Effects of subtypes alpha- and beta-adrenoceptors of the lateral hypothalamus on the water and sodium intake induced by angiotensin II injected into the subfornical organ

Camargo, Luiz Antônio de Arruda; Saad, Wilson Abrão; Camargo, Gabriela

doi:10.1016/s0006-8993(00)02840-7

Cited by 18 publications

(7 citation statements)

References 39 publications

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“…β-Adrenoceptor agonists stimulate water intake through activation of the renin-angiotensin system [20,23). In addition, β-adrenoceptors play a role in the dipsogenic effect of angiotensin II in the preoptic area and hypothalamus [3,8]. However, our data obtained with propranolol rule out any implication of β-adrenoceptors in the increased nocturnal consumption of water exhibited by Y2−/− and Y4−/− mice.…”

Section: Discussionmentioning

confidence: 65%

“…This possibility was envisaged because β-adrenoceptor agonists stimulate water intake [20,23] and NPY is associated with noradrenergic neurons of the central and sympathetic nervous system [16,22]. Thirdly, we examined whether the enhanced water intake in Y2−/− and Y4−/−mice is normalized by the angiotensin AT1 receptor antagonist telmisartan, given that angiotensin II is a central messenger that stimulates drinking [3,12].…”

Section: Introductionmentioning

confidence: 99%

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Selective increase of dark phase water intake in neuropeptide-Y Y2 and Y4 receptor knockout mice

Wultsch

Painsipp

Donner

et al. 2006

Behavioural Brain Research

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Neuropeptide-Y (NPY) is involved in the regulation of ingestive behaviour and energy homeostasis. Since deletion of the NPY Y2 and Y4 receptor gene increases and decreases food intake, respectively, we examined whether water intake during the light and dark phase is altered in Y2 and Y4 receptor knockout mice. The water consumption of mice staying in their home cages was measured by weighing the water bottles at the beginning and end of the light phase during 4 consecutive days. Control, Y2 and Y4 receptor knockout mice did not differ in their water intake during the light phase. However, during the dark phase Y2 and Y4 receptor knockout mice drank significantly more (46-63 %, P<0.05) water than the control mice. The total daily water intake over 24 h was also enhanced. The enhanced water intake during the dark phase was not altered by the β-adrenoceptor antagonist propranolol or the angiotensin AT1 receptor antagonist telmisartan (each injected intraperitoneally at 10 mg/kg). These data indicate that NPY acting via Y2 and Y4 receptors plays a distinctive role in the regulation of nocturnal water consumption. While β-adrenoceptors and angiotensin AT1 receptors do not seem to be involved, water intake in Y2 and Y4 receptor knockout mice may be enhanced because presynaptic autoinhibition of NPY release and inhibition of orexin neurons in the central nervous system are prevented.

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Section: Discussionmentioning

confidence: 65%

Section: Introductionmentioning

confidence: 99%

Selective increase of dark phase water intake in neuropeptide-Y Y2 and Y4 receptor knockout mice

Wultsch

Painsipp

Donner

et al. 2006

Behavioural Brain Research

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“…This pattern, along with the observation that ICV 5-MU did not increase water intake, suggests a specific action of this α 1A -AR antagonist on eating. Camargo et al (2000) infused 5-MU into the lateral hypothalamus, at doses of 20-80 nmol, and did not find a change in water intake over a 4-h postinfusion period. The observation that antagonism of α 1A -ARs by 5-MU increased food intake is consistent with the proposition that α 1 -AR agonist drugs (e.g.…”

Section: Discussionmentioning

confidence: 85%

“…Selective antagonists of the various α 1 -AR subtypes have been developed including the α 1A -AR antagonist 5-methylurapidil (5-MU) (Camargo et al, 2000;Marek and Aghajanian, 1996). In the present study, we assessed the relative impact of ICV administration of 5-MU on cocaine-stimulated locomotion and eating, using a concurrent method.…”

Section: Introductionmentioning

confidence: 99%

Effects of ICV administration of the alpha1A-adrenoceptor antagonist 5-methylurapidil on concurrent measures of eating and locomotion after cocaine in the rat

et al. 2007

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Psychostimulants including amphetamine and cocaine induce locomotion and stereotypy and suppress eating. Although the capacity of cocaine to alter locomotion is usually viewed as related to dopamine neurotransmission, recent studies suggest that norepinephrine, acting through alpha1-adrenergic receptors (alpha1-ARs) can facilitate cocaine-stimulated locomotion. Of the three alpha1-AR subtypes (alpha(1A), alpha(1B), and alpha(1D)) identified to date, inactivation of the alpha(1B)-AR subtype diminishes cocaine-stimulated locomotion, whereas the impact of inactivation of the alpha(1A)-AR subtype on either eating or locomotion is unknown. In the present study, we assessed the relative impact of ICV administration of the alpha(1B)-AR antagonist 5-methylurapidil (5-MU) on cocaine-stimulated hyperlocomotion and hypophagia, using a concurrent method [Wellman, P.J., Ho, D.H., Davis, K.W., 2005. Concurrent measures of feeding and locomotion in rats. Physiology of Behavior 84 (5), 769-774.]. Rats were infused ICV with one of 3 doses of 5-MU (0, 3, or 30 nmol) and then injected (i.p.) with 0, 2.5, 5.0, 10.0, or 20.0 mg/kg cocaine HCl on each of five tests. Rats always received the same 5-MU dose, but a different cocaine dose on each trial. Feeding and locomotion were assessed concurrently during a 45-min postinjection period. Significant suppression of eating was noted at 2.5 mg/kg cocaine, a dose that does not alter forward locomotion in the rat. Administration of 5-MU did not alter locomotion in rats treated with saline, but did significantly increase baseline food intake. Neither cocaine-induced hypophagia nor hyperlocomotion was altered by ICV administration of 5-MU. These results suggest that the capacity of alpha1-AR agonists (e.g. phenylpropanolamine) to suppress eating may be related to activation of the alpha(1A)-AR subtype, whereas cocaine does not act through the alpha(1A)-AR subtype to suppress eating nor does this subtype modulate cocaine-induced hyperlocomotion.

