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7. Palatability profile in spontaneously hypertensive rats.

Author

Pereira, Emilson Donizete, Luca, Laurival A De, Menani, José Vanderlei, and Andrade, Carina Aparecida Fabrício

Abstract

The spontaneously hypertensive rats (SHRs) have enhanced palatability for NaCl taste as measured by the increased number of hedonic versus aversive responses to intraoral infusion (1 mL/1 min) of 0.3 M NaCl, in a taste reactivity test in euhydrated condition or after 24 h of water deprivation + 2 h of partial rehydration (WD-PR). SHRs also ingested more sucrose than normotensive rats, without differences in quinine hydrochloride intake. Here, we investigated the palatability of SHRs (n = 8–10) and normotensive Holtzman rats (n = 8–10) to sucrose and quinine sulphate infused intraorally in the same conditions that NaCl palatability was increased in SHRs. SHRs had similar number of hedonic responses to 2% sucrose in euhydrated condition (95 ± 19) or after WD-PR (142 ± 25), responses increased when compared with normotensive rats in euhydrated condition (13 ± 3) or after WD-PR (21 ± 6). SHRs also showed increased number of aversive responses to 1.4 mM quinine sulphate compared with normotensive rats, whether in euhydrated condition (86 ± 6, vs. normotensive: 54 ± 7) or after WD-PR (89 ± 9, vs. normotensive: 40 ± 9). The results suggest that similar to NaCl taste, sweet taste responses are increased in SHRs and resistant to challenges in bodily fluid balance. They also showed a more intense aversive response in SHRs to bitter taste compared with normotensives. This suggests that the enhanced response of SHRs to taste rewards does not correspond to a decreased response to a typical aversive taste. [ABSTRACT FROM AUTHOR]

Published
2023
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15. Whole body sodium depletion modifies AT 1 mRNA expression and serotonin content in the dorsal raphe nucleus

Author

Porcari, Cintia Yamila, primary, Araujo, Iracema Gomes, additional, Urzedo‐Rodrigues, Lilia, additional, De Luca, Laurival Antonio, additional, Menani, José Vanderlei, additional, Caeiro, Ximena Elizabeth, additional, Imboden, Hans, additional, Antunes‐Rodrigues, José, additional, Reis, Luís Carlos, additional, Vivas, Laura, additional, Godino, Andrea, additional, and Mecawi, André Souza, additional

Published
2019
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19. Role of the Carotid Bodies in the Hypertensive and Natriuretic Responses to NaCl Load in Conscious Rats

Author

da Silva, Elaine Fernanda, primary, de Melo, Aryanne Batista Soares, additional, Lobo Júnior, Eulício de Oliveira, additional, Rodrigues, Karla Lima, additional, Naves, Lara Marques, additional, Coltro, Wendell Karlos Tomazelli, additional, Rebelo, Ana Cristina Silva, additional, Freiria-Oliveira, André Henrique, additional, Menani, José Vanderlei, additional, Pedrino, Gustavo Rodrigues, additional, and Colombari, Eduardo, additional

Published
2018
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22. Increased Expression of Macrophage Migration Inhibitory Factor in the Nucleus of the Solitary Tract Attenuates Renovascular Hypertension in Rats

Author

Barbosa, Rafaela Moreira, primary, Speretta, Guilherme F., additional, Dias, Daniel Penteado Martins, additional, Ruchaya, Prashant Jay, additional, Li, Hongwei, additional, Menani, José Vanderlei, additional, Sumners, Colin, additional, Colombari, Eduardo, additional, and Colombari, Débora S. A., additional

Published
2017
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23. Carotid bodies contribute to sympathoexcitation induced by acute salt overload.

