the neural mechanisms that govern salt appetite are not only activated by the hormones of sodium conservation but appear also to be organized by them for a lifelong increase in avidity for salty substances.

Animals↗

PubMed1986

Salt appetite is suppressed by interference with angiotensin II and aldosterone.

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.

Aldosterone↗