Fos expression in rat brain during depletion-induced  thirst and salt appetite

Thunhorst, Robert L.; Xu, Zhice; Cicha, Michael Z.; Zardetto-Smith, Andrea M.; Johnson, Alan Kim

doi:10.1152/ajpregu.1998.274.6.r1807

Cited by 38 publications

(46 citation statements)

References 38 publications

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“…36 It is proposed that due to the high concentration of the enzyme in this area, 36 the activity of ACE is not effectively blocked by this dose of perindopril, allowing local conversion of Ang I to II and potent stimulation of drinking. 37 It has also been noted that rats treated long term with an AT-1 receptor antagonist have increased urinary volume and increased water intake. 38 Thus, the increase in water intake may be secondary to increased urine loss as opposed to a primary hyperdipsia mediated by the action of angiotensin in the brain.…”

Section: Discussionmentioning

confidence: 99%

Selective reduction in body fat mass and plasma leptin induced by angiotensin-converting enzyme inhibition in rats

et al. 2008

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Objective: There is emerging evidence that angiotensin stimulates adipocyte differentiation and lipogenesis. This study tested the hypothesis that inhibition of angiotensin II by treatment with an angiotensin-converting enzyme inhibitor, perindopril, would reduce fat mass in rats. Design: After a 12-day baseline, rats were divided into two groups: one was untreated and the other received perindopril (1.2 mg kg À1 per day) in drinking water for 26 days. Subjects: In total, 16 male Sprague-Dawley rats aged 10 weeks at the start of the study. Measurements: Plasma leptin was measured in samples collected at baseline, half-way through and at the end of treatment. Body weight, food and water intake were measured daily throughout the experiment. Body fat mass, bone and lean mass were determined by dual energy X-ray absorptiometry (DEXA) at the end of the treatment period. Results: Daily food intake was the same in both groups throughout the study. By the end of treatment, animals receiving perindopril showed a modest reduction in weight gain relative to the untreated animals (62.4 ± 5.0 g vs 73.0 ± 4.0 g; Po0.05). DEXA analysis showed that body composition was greatly altered and the perindopril-treated group had 26% less body fat mass than the untreated group (61.0 ± 5.2 g vs 44.4 ± 4.2 g; Po0.01). The reduction in body fat mass was correlated with reductions in the weight of both the epididymal and retroperitoneal fat pads (Po0.001). Similarly, plasma leptin was reduced by perindopril treatment (4.64 ± 0.56 ng ml À1 ) compared to the untreated group (8.27 ± 1.03 ng ml À1 ; Po0.001). In contrast, there were no differences in lean or bone mass between the two groups. Conclusion: Oral treatment with perindopril selectively reduced body fat mass without influencing daily food intake. In contrast, there were no differences in lean or bone mass between the two groups.

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Section: Discussionmentioning

confidence: 99%

Selective reduction in body fat mass and plasma leptin induced by angiotensin-converting enzyme inhibition in rats

et al. 2008

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“…In rats, furo/cap increases fluid intake and sodium appetite within 2 h, which can be further enhanced by subsequent injections over a period of weeks. Furo/cap increases the activity of cells (as assayed by the number of c-Fos immunoreactive cells) within the SFO, OVLT, MnPO, both magnocellular and parvocellular PVN, PB, area postrema (AP), and NTS (105,113,140). Interestingly, a high dose of captopril blocks this increase in c-fos activity (140).…”

Section: Stimulators Of the Brain Ras And Physiological Effects Of Sfmentioning

confidence: 99%

“…Furo/cap increases the activity of cells (as assayed by the number of c-Fos immunoreactive cells) within the SFO, OVLT, MnPO, both magnocellular and parvocellular PVN, PB, area postrema (AP), and NTS (105,113,140). Interestingly, a high dose of captopril blocks this increase in c-fos activity (140). Presumably this occurs because captopril passes into the brain where it blocks the de novo production of ANG II.…”

Section: Stimulators Of the Brain Ras And Physiological Effects Of Sfmentioning

confidence: 99%

Mechanisms of brain renin angiotensin system-induced drinking and blood pressure: importance of the subfornical organ

