Salt appetite in rat pups: ontogeny of angiotensin II-aldosterone synergy

1991 ◽  
Vol 260 (2) ◽  
pp. R421-R429 ◽  
Author(s):  
C. I. Thompson ◽  
A. N. Epstein
Keyword(s):  
Angiotensin Ii ◽  
Water Intake ◽  
Salt Intake ◽  
Neural Mechanisms ◽  
Salt Appetite ◽  
Ang Ii ◽  
Rat Pups ◽  
Effective Doses ◽  
Old Rats ◽  
Individual Actions

Preweanling rats were tested to determine whether angiotensin II (ANG II) and aldosterone (Aldo) act synergistically to enhance salt appetite at 12 and 17 days. Twelve-day-old pups received one of four hormone treatments in four doses: 1) ANG II only [1, 2, 10, or 100 ng pulse intracerebroventricular (icv)], 2) Aldo only (1, 2, 10, or 40 micrograms/day sc), 3) Aldo + ANG II (four individual doses combined), or 4) vehicle. Seventeen-day-old rats received the same treatments in two doses (2 or 100 ng ANG II; 2 or 40 micrograms Aldo). Pups were presatiated with milk through anterior oral catheters and then given either 4% NaCl or water for 30 min. Intake was assessed by body weight change. At both ages, ANG II enhanced salt (and water) intake, and Aldo enhanced salt (but not water) intake. Minimum effective doses were comparable to those reported for adults. ANG II-Aldo synergy was absent at 12 days and present at 17 days, when salt intake was 590% greater than the summed intakes evoked by ANG II and Aldo alone. The neural mechanisms for ANG II-Aldo synergy thus mature later than those mediating the hormone's individual actions in arousing salt appetite.

Central infusion of the AT1 receptor antagonist losartan inhibits thirst but not sodium appetite in cattle

1997 ◽  
Vol 272 (6) ◽  
pp. R1940-R1945 ◽  
Author(s):  
J. R. Blair-West ◽  
D. A. Denton ◽  
M. J. McKinley ◽  
R. S. Weisinger
Keyword(s):  
Water Intake ◽  
Salt Intake ◽  
Sodium Intake ◽  
High Water ◽  
Salt Appetite ◽  
Ang Ii ◽  
Sodium Depletion ◽  
Water Restriction ◽  
Sodium Appetite ◽  
High Water Intake

Experiments in cattle compared the effects of intracerebroventricular (i.c.v.) infusions of losartan and PD-123319 on water intake caused by water restriction, i.c.v. infusion of hypertonic NaCl, or i.c.v. infusion of angiotensin II (ANG II). The effects of these receptor antagonists on sodium intake caused by sodium depletion were also examined. Losartan infusion caused dose-dependent inhibition of the high water intake caused by the physiological stimulus of water restriction or by ANG II infusion but did not affect salt appetite. PD-123319 infused at equimolar or greater (in ANG II experiments) doses did not affect water intake or salt intake due to sodium depletion. The results of these i.c.v. infusion experiments confirm our earlier proposal that the physiological regulation of water intake in cattle may be mediated by ANG II acting centrally via AT1 receptors. The dose of losartan that inhibited thirst in cattle did not inhibit sodium appetite, nor did an equimolar dose of PD-123319.

scholarly journals Enhanced water and salt intake in transgenic mice with brain-restricted overexpression of angiotensin (AT1) receptors

2008 ◽  
Vol 295 (5) ◽  
pp. R1539-R1545 ◽  
Author(s):  
Eric Lazartigues ◽  
Puspha Sinnayah ◽  
Ginette Augoyard ◽  
Claude Gharib ◽  
Alan Kim Johnson ◽  
...  
Keyword(s):  
Water Intake ◽  
Salt Intake ◽  
Sodium Intake ◽  
Third Ventricle ◽  
Model Neuron ◽  
Neuron Specific Enolase ◽  
Salt Appetite ◽  
Ang Ii ◽  
Sodium Depletion ◽  
Salt Consumption

