Angiotensin and salt appetite of BALB/c mice

Denton, D. A.; Blair‐West, J. R.; McBurnie, M.; Osborne, P.G.; Tarján, É.; Williams, Robert; Weisinger, R. S.

doi:10.1152/ajpregu.1990.259.4.r729

Cited by 29 publications

(31 citation statements)

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“…Injection of Ang II into the brain or into the periphery increases salt appetite and thirst in rodents. 10,32,33 Ang II is a relatively large peptide, and it does not readily cross the blood-brain barrier. The central nervous system effect of the Ang II could be via the circumventricular organ, where the blood-brain barrier is weak or absent.…”

Section: Discussionmentioning

confidence: 99%

Involvement of Tumor Necrosis Factor-α in Angiotensin II–Mediated Effects on Salt Appetite, Hypertension, and Cardiac Hypertrophy

Sriramula

Haque²,

Majid³

et al. 2008

Hypertension

257

201

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Abstract-Hypertension is considered a low-grade inflammatory condition induced by various proinflammatory cytokines, including tumor necrosis factor (TNF)-␣. Recent studies have implicated an involvement of TNF-␣ in the development of salt-sensitive hypertension induced by angiotensin II (Ang II). To understand further the relationship between TNF-␣ and Ang II, we examined the responses to Ang II in TNF-␣ knockout (TNF-␣ Ϫ/Ϫ ) mice in the present study. A continuous infusion of Ang II (1 g/kg per minute) for 2 weeks was given to both TNF-␣ Ϫ/Ϫ and wild-type (WT) mice with implanted osmotic minipumps. Daily measurement of water intake, salt intake, and urine output were performed using metabolic cages. Blood pressure was monitored continuously with implanted radiotelemetry. Ang II administration for 2 weeks caused increases in salt (0.2Ϯ0.07 to 5.6Ϯ0.95 mL/d) and water (5.4Ϯ0.34 to 11.5Ϯ1.2 mL/d) intake and in mean arterial pressure (115Ϯ1 to 151Ϯ3 mm Hg) in wild-type mice, but these responses were absent in TNF-␣ Ϫ/Ϫ mice (0.2Ϯ0.04 to 0.3Ϯ0.09 mL/d, 5.5Ϯ0.2 to 6.1Ϯ0.07 mL/d, and 113Ϯ2 to 123Ϯ3 mm Hg, respectively). Cardiac hypertrophy induced by Ang II was significantly attenuated in TNF-␣ Ϫ/Ϫ mice compared with wild-type mice. In a group of TNF-␣ Ϫ/Ϫ mice, when replacement therapy was made with recombinant TNF-␣, Ang II induced similar responses in salt appetite, mean arterial pressure, and cardiac hypertrophy, as observed in wild-type mice. These results suggest that TNF-␣ plays a mechanistic role in mediating chronic Ang II-induced effects on salt appetite and blood pressure, as well as on cardiac hypertrophy.

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Section: Discussionmentioning

confidence: 99%

Involvement of Tumor Necrosis Factor-α in Angiotensin II–Mediated Effects on Salt Appetite, Hypertension, and Cardiac Hypertrophy

Sriramula

Haque²,

Majid³

et al. 2008

Hypertension

257

201

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“…These studies convincingly show that ANG II production in the SFO plays an important role in both blood pressure and fluid balance. It is notable that unlike rats, mice appear to be resistant to the dipsogenic effects of peripheral ANG II, but will increase water intake after ANG II is directly injected into the brain, albeit with lower sensitivity (31,114).…”

Section: Localization Of Ras Components Required For Ang II Productionmentioning

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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“…The correct placement and functional status of the cannulas in the A y mice receiving low doses of i.c.v. leptin were tested by measuring water intake after infusion of angiotensin II at 3 ng͞hr (21). The animals that did not respond to i.c.v.…”

Section: Physiology: Halaas Et Almentioning

confidence: 99%

“…The i.c.v. infusion was performed using a microsurgical technique for long-term infusion into the third ventricle of mice (21). AKR͞J mice are lean on a chow diet but have a heritable predisposition toward developing obesity when fed a high-fat diet (22).…”

mentioning

confidence: 99%

Physiological response to long-term peripheral and central leptin infusion in lean and obese mice

Halaas

Boozer

Blair‐West

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

942

670

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Recent data have identified leptin as an afferent signal in a negative-feedback loop regulating the mass of the adipose tissue. High leptin levels are observed in obese humans and rodents, suggesting that, in some cases, obesity is the result of leptin insensitivity. This hypothesis was tested by comparing the response to peripherally and centrally administered leptin among lean and three obese strains of mice: diet-induced obese AKR͞J, New Zealand Obese (NZO), and A y . Subcutaneous leptin infusion to lean mice resulted in a dose-dependent loss of body weight at physiologic plasma levels. Chronic infusions of leptin intracerebroventricularly (i.c.v.) at doses of 3 ng͞hr or greater resulted in complete depletion of visible adipose tissue, which was maintained throughout 30 days of continuous i.c.v. infusion. Direct measurement of energy balance indicated that leptin treatment did not increase total energy expenditure but prevented the decrease that follows reduced food intake. Diet-induced obese mice lost weight in response to peripheral leptin but were less sensitive than lean mice. NZO mice were unresponsive to peripheral leptin but were responsive to i.c.v. leptin. A y mice did not respond to subcutaneous leptin and were 1͞100 as sensitive to i.c.v. leptin. The decreased response to leptin in diet-induced obese, NZO, and A y mice suggests that obesity in these strains is the result of leptin resistance. In NZO mice, leptin resistance may be the result of decreased transport of leptin into the cerebrospinal f luid, whereas in A y mice, leptin resistance probably results from defects downstream of the leptin receptor in the hypothalamus.

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Angiotensin and salt appetite of BALB/c mice

Cited by 29 publications

References 0 publications

Involvement of Tumor Necrosis Factor-α in Angiotensin II–Mediated Effects on Salt Appetite, Hypertension, and Cardiac Hypertrophy

Involvement of Tumor Necrosis Factor-α in Angiotensin II–Mediated Effects on Salt Appetite, Hypertension, and Cardiac Hypertrophy

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

Physiological response to long-term peripheral and central leptin infusion in lean and obese mice

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