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Salt apoetite during rehydration in rats
$2-D-2-01
SALT APPETITE DURING REHYDRATION IN RATS Taketoshi Morimoto, Hiroshi Nose, Eizo Sugimoto, Takiko Yawata and Tadashi Okuno Department of Physiology, Kyoto Prefectural University of Medicine Kamigyoku, Kyoto 602 Japan To analyze the role of salt appetite for the recovery from thermat dehydration, we performed a series of experiments in rats which spread saliva for heat dissipation and loss NaCI via saliva. When only water was provided to thermally dehydrated rats (dehydrated by 7-8% of their initial body weight), the fluid balance reached a steady state prior to replacement of their fluid loss with a reduction of fluid intake and an increase in urine output. In contrast, complete rehydration was achieved by rats provided with either 0.45% or 0.9% NaCI solution. In addition, determination of the difference between intake and urine output of water and NaCI indicated that rats given 0.9% or 0.45% NaCI solution regained their fluid loss completely in 3-3.5 hr and then they showed positive balances of water and NaCI. When dehydrated rats were given a choice of tap water and NaCI solution, rats consumed more water than saline for about 2 hr after the start of fluid replacement, but consumed more saline thereafter. The average NaCI concentration chosen by the rats was about 55 mM for the initial 2 hr, and then the average concentration of the fluid consumed shifted to about 125 mM. This shift of salt appetite was found in rats dehydrated by 6-8% of their initial body weight, but not in rats dehydrated by 3%. Using techniques of continuous determinations of circulating blood volume and plasma Na+ concentration, it was shown that during the initial stage of rehydration, rats chose a dilute NaCI solution to decrease their blood osmolality and to restore the lost sodium. Thereafter, blood volume was expanded with consumption of almost isotonic NaCI solution. From these results, it is concluded that the osmoregulation precedes the volume regulation and sodium is required for complete recovery of blood volume.
$2-D-2-02 NEURONAL AND NEUROENDOCRINE MECHANISMS OF SODIUM APPETITE S. Nicola'idis Lab. de Neurobiologie des Rrgulations, CNRS, URA 1860, Coll~ge de France, Paris 75231 France Sodium appetite(SA) is a (neuro)hormone-dependent state and behavior. Mineralocorticoids and angiotensin II(AII) and III enhance it while ANF or BNF and oxytocin seem to inhibit it. The motivated behavior starts with the deficiency in plasma [Na+](sweating, diarrhea, hemorrhage) brings about extracellular dehydration and hypovolemia that induces the release of All and aldosterone(AL) both of which must reach brain structures to produce SA (Sakai Epstein and Nicola'fdis; Amer J Physiol 251: R762-768(1986). This mechanism of SA is need-induced or regulatory. But a robust SA can be also induced under need-free (in terms of [Na+] conditions due to administration of the hormones themselves. Need-free SA is often observed in humans and rats, following a history of episodes of [Na+| deficiency, either in their post natal or, even pre-natal life (Nicola'/dis et al; Amer J Physiol 258: R 281-283 (1990). The mechanism of this worldwide nutritional and epidemiological problem is important to understand. It deals with the capacity of the hormones AII and AL to imprint a long-lasting "memory" in specific areas of brain that entrain an enhancement of gustatory message of salty taste. Note that both the renin-AII system and, according to our very recent findings, AL are also generated by brain structures and so do not depend necessarily on peripheral production. Using 7-barrel iontophotetic technique on single units we have investigated the neuronal mechanism of the need free enhancement of salty taste. We found that, in a mid-forebrain continuum extending from the preoptic area above the OVLT up to the anterior septum surrounding the organum cavum pre-lamina terminalis (Nicola'idis Ghissassi; Amer J Physiol 260: R396-406(1991), there are neurons that become overresponsive to iontophoretically applied AII following a pretreatment by DOCA (Thornton, Nicola'fdis; Amer J Physiol; 265: R826-833(1993) which is known to sensitize the animal to All for the expression of a need-free SA. Moreover, using unanesthetized stereotaxicaUy restrained rats, we showed that not only does the same septopreoptic area receive gustatory projections in response to drinking saline but also it is capable of triggering saline drinking in response to a minimal stimulation by All applied iontophoretically (Nicola'/dis et al; Proc 22nd ann meeting Soc for Neurosc 1992 p373.14). The subtypes of AII receptors seem to play an important role in the expression of SA as shown in our recent investigations. In conclusion, the septopreoptic sagittal area possesses neurons that keep in "memory" the history of hormonally translated past events of [Na+] deficiency and become over-responsive to salt taste and initiate the consummatory behavior. Supported by NIH MH 43787 and the Evian Company.
