scholarly journals Circumventricular organs and ANG II-induced salt appetite: blood pressure and connectivity

2000 ◽  
Vol 279 (6) ◽  
pp. R2277-R2286 ◽  
Author(s):  
Douglas A. Fitts ◽  
Elizabeth M. Starbuck ◽  
Alexandra Ruhf
Keyword(s):  
Blood Pressure ◽  
Water Intake ◽  
Femoral Vein ◽  
Circumventricular Organs ◽  
Subfornical Organ ◽  
Salt Appetite ◽  
Ang Ii ◽  
Sodium Depletion ◽  
Apparent Contradiction ◽  
Organum Vasculosum Laminae Terminalis

A lesion of the subfornical organ (SFO) may reduce sodium depletion-induced salt appetite, which is largely dependent on ANG II, and yet ANG II infusions directly into SFO do not provoke salt appetite. Two experiments were designed to address this apparent contradiction. In experiment 1 sustained infusions of ANG II into SFO did not produce a sustained elevation of blood pressure, and neither a reduction of blood pressure alone with minoxidil and captopril nor a reduction of both blood pressure and volume with furosemide and captopril enhanced salt appetite. Infusions of ANG II in the organum vasculosum laminae terminalis (OVLT) did evoke salt appetite without raising blood pressure. In experiment 2 knife cuts of the afferent and efferent fibers of the rostroventral pole of the SFO abolished water intake during an infusion of ANG II into the femoral vein but failed to reduce salt appetite during an infusion of ANG II into the OVLT. We conclude that 1) hypertension does not account for the failure of infusions of ANG II in the SFO to generate salt appetite and 2) the OVLT does not depend on its connectivity with the SFO to generate salt appetite during ANG II infusions.

Central actions of angiotensin in cardiovascular control: Multiple roles for a single peptide

1992 ◽  
Vol 70 (5) ◽  
pp. 779-785 ◽  
Author(s):  
Alastair V. Ferguson ◽  
Katharine M. Wall
Keyword(s):  
Blood Pressure ◽  
Area Postrema ◽  
Circumventricular Organs ◽  
Subfornical Organ ◽  
Cardiovascular Control ◽  
Multiple Roles ◽  
Ang Ii ◽  
Electrophysiological Studies ◽  
The Central Nervous System ◽  
Central Actions

Angiotensin II (ANG II) acts peripherally as a hormone, with actions on the vasculature, adrenals, and kidney. In addition, certain actions of ANG II in the central nervous system are directed toward cardiovascular control and fluid volume homeostasis. Dense binding sites for ANG II are found at circumventricular organs, which apparently have the ability to relay information to cardiovascular centers via neural circuitry. Microinjection of ANG II into the subfornical organ (SFO) or area postrema (AP) produces site-specific increases in blood pressure. In addition, electrophysiological studies demonstrate profound effects of ANG II, acting at the SFO, on activity of neurohypophysial neurons and release of oxytocin and vasopressin, which can be antagonized by ANG II blockers or attenuated by SFO lesions. Evidence from microinjection, electrophysiological, and lesion studies indicate a complex interaction between central sites involved in mechanisms of cardiovascular control: the SFO, AP, organum vasculosum of the lamina terminalis, and paraventricular and supraoptic nuclei of the hypothalamus. Not only is ANG II a humoral messenger in this central scenario, but evidence suggests it acts as a neurotransmitter or neuroendocrine substance within specific CNS pathways, suggesting multiple roles for this peptide in central cardiovascular control.Key words: blood pressure regulation, circumventricular organs, vasopressin, area postrema, subfornical organ.

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.