To address the relative contribution of central and peripheral angiotensin II (ANG II) type 1A receptors (AT1A) to blood pressure and volume homeostasis, we generated a transgenic mouse model [neuron-specific enolase (NSE)-AT1A] with brain-restricted overexpression of AT1A receptors. These mice are normotensive at baseline but have dramatically enhanced pressor and bradycardic responses to intracerebroventricular ANG II or activation of endogenous ANG II production. Here our goal was to examine the water and sodium intake in this model under basal conditions and in response to increased ANG II levels. Baseline water and NaCl (0.3 M) intakes were significantly elevated in NSE-AT1A compared with nontransgenic littermates, and bolus intracerebroventricular injections of ANG II (200 ng in 200 nl) caused further enhanced water intake in NSE-AT1A. Activation of endogenous ANG II production by sodium depletion (10 days low-sodium diet followed by furosemide, 1 mg sc) enhanced NaCl intake in NSE-AT1A mice compared with wild types. Fos immunohistochemistry, used to assess neuronal activation, demonstrated sodium depletion-enhanced activity in the anteroventral third ventricle region of the brain in NSE-AT1A mice compared with control animals. The results show that brain-selective overexpression of AT1A receptors results in enhanced salt appetite and altered water intake. This model provides a new tool for studying the mechanisms of brain AT1A-dependent water and salt consumption.

Angiotensin II-induced thirst, but not sodium appetite, via AT1 receptors in organum cavum prelamina terminalis

1995 ◽  
Vol 268 (6) ◽  
pp. R1401-R1405 ◽  
Author(s):  
M. el Ghissassi ◽  
S. N. Thornton ◽  
S. Nicolaidis
Keyword(s):  
Angiotensin Ii ◽  
Salt Intake ◽  
High Sensitivity ◽  
Ang Ii ◽  
Nacl Solution ◽  
At1 Receptors ◽  
Sodium Appetite ◽  
Specific Antagonist

The angiotensin receptor specificity, with respect to fluid intake, of the organum cavum prelamina terminalis (OCPLT), a recently discovered discrete forebrain structure with high sensitivity to angiotensin II (ANG II), was investigated. ANG II (10 ng) microinjected into the OCPLT significantly increased water consumption but did not induce intake of a hypertonic (3%) NaCl solution. Losartan, an ANG II type 1 (AT1) receptor-specific antagonist, produced dose-related (1-100 ng) inhibition of ANG II-induced drinking. The ANG II type 2 receptor-specific antagonist CGP-42112A was ineffective. Intake of the 3% NaCl solution in response to microinjection of either of the antagonists into the OCPLT was never observed. These findings suggest that water intake produced by microinjection of ANG II into the OCPLT is mediated by AT1 receptors uniquely and that, in contrast to other regions of the brain, these receptors do not induce salt intake when stimulated by ANG II.

Angiotensin and Na appetite of sheep

1986 ◽  
Vol 251 (4) ◽  
pp. R690-R699 ◽  
Author(s):  
R. S. Weisinger ◽  
D. A. Denton ◽  
M. J. McKinley ◽  
A. F. Muller ◽  
E. Tarjan
Keyword(s):  
Cerebrospinal Fluid ◽  
Angiotensin Ii ◽  
Water Intake ◽  
Ang Ii ◽  
Nacl Solution ◽  
Parotid Saliva ◽  
Continuous Access ◽  
Access To Water

The effect of both intravenous (iv; 24 micrograms/h) and intracerebroventricular (ivt; 3.8 micrograms/h) infusion over 1-2 days of angiotensin II (ANG II) on Na intake of both Na-replete and -deplete sheep (i.e., 22 h loss of parotid saliva) was observed. In Na-replete sheep with continuous access to water and 2-h daily access to 0.5 M NaCl solution, both iv and ivt ANG II caused an increase in Na intake. The increase in Na intake caused by iv or ivt ANG II was preceded by a Na deficit due to increased urinary Na excretion. The increase in Na intake was eliminated by the continuous return of urine. In Na-deplete sheep with continuous access to water and 2-h daily access to 0.6 M NaHCO3 solution, iv ANG II caused no change in Na loss but a small increase in Na intake during the 1st day of infusion. The ivt ANG II caused no change in Na loss or in Na intake. The iv ANG II caused a small and inconsistent increase in water intake in Na-replete sheep but did not cause any change in water intake of Na-deplete sheep. The ivt ANG II caused a large increase in water intake in both Na-replete and -deplete sheep. In both Na-replete and -deplete sheep, iv ANG II did not alter cerebrospinal fluid or plasma [Na] or osmolality but decreased plasma [K]. The ivt ANG II decreased both cerebrospinal fluid and plasma [Na] and osmolality. The results of the present experiments are consistent with the proposition that the ANG II-induced Na appetite in sheep is largely due to an ANG II-induced Na loss preceding the development of appetite.

