Osmoregulatory fluid intake but not hypovolemic thirst is intact in mice lacking angiotensin

Walker, Lesley; Alexiou, Theodora; Allen, Andrew M.; Campbell, Duncan J.; Nicolantonio, R. Di; Oldfield, Brian J.; Denton, Derek A.

doi:10.1152/ajpregu.00848.2007

Cited by 35 publications

(31 citation statements)

References 49 publications

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“…It has been proposed that AT 2 R may be acting as a mechanosensor of cellular swelling in response to intracellular dehydration rather than being activated by angiotensin peptides. This is supported by data suggesting that angiotensin peptides were not needed for intracellular dehydration-induced polydipsia in AGTϪ/Ϫ mice (90). Thus fluid intake can occur centrally through different ANG II receptors.…”

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

confidence: 56%

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

confidence: 56%

“…AGT-deficient mice (AGTϪ/Ϫ) exhibit an impaired dipsogenic response to acute extracellular dehydration suggesting a requirement for de novo synthesis of ANG II (90). In contrast, intracellular dehydration (discussed in more detail below) induced water intake in AGTϪ/Ϫ mice.…”

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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“…Moreover, AII acts as a major system regulating water intake independent of osmolality and extracellular volume [28]. Centrally administered 4a-PDD inhibited AII-induced water intake and did not change hyperosmolality-induced water intake [4].…”

Section: Discussionmentioning

confidence: 97%

Centrally administered ghrelin potently inhibits water intake induced by angiotensin II and hypovolemia in rats

et al. 2009

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Ghrelin is a potent, centrally acting orexigenic hormone. Recently, we showed that centrally administered ghrelin is a potent antidipsogenic hormone in 24-h water deprived rats. In this study, we examined the effect of intracerebroventricular (icv) injection of ghrelin on angiotensin II (AII)-induced water intake in rats. We also examined the effects of icv injection of ghrelin on drinking induced by intraperitoneal injection of an isotonic polyethylene glycol (PEG) solution that causes isotonic hypovolemia. Water intake induced by the icv injection of AII or ip injection of PEG was significantly reduced after icv injection of ghrelin, although food intake was stimulated by the hormone. The drinking induced by AII was also inhibited by the icv administration of 4alpha-phorbol 12, 13-didecanoate, an agonist of the osmosensitive TRPV4 channel. This study showed that ghrelin is a potent antidipsogenic peptide by antagonizing general dipsogenic mechanisms including those activated by AII and hypovolemia in rats.

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“…AII acts to regulate water intake independent of osmolality and extracellular volume [80]. Centrally administered 4 -PDD inhibited AII-induced water intake but did not change hyperosmolality-induced water intake [74].…”

Section: Central Effects Of Ghrelin On Body Fluid Homeostasismentioning

confidence: 95%

Central Effects of Ghrelin, a Unique Peptide, on Appetite and Fluid/Water Drinking Behavior

Hashimoto¹,

Ueta

2011

CPPS

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Ghrelin is a stomach-derived peptide discovered as a ligand of the orphan G-protein coupled receptor. Ghrelin is now recognized as a major orexigenic neuropeptide. Immunohistochemical studies demonstrated that centrally administered ghrelin induced c-fos protein expression in many areas in the brain. Indeed, centrally administered ghrelin has various effects such as stimulating feeding, arousal, increasing gastric acid secretion, release of hormones from the pituitary, and inhibition of water intake. In particular, we recently showed that ghrelin was an antidipsogenic peptide with a simultaneous orexigenic effect. This may be of important, because most spontaneous daily water intake is temporally associated with feeding. Here, we summarise recent findings on the integration of central effects of ghrelin that regulate feeding, release hormones from the pituitary and inhibit fluid/water intake.

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Osmoregulatory fluid intake but not hypovolemic thirst is intact in mice lacking angiotensin

Cited by 35 publications

References 49 publications

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

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

Centrally administered ghrelin potently inhibits water intake induced by angiotensin II and hypovolemia in rats

Central Effects of Ghrelin, a Unique Peptide, on Appetite and Fluid/Water Drinking Behavior

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