Effects of forebrain circumventricular organ ablation on drinking or salt appetite after sodium depletion or hypernatremia

2004 ◽  
Vol 287 (6) ◽  
pp. R1325-R1334 ◽  
Author(s):  
Douglas A. Fitts ◽  
Julia A. Freece ◽  
Julie E. Van Bebber ◽  
Dannielle K. Zierath ◽  
John E. Bassett
Keyword(s):  
Hypertonic Saline ◽  
Physiological Responses ◽  
Daily Basis ◽  
Subfornical Organ ◽  
The Other ◽  
Salt Appetite ◽  
Circumventricular Organ ◽  
Sodium Depletion ◽  
Organum Vasculosum Laminae Terminalis ◽  
Single Lesion

In many previous studies, one or the other forebrain circumventricular organ, the subfornical organ (SFO) or organum vasculosum laminae terminalis (OVLT), was lesioned to test whether it was critical for the behavioral or physiological responses to sodium depletion and hypernatremia. These studies conflict in their conclusions. The present study was designed to create discrete lesions of both the SFO and OVLT in the same animals and to compare these with rats having a lesion of only the SFO or OVLT. Both the OVLT-lesioned group and the combined SFO + OVLT-lesioned group drank significantly more water and saline on a daily basis than Controls or SFO-lesioned rats. In both sodium depletion and hypertonic saline testing, rats with SFO lesions displayed transient deficits in salt appetite or thirst responses, whereas the rats with single OVLT lesions did not. In the sodium depletion test, but not in the hypernatremia test, rats with lesions of both the SFO and OVLT exhibited the largest deficit. The data support the hypothesis that a combined lesion eliminates redundancy and is more effective than a single lesion in sodium depletion tests. The interpretation of the OVLT lesion-only data may have been complicated by a tendency to drink more fluid on a daily basis, because some of those animals drank copious water in addition to saline even very early during the salt appetite test.

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.

Synergy between angiotensin and aldosterone in evoking sodium appetite in baboons

2002 ◽  
Vol 283 (5) ◽  
pp. R1070-R1078 ◽  
Author(s):  
R. E. Shade ◽  
J. R. Blair-West ◽  
K. D. Carey ◽  
L. J. Madden ◽  
R. S. Weisinger ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Food Intake ◽  
Water Intake ◽  
Daily Intake ◽  
Salt Appetite ◽  
Ang Ii ◽  
Vasopressin Release ◽  
Arterial Blood ◽  
Excretion Rates ◽  
Acth Release

The synergy between ANG II and aldosterone (Aldo) in the induction of salt appetite, extensively studied in rats, has been tested in baboons. ANG II was infused intracerebroventricularly at 0.5 or 1.0 μg/h; Aldo was infused subcutaneously at 20 μg/h. Separate infusions over 7 days had no significant effect on the daily intake of 300 mM NaCl. Concurrent infusions, however, increased daily NaCl intake ∼10-fold and daily water intake ∼2.5-fold. In addition, the combined infusions caused 1) a reduction in daily food intake, 2) changes in blood composition indicative of increased vasopressin release, and 3) changes of urinary excretion rates of cortisol and Aldo indicative of increased ACTH release. Arterial blood pressure, measured in two baboons, rose during concurrent ANG II and Aldo treatment. These results indicate a potent synergy between central ANG II and peripheral Aldo in stimulating salt appetite in baboons. At the same time, other ANG II-specific brain mechanisms concerned with water intake, food intake, vasopressin release, ACTH release, and blood pressure regulation appear to have been activated by the same type of synergy. These central enhancement processes have never been previously demonstrated in primates.

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.

Effects of central oxytocin receptor blockade on water and saline intake, mean arterial pressure, and c-Fos expression in rats

2003 ◽  
Vol 285 (6) ◽  
pp. R1331-R1339 ◽  
Author(s):  
Douglas A. Fitts ◽  
Simon N. Thornton ◽  
Alexandra A. Ruhf ◽  
Dannielle K. Zierath ◽  
Alan Kim Johnson ◽  
...  
Keyword(s):  
Pressor Response ◽  
Inhibitory Effect ◽  
Salt Appetite ◽  
Ang Ii ◽  
Preoptic Nucleus ◽  
Organum Vasculosum Laminae Terminalis ◽  
Fos Expression ◽  
Oxytocinergic Neurons ◽  
Oxytocin Antagonist ◽  
First Time