Role of arteria baroreceptor input on thirst and urinary responses to intracerebroventricular angiotensin II

1993 ◽  
Vol 265 (3) ◽  
pp. R591-R595 ◽  
Author(s):  
R. L. Thunhorst ◽  
S. J. Lewis ◽  
A. K. Johnson
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Arterial Blood Pressure ◽  
Water Intake ◽  
Enzyme Inhibitor ◽  
Ang Ii ◽  
Converting Enzyme ◽  
Arterial Blood ◽  
Endogenous Formation

Intracerebroventricular (icv) infusion of angiotensin II (ANG II) in rats elicits greater water intake under hypotensive, compared with normotensive, conditions. The present experiments used sinoaortic baroreceptor-denervated (SAD) rats and sham-operated rats to examine if the modulatory effects of arterial blood pressure on water intake in response to icv ANG II are mediated by arterial baroreceptors. Mean arterial blood pressure (MAP) was raised or lowered by intravenous (i.v.) infusions of phenylephrine (1 or 10 micrograms.kg-1 x min-1) or minoxidil (25 micrograms.kg-1 x min-1), respectively. The angiotensin-converting enzyme inhibitor captopril (0.33 mg/min) was infused i.v. to prevent the endogenous formation of ANG II during testing. Urinary excretion of water and solutes was measured throughout. Water intake elicited by icv ANG II was inversely related to changes in MAP. Specifically, rats drank more water in response to icv ANG II when MAP was reduced by minoxidil but drank less water when MAP was elevated by phenylephrine. The influence of changing MAP on the icv ANG II-induced drinking responses was not affected by SAD. These results suggest that the modulatory effects of arterial blood pressure on icv ANG II-induced drinking can occur in the absence of sinoaortic baroreceptor input.

scholarly journals Central and peripheral slow-pressor mechanisms contributing to Angiotensin II-salt hypertension in rats

2017 ◽  
Vol 114 (2) ◽  
pp. 233-246 ◽  
Author(s):  
Jiao Lu ◽  
Hong-Wei Wang ◽  
Monir Ahmad ◽  
Marzieh Keshtkar-Jahromi ◽  
Mordecai P Blaustein ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Adrenal Cortex ◽  
Salt Intake ◽  
Plasma Corticosterone ◽  
High Salt ◽  
Ang Ii ◽  
Intracerebroventricular Infusion ◽  
High Salt Intake ◽  
Endogenous Ouabain ◽  
Salt Hypertension

AbstractAimsHigh salt intake markedly enhances hypertension induced by angiotensin II (Ang II). We explored central and peripheral slow-pressor mechanisms which may be activated by Ang II and salt.Methods and resultsIn protocol I, Wistar rats were infused subcutaneously with low-dose Ang II (150 ng/kg/min) and fed regular (0.4%) or high salt (2%) diet for 14 days. In protocol II, Ang II-high salt was combined with intracerebroventricular infusion of mineralocorticoid receptor (MR) blockers (eplerenone, spironolactone), epithelial sodium channel (ENaC) blocker (benzamil), angiotensin II type 1 receptor (AT1R) blocker (losartan) or vehicles. Ang II alone raised mean arterial pressure (MAP) ∼10 mmHg, but Ang II-high salt increased MAP ∼50 mmHg. Ang II-high salt elevated plasma corticosterone, aldosterone and endogenous ouabain but not Ang II alone. Both Ang II alone and Ang II-high salt increased mRNA and protein expression of CYP11B2 (aldosterone synthase gene) in the adrenal cortex but not of CYP11B1 (11-β-hydroxylase gene). In the aorta, Ang II-high salt increased sodium-calcium exchanger-1 (NCX1) protein. The Ang II-high salt induced increase in MAP was largely prevented by central infusion of MR blockers, benzamil or losartan. Central blockades significantly lowered plasma aldosterone and endogenous ouabain and markedly decreased Ang II-high salt induced CYP11B2 mRNA expression in the adrenal cortex and NCX1 protein in the aorta.ConclusionThese results suggest that in Ang II-high salt hypertension, MR-ENaC-AT1R signalling in the brain increases circulating aldosterone and endogenous ouabain, and arterial NCX1. These factors can amplify blood pressure responses to centrally-induced sympatho-excitation and thereby contribute to severe hypertension.