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SALT APPETITE DURING REHYDRATION IN RATS Taketoshi Morimoto, Hiroshi Nose, Eizo Sugimoto, Takiko Yawata and Tadashi Okuno Department of Physiology, Kyoto Prefectural University of Medicine Kamigyoku, Kyoto 602 Japan To analyze the role of salt appetite for the recovery from thermat dehydration, we performed a series of experiments in rats which spread saliva for heat dissipation and loss NaCI via saliva. When only water was provided to thermally dehydrated rats (dehydrated by 7-8% of their initial body weight), the fluid balance reached a steady state prior to replacement of their fluid loss with a reduction of fluid intake and an increase in urine output. In contrast, complete rehydration was achieved by rats provided with either 0.45% or 0.9% NaCI solution. In addition, determination of the difference between intake and urine output of water and NaCI indicated that rats given 0.9% or 0.45% NaCI solution regained their fluid loss completely in 3-3.5 hr and then they showed positive balances of water and NaCI. When dehydrated rats were given a choice of tap water and NaCI solution, rats consumed more water than saline for about 2 hr after the start of fluid replacement, but consumed more saline thereafter. The average NaCI concentration chosen by the rats was about 55 mM for the initial 2 hr, and then the average concentration of the fluid consumed shifted to about 125 mM. This shift of salt appetite was found in rats dehydrated by 6-8% of their initial body weight, but not in rats dehydrated by 3%. Using techniques of continuous determinations of circulating blood volume and plasma Na+ concentration, it was shown that during the initial stage of rehydration, rats chose a dilute NaCI solution to decrease their blood osmolality and to restore the lost sodium. Thereafter, blood volume was expanded with consumption of almost isotonic NaCI solution. From these results, it is concluded that the osmoregulation precedes the volume regulation and sodium is required for complete recovery of blood volume.
$2-D-2-02 NEURONAL AND NEUROENDOCRINE MECHANISMS OF SODIUM APPETITE S. Nicola'idis Lab. de Neurobiologie des Rrgulations, CNRS, URA 1860, Coll~ge de France, Paris 75231 France Sodium appetite(SA) is a (neuro)hormone-dependent state and behavior. Mineralocorticoids and angiotensin II(AII) and III enhance it while ANF or BNF and oxytocin seem to inhibit it. The motivated behavior starts with the deficiency in plasma [Na+](sweating, diarrhea, hemorrhage) brings about extracellular dehydration and hypovolemia that induces the release of All and aldosterone(AL) both of which must reach brain structures to produce SA (Sakai Epstein and Nicola'fdis; Amer J Physiol 251: R762-768(1986). This mechanism of SA is need-induced or regulatory. But a robust SA can be also induced under need-free (in terms of [Na+] conditions due to administration of the hormones themselves. Need-free SA is often observed in humans and rats, following a history of episodes of [Na+| deficiency, either in their post natal or, even pre-natal life (Nicola'/dis et al; Amer J Physiol 258: R 281-283 (1990). The mechanism of this worldwide nutritional and epidemiological problem is important to understand. It deals with the capacity of the hormones AII and AL to imprint a long-lasting "memory" in specific areas of brain that entrain an enhancement of gustatory message of salty taste. Note that both the renin-AII system and, according to our very recent findings, AL are also generated by brain structures and so do not depend necessarily on peripheral production. Using 7-barrel iontophotetic technique on single units we have investigated the neuronal mechanism of the need free enhancement of salty taste. We found that, in a mid-forebrain continuum extending from the preoptic area above the OVLT up to the anterior septum surrounding the organum cavum pre-lamina terminalis (Nicola'idis Ghissassi; Amer J Physiol 260: R396-406(1991), there are neurons that become overresponsive to iontophoretically applied AII following a pretreatment by DOCA (Thornton, Nicola'fdis; Amer J Physiol; 265: R826-833(1993) which is known to sensitize the animal to All for the expression of a need-free SA. Moreover, using unanesthetized stereotaxicaUy restrained rats, we showed that not only does the same septopreoptic area receive gustatory projections in response to drinking saline but also it is capable of triggering saline drinking in response to a minimal stimulation by All applied iontophoretically (Nicola'/dis et al; Proc 22nd ann meeting Soc for Neurosc 1992 p373.14). The subtypes of AII receptors seem to play an important role in the expression of SA as shown in our recent investigations. In conclusion, the septopreoptic sagittal area possesses neurons that keep in "memory" the history of hormonally translated past events of [Na+] deficiency and become over-responsive to salt taste and initiate the consummatory behavior. Supported by NIH MH 43787 and the Evian Company.
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