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“…For the intracerebral injection, the ODNs were diluted to a final concentration of 100 ng/ l artificial cerebrospinal fluid (22). Under pentobarbital (7.5 mg/kg body weight) and ketamine hydrochloride (25 mg/kg body weight) anesthesia, a polyethylene cannula (outer diameter, 1.05 mm; inner diameter, 0.35 mm) was stereotaxically implanted into the brain with its opening protruding onto the top of the SFO (coordinates: AP ϭ 1.3 mm caudal to the bregma; V ϭ 4.3 mm from the dura mater; L ϭ 0.0 mm from the midsagittal line) as recommended (37). After a week of recovery, the ODNs (2 nmol in 4 l of artificial cerebrospinal fluid) were injected with a Hamilton syringe, and water intake, urine excretion, and body weight were measured.…”

Section: Methodsmentioning

confidence: 99%

TTF-1, a Homeodomain-containing Transcription Factor, Participates in the Control of Body Fluid Homeostasis by Regulating Angiotensinogen Gene Transcription in the Rat Subfornical Organ

Son

Hur

Ryu

et al. 2003

Journal of Biological Chemistry

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In recent years, it has become increasingly evident that angiotensins synthesized in the brain contribute to regulating body fluid homeostasis. Although angiotensinogen, the unique angiotensin precursor, is produced in the brain, the factors that regulate its gene expression remain unknown. We recently found that TTF-1, a homeodomain-containing transcription factor essential for the development of the fetal diencephalon, is postnatally expressed in discrete areas of the hypothalamus. We now report that the subfornical organ, an important site of angiotensinogen synthesis, is an extrahypothalamic site of TTF-1 expression. Double in situ hybridization histochemistry demonstrated the presence of TTF-1 mRNA in angiotensinogen-producing cells of the rat subfornical organ. RNase protection assays showed that TTF-1 and angiotensinogen mRNA levels are simultaneously increased in the subfornical organ by water deprivation. The angiotensinogen promoter contains seven presumptive TTF-1 binding motifs, four of which are recognized by the TTF-1 homeodomain. In the C6 glioma cell line, TTF-1 transactivates the angiotensinogen promoter in a dose-dependent manner. This transactivation is abolished by deletion of the TTF-1 binding motif at ؊125. Intracranial administration of an antisense TTF-1 oligodeoxynucleotide decreased angiotensinogen mRNA in the subfornical organ and dramatically reduced the animal's water intake while increasing urine excretion. Moreover, plasma arginine vasopressin content was decreased by the same treatment. These results demonstrate a novel role for TTF-1 in the regulation of body fluid homeostasis, exerted via the transactivational control of angiotensinogen synthesis in the subfornical organ.The control of body fluid volume and blood pressure is a critical homeostatic process required for normalcy of the internal environment and for the preservation of life. Many studies have demonstrated that the renin-angiotensin system (RAS) 1 plays an important role in the regulation of fluid volume balance, blood pressure, and other related biological responses through the generation of angiotensin II (ANG II) (1). The existence of a brain RAS in addition to the peripheral RAS has also been established (2, 3). All components of the peripheral RAS have been found in the brain, most notably in the subfornical organ (SFO). The SFO is a circumventricular organ (CVO) of the lamina terminalis located at the top of the dorsal third ventricle (4). It is composed of fenestrated capillary loops in addition to glial cells, but in contrast to other CVOs such as the median eminence of the hypothalamus, it also contains neuronal cell bodies (1, 5). The SFO of rats contains high concentrations of angiotensinogen (AoGen) (6), the angiotensin precursor; renin-like activity (that converts AoGen to ANG I) (7); angiotensin-converting enzyme (which converts ANG I to ANG II) (8); the peptide ANG II (9); and AT 1 -type ANG II receptors (3). Thus, the SFO is not only a target for circulating ANG II, which exerts a potent dipsogenic ef...

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Effects of subtypes alpha- and beta-adrenoceptors of the lateral hypothalamus on the water and sodium intake induced by angiotensin II injected into the subfornical organ

Cited by 18 publications

References 39 publications

Selective increase of dark phase water intake in neuropeptide-Y Y2 and Y4 receptor knockout mice

Selective increase of dark phase water intake in neuropeptide-Y Y2 and Y4 receptor knockout mice

Effects of ICV administration of the alpha1A-adrenoceptor antagonist 5-methylurapidil on concurrent measures of eating and locomotion after cocaine in the rat

TTF-1, a Homeodomain-containing Transcription Factor, Participates in the Control of Body Fluid Homeostasis by Regulating Angiotensinogen Gene Transcription in the Rat Subfornical Organ

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