Author

da Silva, Elaine Fernanda, Bassi, Mirian, Menani, José Vanderlei, Colombari, Débora Simões Almeida, Zoccal, Daniel Breseghello, Pedrino, Gustavo Rodrigues, and Colombari, Eduardo

Subjects
CAROTID artery, SALT, HYPOTHALAMUS, TACHYPNEA, CAROTID sinus
Abstract

New Findings: What is the central question of this study?Does carotid body input contribute to the hyperosmotic responses?What is the main finding and its importance?The response to NaCl overload is sympathorespiratory excitation. Eliminating the carotid body input reduced sympathoexcitation but did not affect the increase in phrenic burst frequency, whereas eliminating the hypothalamus prevented the tachypnoea and sympathoexcitation. We conclude that the carotid body inputs are essential for the full expression of the sympathetic activity during acute NaCl overload, whereas the tachypnoea depends on hypothalamic mechanisms. Acute salt excess activates central osmoreceptors, which trigger an increase in sympathetic and respiratory activity. The carotid bodies also respond to hyperosmolality of the extracellular compartment, but their contribution to the sympathoexcitatory and ventilatory responses to NaCl overload remains unknown. To evaluate their contribution to acute NaCl overload, we recorded thoracic sympathetic (tSNA), phrenic (PNA) and carotid sinus nerve activities in decorticate in situ preparations of male Holtzman rats (60–100 g) while delivering intra‐arterial infusions of hyperosmotic NaCl (0.17, 0.3, 0.7, 1.5 and 2.0 mol l−1; 200 μl infusion over 25–30 s, with a 10 min time interval between solutions) or mannitol (0.3, 0.5, 1.0, 2.7 and 3.8 mol l−1) progressively. The cumulative infusions of hyperosmotic NaCl increased the perfusate osmolality to 341 ± 5 mosmol (kg water)−1 and elicited an immediate increase in PNA and tSNA (n = 6, P < 0.05) in sham‐denervated rats. Carotid body removal attenuated sympathoexcitation (n = 5, P < 0.05) but did not affect the tachypnoeic response. A precollicular transection disconnecting the hypothalamus abolished the sympathoexcitatory and tachypnoeic responses to NaCl overload (n = 6, P < 0.05). Equi‐osmolar infusions of mannitol did not alter the PNA and tSNA in sham‐denervated rats (n = 5). Sodium chloride infusions increased carotid sinus nerve activity (n = 10, P < 0.05), whereas mannitol produced negligible changes (n = 5). The results indicate that carotid bodies are activated by acute NaCl overload, but not by mannitol. We conclude that the carotid bodies contribute to the increased sympathetic activity during acute NaCl overload, whereas the ventilatory response is mainly mediated by hypothalamic mechanisms. [ABSTRACT FROM AUTHOR]

Published
2019
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26. Cardiovascular responses to hydrogen peroxide into the nucleus tractus solitarius

Author

Cardoso, Leonardo Máximo, Colombari, Débora Simões de Almeida, Menani, José Vanderlei, Toney, Glenn M., Chianca Júnior, Deoclécio Alves, and Colombari, Eduardo

Subjects
Catalase inhibition, nervous system, Heart rate, Blood pressure, Reactive oxygen species, circulatory and respiratory physiology, Kynurenic acid
Abstract

The nucleus tractus solitarius (NTS), a major hindbrain area involved in cardiovascular regulation, receives primary afferent fibers from peripheral baroreceptors and chemoreceptors. Hydrogen peroxide (H(2)O(2)) is a relatively stable and diffusible reactive oxygen species (ROS), which acting centrally, may affect neural mechanisms. In the present study, we investigated effects of H(2)O(2) alone or combined with the glutamatergic antagonist kynurenate into the NTS on mean arterial pressure (MAP) and heart rate (HR). Conscious or anesthetized (urethane and alpha-chloralose) male Holtzman rats (280-320 g) were used. Injections of H(2)O(2) (125 to 1500 pmol/40 nl) into the intermediate NTS of anesthetized rats evoked dose-dependent and transient hypotension (-18 +/- 3 to -55 +/- 11 mmHg) and bradycardia (-16 +/- 5 to -116 +/- 40 bpm). Injection of the catalase inhibitor 3-amino-1,2,4-triazole (100 nmol/40 nl) into the NTS also produced hypotension and bradycardia. Previous injection of the ionotropic L-glutamate receptor antagonist kynurenate (7 nmol/40 nl) attenuated by 48% the bradycardic response, without changing the hypotension evoked by H(2)O(2) (500 pmol/40 nl) in anesthetized rats. The antioxidant L-ascorbate (600 pmol/80 nl) injected into the NTS attenuated the bradycardic (42%) and hypotensive (67%) responses to H(2)O(2) (500 pmol/40 nl) into the NTS. In conscious rats, injection of H(2)O(2) (50 nmol/100 nl) into the NTS also evoked intense bradycardia (-207 +/- 8 bpm) and hypotension (-54 +/- 6 mmHg) that were abolished by prior injection of kynurenate (7 nmol/100 nl). The results show that H(2)O(2) into the NTS induces hypotension and bradycardia probably due to activation of glutamatergic mechanisms.