Intracerebroventricular infusion of angiotensin II increases water and ethanol intake in rats

1999 ◽  
Vol 277 (1) ◽  
pp. R162-R172 ◽  
Author(s):  
R. S. Weisinger ◽  
J. R. Blair-West ◽  
P. Burns ◽  
D. A. Denton
Keyword(s):  
Angiotensin Ii ◽  
Direct Effect ◽  
Water Intake ◽  
Indirect Effect ◽  
Taste Preference ◽  
Ethanol Solution ◽  
Ethanol Intake ◽  
Ang Ii ◽  
Intracerebroventricular Infusion ◽  
Stimulation Of

The influence of prolonged ingestion of ethanol on stimulation of water or ethanol intake by intracerebroventricular infusion of ANG II was evaluated in rats. Animals were maintained for 5–6 mo with either 10% ethanol solution or water as their only source of fluid. In both groups of rats, infusion of ANG II caused a large increase in water intake (7-fold) and a lesser increase in 10% ethanol intake (2-fold). The effect of ANG II on the volume of ethanol solution ingested, however, was inversely related to the concentration of the ethanol solution. As the concentration of ethanol solution was decreased, frequency and duration of drinking bouts increased. The intake of sweetened 10% ethanol solution or commercially produced wine during infusion of ANG II was similar to the intake of 10% ethanol and not related to taste preference. In conclusion, chronic consumption of ethanol solution did not appear to adversely effect ANG II stimulation of water intake. The intake of ethanol solution during infusion of ANG II was inhibited by a direct effect of ingested ethanol and/or by indirect effect from metabolized ethanol.

Angiotensin II enhances β-adrenergic receptor-mediated vasorelaxation in aortas from young but not old rats

2000 ◽  
Vol 279 (6) ◽  
pp. H2807-H2814 ◽  
Author(s):  
William E. Schutzer ◽  
Hong Xue ◽  
John F. Reed ◽  
Jean-Baptiste Roullet ◽  
Sharon Anderson ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Adrenergic Receptor ◽  
Age Groups ◽  
Ang Ii ◽  
Camp Production ◽  
Fischer 344 ◽  
Age Related ◽  
Old Rats ◽  
Potent Vasoconstrictor ◽  
Direct Activator

β-Adrenergic receptor (β-AR)-mediated (cAMP-dependent) vasorelaxation declines with advancing age. It has been shown that angiotensin II (ANG II), a potent vasoconstrictor, enhances cAMP-mediated vasorelaxation. Therefore, we questioned whether ANG II could reverse age-related, impaired β-AR-mediated vasorelaxation and cAMP production. Pretreatment of aortic rings from 6-wk-old or 6-mo-old male Fischer 344 rats with ANG II significantly enhanced vasorelaxation induced by isoproterenol (Iso), a β-AR agonist, and forskolin, a direct activator of adenylyl cyclase, but not dibutyryl-cAMP or isobutylmethylxanthine. The ANG II effect was blocked by losartan but not PD-123319 and was not observed in the aortas from 12- and 24-mo-old animals. Iso-stimulated cAMP production in the aorta was enhanced in the presence of ANG II in the 6-wk-old and 6-mo-old age groups only. Results suggest ANG II cannot reverse the age-related impairment in β-AR-dependent vasorelaxation. We conclude aging may affect a factor common to both ANG II-receptors and β-AR signaling pathways or aging may impair cross-talk between these two receptor pathways.

