Potassium intake during cell dehydration

Pereira, D.T.B.; David, Richard B.; Vendramini, Regina Célia; Menani, José Vanderlei; Luca, Laurival A. De

doi:10.1016/j.physbeh.2005.03.004

Cited by 10 publications

(15 citation statements)

References 23 publications

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“…The main implication of this conclusion is that thirst drives a rat to ingest not only water, but also salt. One may agree in part with this view, because water is not always the most preferred liquid compared to mineral solutions under conditions of selective acute dehydration of either the extracellular or the intracellular compartment occurring within hours (7). Moreover, the total amount of fluid ingested by water-deprived rats is strongly influenced by taste (8,9).…”

Section: Thirst and Sodium Appetite Results From Water Deprivationmentioning

confidence: 98%

Water deprivation and the double- depletion hypothesis: common neural mechanisms underlie thirst and salt appetite

Luca

Vendramini

Pereira

et al. 2007

Braz J Med Biol Res

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Water deprivation-induced thirst is explained by the double-depletion hypothesis, which predicts that dehydration of the two major body fluid compartments, the extracellular and intracellular compartments, activates signals that combine centrally to induce water intake. However, sodium appetite is also elicited by water deprivation. In this brief review, we stress the importance of the water-depletion and partial extracellular fluid-repletion protocol which permits the distinction between sodium appetite and thirst. Consistent enhancement or a de novo production of sodium intake induced by deactivation of inhibitory nuclei (e.g., lateral parabrachial nucleus) or hormones (oxytocin, atrial natriuretic peptide), in water-deprived, extracellular-dehydrated or, contrary to tradition, intracellular-dehydrated rats, suggests that sodium appetite and thirst share more mechanisms than previously thought. Water deprivation has physiological and health effects in humans that might be related to the salt craving shown by our species.

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Section: Thirst and Sodium Appetite Results From Water Deprivationmentioning

confidence: 98%

Water deprivation and the double- depletion hypothesis: common neural mechanisms underlie thirst and salt appetite

Luca

Vendramini

Pereira

et al. 2007

Braz J Med Biol Res

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“…The different effects of ATP in different protocols of water intake may be the result of the different interactions between facilitatory and inhibitory mechanisms activated in each situation. For example, rats acutely treated with furosemide have increased renin activity together with hypovolemia (24,25) that is an additional signal to increase water intake, while central injection of ANG II induces water intake in spite of the pressor response that is an inhibitory signal for water intake.…”

Section: Discussionmentioning

confidence: 99%

“…Food, 1.8% NaCl and water were removed from the cages and the rats were injected sc with the diuretic/natriuretic furosemide (20 mg/kg body weight). This dose of furosemide induces a rapid and maximum loss of water and electrolytes, including sodium and potassium, within 1 h (24,25). Fifty minutes after the sc injection of furosemide, ATP (300 nmol/μL) or vehicle (saline) was injected icv.…”

Section: Experimental Protocols Testedmentioning

confidence: 99%

“…In addition, we also tested the effects of icv ATP on water intake induced by intragastric gavage with 12% NaCl (a model of intracellular dehydration) (23), acute treatment with the diuretic/natriuretic furosemide (a model of extracellular dehydration) (24,25), icv angiotensin II (ANG II, the main mechanism activated by extracellular dehydration to induce thirst) (21), and icv carbachol (a cholinergic agonist suggested to activate the same central mechanisms involved in intracellular dehydration-induced thirst) (26,27). To determine the specificity of central ATP for the control of water intake in comparison to another type of ingestive behavior, we also tested the effects of icv ATP on sodium depletion-induced 1.8% NaCl intake and on food deprivation-induced food intake.…”

Section: Introductionmentioning

confidence: 99%

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Antidipsogenic effects of central adenosine-5'-triphosphate