Published
2009

27. Central blockade of nitric oxide synthesis reduces moxonidine-induced hypotension

Author

Moreira, T. S., Takakura, ACT, Menani, José Vanderlei [UNESP], Sato, M. A., Colombari, Eduardo [UNESP], Universidade Federal de São Paulo (UNIFESP), Universidade Estadual Paulista (Unesp), and Fac Med ABC

Subjects
hypertension, vascular resistance, nitric oxide, imidazoline receptors, alpha(2)-adrenoceptors, blood flow, blood pressure
Abstract

Submitted by Guilherme Lemeszenski (guilherme@nead.unesp.br) on 2014-02-26T17:19:36Z No. of bitstreams: 1 WOS000222532400016.pdf: 166354 bytes, checksum: 2aa40912a282f3f80f68aefd70f34c4d (MD5) Made available in DSpace on 2014-02-26T17:19:36Z (GMT). No. of bitstreams: 1 WOS000222532400016.pdf: 166354 bytes, checksum: 2aa40912a282f3f80f68aefd70f34c4d (MD5) Previous issue date: 2004-06-01 Submitted by Vitor Silverio Rodrigues (vitorsrodrigues@reitoria.unesp.br) on 2014-05-20T13:45:41Z No. of bitstreams: 1 WOS000222532400016.pdf: 166354 bytes, checksum: 2aa40912a282f3f80f68aefd70f34c4d (MD5) Made available in DSpace on 2014-05-20T13:45:41Z (GMT). No. of bitstreams: 1 WOS000222532400016.pdf: 166354 bytes, checksum: 2aa40912a282f3f80f68aefd70f34c4d (MD5) Previous issue date: 2004-06-01 1 Nitric oxide (NO) and alpha(2)-adrenoceptor and imidazoline agonists such as moxonidine may act centrally to inhibit sympathetic activity and decrease arterial pressure.2 In the present study, we investigated the effects of pretreatment with L-NAME ( NO synthesis inhibitor), injected into the 4th ventricle (4th V) or intravenously (i.v.), on the hypotension, bradycardia and vasodilatation induced by moxonidine injected into the 4th V in normotensive rats.3 Male Wistar rats with a stainless steel cannula implanted into the 4th V and anaesthetized with urethane were used. Blood flows were recorded by use of miniature pulsed Doppler flow probes implanted around the renal, superior mesenteric and low abdominal aorta.4 Moxonidine (20 nmol), injected into the 4th V, reduced the mean arterial pressure (-42+/-3 mmHg), heart rate (-22+/-7 bpm) and renal (-62+/-15%), mesenteric (-41+/-8%) and hindquarter (-50+/-8%) vascular resistances.5 Pretreatment with L-NAME (10 nmol into the 4th V) almost abolished central moxonidine-induced hypotension (-10+/-3 mmHg) and renal (-10+/-4%), mesenteric (-11+/-4%) and hindquarter (-13+/-6%) vascular resistance reduction, but did not affect the bradycardia (-18+/-8 bpm).6 the results indicate that central NO mechanisms are involved in the vasodilatation and hypotension, but not in the bradycardia, induced by central moxonidine in normotensive rats. British Journal of Pharmacology (2004). Univ Fed São Paulo, Escola Paulista Med, Dept Physiol, BR-04023060 São Paulo, Brazil Univ Estadual Paulista, Fac Odontol, Dept Physiol & Pathol, BR-14801903 Araraquara, SP, Brazil Fac Med ABC, Dept Physiol, BR-09060650 Santo Andre, SP, Brazil Univ Estadual Paulista, Fac Odontol, Dept Physiol & Pathol, BR-14801903 Araraquara, SP, Brazil