Coble¹,

Grobe

Johnson³

et al. 2015

American Journal of Physiology-Regulatory, Integrative and Comp

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Coble JP, Grobe JL, Johnson AK, Sigmund CD. Mechanisms of brain renin angiotensin system-induced drinking and blood pressure: importance of the subfornical organ. Am J Physiol Regul Integr Comp Physiol 308: R238 -R249, 2015. First published December 17, 2014 doi:10.1152/ajpregu.00486.2014.-It is critical for cells to maintain a homeostatic balance of water and electrolytes because disturbances can disrupt cellular function, which can lead to profound effects on the physiology of an organism. Dehydration can be classified as either intra-or extracellular, and different mechanisms have developed to restore homeostasis in response to each. Whereas the renin-angiotensin system (RAS) is important for restoring homeostasis after dehydration, the pathways mediating the responses to intra-and extracellular dehydration may differ. Thirst responses mediated through the angiotensin type 1 receptor (AT 1R) and angiotensin type 2 receptors (AT 2R) respond to extracellular dehydration and intracellular dehydration, respectively. Intracellular signaling factors, such as protein kinase C (PKC), reactive oxygen species (ROS), and the mitogen-activated protein (MAP) kinase pathway, mediate the effects of central angiotensin II (ANG II). Experimental evidence also demonstrates the importance of the subfornical organ (SFO) in mediating some of the fluid intake effects of central ANG II. The purpose of this review is to highlight the importance of the SFO in mediating fluid intake responses to dehydration and ANG II.angiotensin; blood pressure; barin; fluid; renin FLUID BALANCE is crucial for the homeostasis and survival of organisms because they have to properly maintain fluid and electrolyte concentrations for the normal function of all cells. Fluid balance can go awry in pathological states such as in chronic kidney disease and diabetes. Among its many roles in maintaining homeostasis, the renin-angiotensin system (RAS) is an important regulator of fluid balance. The RAS achieves this through the actions of its main effector peptide, angiotensin II (ANG II) through the ANG II type 1 (AT 1 R) and type 2 (AT 2 R) receptors. Activation of AT 1 R by blood-borne ANG II in target tissues causes increases in sodium and water retention, arginine vasopressin (AVP), and aldosterone release, vasoconstriction, increased sympathetic nervous system activity, and increased fluid intake. ANG II is produced by the consecutive enzymatic action of renin on its substrate angiotensinogen (AGT) and by angiotensin-converting enzyme (ACE) on its substrate angiotensin I (ANG I). The renin-AGT cleavage step is generally the rate-limiting step in the production of ANG II, and this is certainly true in the brain where the amount of renin is limiting. The RAS exists in two forms: a circulatory form where ANG II acts as an endocrine factor, and a tissue-specific form, where local production of ANG II acts in an autocrine or paracrine manner to induce AT 1 R signaling on ANG II producing or nearby cells (75). Intracrine, or intracellular forms of the RAS, hav...

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“…Also, unlike previous Fos studies (Rowland et al, 1996;Houpt et al, 1998;Thunhorst et al, 1998), the present experiments were focused on a specific neuronal phenotype. A profound change in c-Fos expression was observed in the subgroup of NTS neurons that express HSD2 (Fig.…”

Section: Hsd2 Neurons Signal Sodium Depletionmentioning

confidence: 99%

“…3), but when c-Fos-positive nuclei were counted throughout the entire NTS, there was no consistent association with sodium status (see Results). This problem may have limited previous studies that considered Fos location, but not the specific neuronal phenotypes involved (Houpt et al, 1998;Thunhorst et al, 1998).…”

Section: Hsd2 Neurons Signal Sodium Depletionmentioning

confidence: 99%

Aldosterone Target Neurons in the Nucleus Tractus Solitarius Drive Sodium Appetite

Geerling¹,

Engeland²,

Kawata³

et al. 2006

J. Neurosci.

135

187

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Sodium appetite can be enhanced by the adrenal steroid aldosterone via an unknown brain mechanism. A novel group of neurons in the nucleus tractus solitarius expresses the enzyme 11-␤-hydroxysteroid dehydrogenase type 2, which makes them selectively responsive to aldosterone. Their activation parallels sodium appetite in different paradigms of salt loss even in the absence of aldosterone. These unique aldosterone target neurons may represent a previously unrecognized central convergence point at which hormonal and neural signals can be integrated to drive sodium appetite.

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Fos expression in rat brain during depletion-induced thirst and salt appetite

Cited by 38 publications

References 38 publications

Selective reduction in body fat mass and plasma leptin induced by angiotensin-converting enzyme inhibition in rats

Selective reduction in body fat mass and plasma leptin induced by angiotensin-converting enzyme inhibition in rats

Mechanisms of brain renin angiotensin system-induced drinking and blood pressure: importance of the subfornical organ

Aldosterone Target Neurons in the Nucleus Tractus Solitarius Drive Sodium Appetite

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