Intracerebroventricular losartan inhibits postprandial drinking in sheep

1997 ◽  
Vol 272 (4) ◽  
pp. R1055-R1059 ◽  
Author(s):  
M. Mathai ◽  
M. D. Evered ◽  
M. J. McKinley
Keyword(s):  
Cerebrospinal Fluid ◽  
Angiotensin Ii ◽  
Food Intake ◽  
Water Intake ◽  
Fluid Balance ◽  
Intravenous Infusion ◽  
Ang Ii ◽  
Intracerebroventricular Infusion ◽  
Drinking Response ◽  
Dependent Mechanism

We investigated the contribution of brain angiotensinergic mechanisms to postprandial drinking in sheep. Sheep in fluid balance were given 0.8 kg chaff for 30 min, and water intake was measured for the next hour. Intracerebroventricular infusion of the AT1 type angiotensin II (ANG II) receptor blocker losartan (1 mg/h) reduced postprandial drinking by approximately 70% (n = 7, P < 0.01) but did not affect food intake. The same losartan dose given intravenously had little or no effect on prandial drinking. Feeding increased Na+ concentrations in plasma and cerebrospinal fluid (CSF; n = 5, P < 0.05). Intracerebroventricular losartan (1 mg/h) inhibited the drinking responses to intracarotid infusion of ANG II (0.8 microg/min for 30 min, n = 4, P < 0.01) and to intracerebroventricular infusion of 0.5 M NaCl (1 ml/h for 1 h, n = 5, P < 0.05) but had no effect on drinking responses to intravenous infusion of 4 M NaCl (1.3 ml/min for 30 min). These findings indicate that a brain ANG II-dependent mechanism is involved in postprandial drinking in sheep. They suggest also that the mechanism by which increasing CSF Na+ causes thirst involves brain ANG II and is different from the mechanism subserving the drinking response to changes in blood Na+.

scholarly journals mTORC1 Signaling Contributes to Drinking But Not Blood Pressure Responses to Brain Angiotensin II

Endocrinology ◽  
2016 ◽  
Vol 157 (8) ◽  
pp. 3140-3148 ◽  
Author(s):  
Kenjiro Muta ◽  
Donald A. Morgan ◽  
Justin L. Grobe ◽  
Curt D. Sigmund ◽  
Kamal Rahmouni
Keyword(s):  
Angiotensin Ii ◽  
Water Intake ◽  
Drinking Behavior ◽  
Subfornical Organ ◽  
Dependent Manner ◽  
Ang Ii ◽  
Mtorc1 Signaling ◽  
Wide Range ◽  
The Brain

Mechanistic target of rapamycin complex 1 (mTORC1) is a molecular node that couples extracellular cues to a wide range of cellular events controlling various physiological processes. Here, we identified mTORC1 signaling as a critical mediator of angiotensin II (Ang II) action in the brain. In neuronal GT1–7 cells, we show that Ang II stimulates neuronal mTORC1 signaling in an Ang II type 1 receptor-dependent manner. In mice, a single intracerebroventricular (ICV) injection or chronic sc infusion of Ang II activated mTORC1 signaling in the subfornical organ, a critical brain region in cardiovascular control and fluid balance. Moreover, transgenic sRA mice with brain-specific overproduction of Ang II displayed increased mTORC1 signaling in the subfornical organ. To test the functional role of brain mTORC1 in mediating the action of Ang II, we examined the consequence of mTORC1 inhibition with rapamycin on Ang II-induced increase in water intake and arterial pressure. ICV pretreatment with rapamycin blocked ICV Ang II-mediated increases in the frequency, duration, and amount of water intake but did not interfere with the pressor response evoked by Ang II. In addition, ICV delivery of rapamycin significantly reduced polydipsia, but not hypertension, of sRA mice. These results demonstrate that mTORC1 is a novel downstream pathway of Ang II type 1 receptor signaling in the brain and selectively mediates the effect of Ang II on drinking behavior.

Sign in / Sign up

Export Citation Format

Share Document