Central injection of ANG II has been proposed to have dual effects on salt appetite including a direct stimulatory effect and an indirect inhibitory effect through an activation of central oxytocinergic neurons. The inhibition was demonstrated by pretreating rats with central ornithine vasotocin (OVT; oxytocin antagonist) 30 min before a central ANG II injection. The OVT pretreatment produced a large increase in ANG II-induced saline intake. The present paper reports a failure to replicate that influential experiment. However, we also report for the first time that OVT by itself: 1) provokes drinking of both water and saline solution with a latency almost as short as that produced by ANG II; 2) produces a mild pressor response; and 3) increases c-Fos expression in the organum vasculosum laminae terminalis (OVLT) and the median preoptic nucleus (MnPO). Oxytocin activity may provide an inhibitory control of drinking responses as has been suggested, but the inhibition is tonic and includes both water and saline drinking. Inhibition of this tonic activity may stimulate drinking by increasing neural activity in the OVLT and MnPO.

Angiotensin II receptors in SFO but not in OVLT mediate isoproterenol-induced thirst

1994 ◽  
Vol 267 (1) ◽  
pp. R7-R15 ◽  
Author(s):  
D. A. Fitts
Keyword(s):  
Angiotensin Ii ◽  
Circumventricular Organs ◽  
Ang Ii ◽  
Circumventricular Organ ◽  
Adrenergic Agonist ◽  
Receptor Sites ◽  
Organum Vasculosum Laminae Terminalis ◽  
Reduced Drinking ◽  
Beta Adrenergic Agonist ◽  
The Brain

Thirst elicited by the beta-adrenergic agonist isoproterenol in rats depends in part on the secretion of renin, the consequent synthesis of angiotensin II (ANG II), and the binding of circulating ANG II to dipsogenic receptors in the brain. These receptors probably reside in either of two forebrain circumventricular organs, the subfornical organ (SFO) or organum vasculosum laminae terminalis (OVLT). Experiments determined that lesions of the SFO, but not of the OVLT, reduced drinking induced by isoproterenol treatment. Competitive ANG II-receptor antagonism with sarthran reduced isoproterenol-induced drinking when the blocker was infused into the SFO but not when it was infused into the OVLT or into the lateral ventricles at a 25-fold greater dose. The findings confirm the widely held belief that renin-dependent thirst elicited by isoproterenol relies on ANG II binding to receptor sites at a circumventricular organ in the brain. The results demonstrate that this site is the SFO and not the OVLT.

Drinking and blood pressure during sodium depletion or ANG II infusion in chronic cholestatic rats

1999 ◽  
Vol 276 (1) ◽  
pp. R23-R31 ◽  
Author(s):  
Douglas A. Fitts ◽  
Jeannine R. Lane ◽  
Elizabeth M. Starbuck ◽  
Chi-Pei Li
Keyword(s):  
Blood Pressure ◽  
Saline Solution ◽  
Ang Ii ◽  
Sodium Depletion ◽  
Drinking Response ◽  
Pressor Responses ◽  
The Common ◽  
Ad Libitum ◽  
Long Evans ◽  
Rapid Intake

After a chronic ligation of the common bile duct (BDL), Long-Evans rats are hypotensive and have elevated saline intake during both sodium-depleted and nondepleted conditions. We tested whether BDL rats have exaggerated hypotension during sodium depletion or an elevated dipsogenic response to angiotensin II (ANG II) that might help to explain the saline intake. After 4 wk of BDL, rats were hypotensive at baseline and developed exaggerated hypotension during acute furosemide-induced diuresis. Without saline to drink, BDL rats increased water intake during depletion equal to sham-ligated rats. However, with saline solution available at 22 h after sodium depletion, the BDL rats drank more water and saline than did sham-ligated rats. This rapid intake temporarily increased their mean arterial pressure to equal that of sham-ligated rats. Intravenous infusion of ANG II induced equal drinking responses despite reduced pressor responses in the BDL rats relative to sham-ligated rats during both ad libitum and sodium-depleted conditions. Thus BDL rats have exaggerated hypotension during diuresis, and their hypotension is corrected by drinking an exaggerated volume of saline, but they do not have an increased drinking response to ANG II.

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