Furosemide, sodium appetite, and ingestive behavior

Lundy, Robert F.; Blair, Mary E.; Horvath, Nelli; Norgren, Ralph

doi:10.1016/s0031-9384(03)00017-9

Cited by 26 publications

(22 citation statements)

References 18 publications

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“…In experiment 2, the Furo dose was 10 mg/kg sc (range 5.3-5.5 mg). Prior data indicate that the Na appetites produced by 5.0 to 7.0 mg doses do not differ significantly (19). During this experiment, urine was collected and the volume measured three times: 24 h prior to the Furo and saline injections, 3 h immediately after the injections, and again from 3 to 21 h postinjection.…”

Section: Methodsmentioning

confidence: 95%

Parabrachial and hypothalamic interaction in sodium appetite

Dayawansa

Peckins

Ruch

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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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. ibotenic acid; lateral hypothalamus; asymmetric lesions; parabrachial nuclei SALT APPETITE ARISES DURING sodium need or its hormonal mimics. It is usually assessed by measuring NaCl intake at concentrations rejected by animals in hydromineral balance (5,38). Although the hormonal precursors of the Na (sodium) appetite and their neural targets are yielding to investigation, the neural mechanisms that change the hedonic value of the sapid stimulus remain elusive (6, 10). Bilateral lesions centered in the parabrachial nuclei (PBN), the second central gustatory relay in rodents, eliminate the expression of salt appetite (7,8,41,(43)(44)(45). Chronic decerebrate rats that have an intact PBN but no connections between the hind-and forebrain also fail to express Na appetite (12). Thus, the PBN is necessary for the expression of sodium appetite, but is not sufficient unless its axonal connections to the forebrain are intact. In the forebrain, however, neither the thalamic nor the cortical gustatory areas are required for the expression of this behavior (7,8,41,51,55). Based on these observations, it follows that the gustatory neural activity required for salt appetite reaches the forebrain via the PBN projections to the limbic system (29). Nevertheless, the intermediate structures and functional relationships remain to be deciphered.The major terminal areas of the PBN in the limbic system: 1) amygdala, 2) bed nucleus of the stria terminalis, and 3) lateral hypothalamus (LH), each influence Na appetite to one degree or another (9,36,42,56). These same areas also are connected to the PBN reciprocally, to one another (3, 21), and to key components in a proposed reward system: the prefrontal cortex, ventral tegmental area, and nucleus accumbens (22,24,47). This anatomical complexity confounds any simple prediction about the mechanisms through which the hedonic sign of parabrachial gustatory activity is altered by body sodium deficit.The conventional approach to such an embarrassment of riches is to damage each of the forebrain targets in turn. As menti...

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Section: Methodsmentioning

confidence: 95%

Parabrachial and hypothalamic interaction in sodium appetite

Dayawansa

Peckins

Ruch

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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“…First, although the diuretic action of Furo was a linear function of dose, its effect on salt appetite was not (13). Specifically, 2.0 mg of Furo produced as much NaCl intake as 10 mg. Second, the dose of Furo used in the standard protocol, 10 mg, also supported a conditioned taste aversion (CTA), but the lower, 2.0-mg dose did not (14).…”

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confidence: 98%

Low-dose furosemide modulates taste responses in the nucleus of the solitary tract of the rat

Cho

Smith

Norgren

2004

American Journal of Physiology-Regulatory, Integrative and Comp

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Taste-evoked neural responses in the nucleus of the solitary tract (NST) are subject to both excitatory and inhibitory modulation by physiological conditions that influence ingestion. Treatments that induce sodium appetite predominantly reduce NST gustatory responsiveness to sapid stimuli. When sodium appetite is aroused with 10 mg of the diuretic furosemide (Furo), however, NST gustatory neurons exhibit an enhanced responsiveness to NaCl. In addition to inducing a sodium appetite, 10 mg Furo supports a conditioned taste aversion (CTA). A lower, 2-mg dose of Furo induces an equivalent sodium appetite, but not a CTA. To determine whether the anomalous electrophysiological results reflected the adverse effects of the 10-mg dose, we replicated the original experiment but instead used 2 mg of Furo. In chronically prepared, lightly anesthetized rats, the responses of 49 single NST neurons to 12 taste stimuli were recorded after subcutaneous injections of either 2 mg Furo or saline. There was no effect of treatment on NST neural responses to the four standard taste stimuli. In the NaCl concentration series, however, 2 mg Furo evoked significantly higher responses to the two highest concentrations of NaCl. There was no effect of treatment in the sucrose concentration series. Thus, unlike other methods that induce a sodium appetite, Furo increases NST neural responsiveness to NaCl. At least as far as the first central relay, sodium appetite apparently does not depend on specific changes in the sensory neural code for taste.

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“…An observation made in animal heart failure models using loop diuretics [14,23], was an activation of mediators involved in the activation of the RAAS. Furosemide treatment has been shown to yield increased plasma activity of renin [23], angiotensin II [15], and aldosterone [23]. Given that an activated RAAS accounts for the worsening of CHF, these results can be seen as indicators of a higher risk for mortality.…”

Section: Results From Previous Experimental Studiesmentioning

confidence: 99%

“…Assuming a bodyweight of around 300 g and a daily water uptake of about 35 mL per rat, the substance was given in a dose of 86 mg/L via drinking water. As shown previously, daily water intake is around 10 mL/100 g body weight in Sprague Dawley rats, and this ratio seems to remain constant even after coronary ligation [15,16]. We used the following formula: 86 mg = L ½ × 0:035 L = day ½ Ä 0:3 kg ½ ≅10 mg = kg dayÞ ½…”

Section: Drugs and Dosingmentioning

confidence: 99%