Faria

Sant'Ana

Menani

et al. 2009

Braz J Med Biol Res

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Besides other physiological functions, adenosine-5'-triphosphate (ATP) is also a neurotransmitter that acts on purinergic receptors. In spite of the presence of purinergic receptors in forebrain areas involved with fluid-electrolyte balance, the effect of ATP on water intake has not been investigated. Therefore, we studied the effects of intracerebroventricular (icv ) injections of ATP (100, 200 and 300 nmol/μL) alone or combined with DPCPX or PPADS (P1 and P2 purinergic antagonists, respectively, 25 nmol/μL) on water intake induced by water deprivation. In addition, the effect of icv ATP was also tested on water intake induced by intragastric load of 12% NaCl (2 mL/rat), acute treatment with the diuretic/natriuretic furosemide (20 mg/kg), icv angiotensin II (50 ng/μL) or icv carbachol (a cholinergic agonist, 4 nmol/μL), on sodium depletion-induced 1.8% NaCl intake, and on food intake induced by food deprivation. Male Holtzman rats (280-320 g, N = 7-11) had cannulas implanted into the lateral ventricle. Icv ATP (300 nmol/μL) reduced water intake induced by water deprivation (13.1 ± 1.9 vs saline: 19.0 ± 1.4 mL/2 h; P < 0.05), an effect blocked by pre-treatment with PPADS, but not DPCPX. Icv ATP also reduced water intake induced by NaCl intragastric load (5.6 ± 0.9 vs saline: 10.3 ± 1.4 mL/2 h; P < 0.05), acute furosemide treatment (0.5 ± 0.2 vs saline: 2.3 ± 0.6 mL/15 min; P < 0.05), and icv angiotensin II (2.2 ± 0.8 vs saline: 10.4 ± 2.0 mL/2 h; P < 0.05), without changing icv carbachol-induced water intake, sodium depletion-induced 1.8% NaCl intake and food deprivation-induced food intake. These data suggest that central ATP, acting on purinergic P2 receptors, reduces water intake induced by intracellular and extracellular dehydration.

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“…The animals in our study were fed only with water supply. Studies by Pereira et al [10] reported that the dose of 10 mg/kg (SC route) of furosemide induces a maximum and rapid loss of water and electrolytes -including Na + and K + . Our results, however, showed no hypokalemia using this dose.…”

Section: Discussionmentioning

confidence: 99%

Influência do veículo na eficácia da reposição de potássio em ratos hipocalêmicos

Petenusso

Valenti

Abreu³

et al. 2009

Rev Bras Cir Cardiovasc

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Influência do veículo na eficácia da reposição de potássio em ratos hipocalêmicosVehicle influence on potassium replacement effectiveness in hypokalemic rats Abstract Introduction: Patients who undergo cardiac surgery are commonly treated with diuretic therapy for the management of volume overload. The concern of hypokalemia in adult before, during and after surgery has already been described since there is risk of cardiac arrhythmia. Clinically, intravenous potassium (K+) replacement dilution is only recommended with sodium chloride 0.9% solution (SF0.9%), likely due to the putative effects of glucose solution 5% (SG5%) on insulin secretion, which influence K+ replacement quality. However, it is not yet experimentally proved the influence of SF0.9% and SG5% on K+ replacement quality in patients with hypokalemia.Objectives: To assess the effects of different vehicles of K+ replacement on blood K+ levels in furosemide hypokalemic rats.Methods: Male Wistar rats were divided into four groups: K++SF, K++SG, SF and SG. Jugular vein was cannulated for K+ replacement and femoral vein was cannulated for blood analysis were performed. Furosemide (50mg/kg) was injected S.C. to induce hypokalemia. It was analyzed potassium plasmatic levels 24 hours before furosemide injection, 24 hours after furosemide injection and after 30 minutes post-replacement.Results: There was reduction in post-injection of K+ levels when compared to the basal values (pre-furosemide) in all groups. However, the levels [K+] returned to baseline in both groups receiving K++SF or K++SG, which was not observed in groups receiving only SF and SG. Only K+SF presented increased after K+ replacement (P< 0.05).Conclusion: K+ replacement diluted both in SF and SG did not affect blood K+ levels in rats. 368 PETENUSSO, M ET AL -Vehicle influence on potassium replacement effectiveness in hypokalemic rats Bras Cir Cardiovasc 2009; 24(3): 367-372 Descriptors Rev

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Potassium intake during cell dehydration

Cited by 10 publications

References 23 publications

Water deprivation and the double- depletion hypothesis: common neural mechanisms underlie thirst and salt appetite

Water deprivation and the double- depletion hypothesis: common neural mechanisms underlie thirst and salt appetite

Antidipsogenic effects of central adenosine-5'-triphosphate

Influência do veículo na eficácia da reposição de potássio em ratos hipocalêmicos

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