Published
2004

29. Multifactorial control of water and saline intake: Role of α2-adrenoceptors

Author

De-Luca, L. A. [UNESP], Menani, José Vanderlei [UNESP], and Universidade Estadual Paulista (Unesp)

Subjects
Water intake, Dehydration, noradrenalin, drug effect, alpha adrenergic receptor stimulating agent, review, Drinking, Sodium Chloride, Clonidine, α2-Adrenergic agonist, Renin-Angiotensin System, Norepinephrine, Receptors, Adrenergic, alpha-2, renin angiotensin aldosterone system, physiology, Noradrenaline, alpha 2 adrenergic receptor, Animals, animal, metabolism, Adrenergic alpha-Agonists, Sodium intake
Abstract

Submitted by Vitor Silverio Rodrigues (vitorsrodrigues@reitoria.unesp.br) on 2014-05-27T11:18:13Z No. of bitstreams: 0Bitstream added on 2014-05-27T14:33:46Z : No. of bitstreams: 1 2-s2.0-0031110231.pdf: 218550 bytes, checksum: f1ded0f5e9d54d1fba04a92155ede337 (MD5) Made available in DSpace on 2014-05-27T11:18:13Z (GMT). No. of bitstreams: 0 Previous issue date: 1997-04-01 Water and saline intake is controlled by several mechanisms activated during dehydration. Some mechanisms, such as the production of angiotensin II and unloading of cardiovascular receptors, activate both behaviors, while others, such as the increase in blood osmolality or sodium concentration, activate water, but inhibit saline intake. Aldosterone probably activates only saline intake. Clonidine, anα2-adrenergic agonist, inhibits water and saline intake induced by these mechanisms. One model to describe the interactions between these multiple mechanisms is a wire-block diagram, where the brain circuit that controls each intake is represented by a summing point of its respective inhibiting and activating factors. The α2-adrenoceptors constitute an inhibitory factor common to both summing points. Depto. de Cie. Fisiológicas Faculdade de Odontologia Universidade Estadual Paulista, 14801-903 Araraquara, SP Depto. de Cie. Fisiológicas Faculdade de Odontologia Universidade Estadual Paulista, 14801-903 Araraquara, SP

Published
1997

30. PERIPHERAL PRAZOSIN COMBINED WITH NORADRENALINE INTO THE LATERAL PARABRACHIAL NUCLEUS FACILITATES CHOLINERGIC‐INDUCED SODIUM APPETITE

Author

Gasparini, Silvia, primary, Gomide, Joelma Maria Cardoso, additional, Andrade-Franzé, Glaucia Maria Fabricio, additional, Andrade, Carina Aparecida Fabricio, additional, Almeida Colombari, Débora Simões, additional, De Luca, Laurival Antônio, additional, De Paula, Patrícia Maria, additional, Moreira, Thiago Santos, additional, and Menani, José Vanderlei, additional

Published
2012
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34. Taste Preference Measure

Author

de Souza, Juli Thomaz, primary, Matsubara, Luiz S., additional, Menani, José Vanderlei, additional, Matsubara, Beatriz B., additional, Johnson, Alan Kim, additional, and De Gobbi, Juliana Irani Fratucci, additional

Published
2012
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40. THE EFFECT OF ANALOGS OF ANGIOTENSIN-II ON DRINKING AND CARDIOVASCULAR-RESPONSES TO CENTRAL ANGIOTENSIN-II IN THE RAT

Author

Camargo, LAA, Deluca, L. A., Menani, José Vanderlei [UNESP], Renzi, Antonio [UNESP], Saad, W. A., Silveira, JEN, Universidade de São Paulo (USP), and Universidade Estadual Paulista (Unesp)

Subjects
cardiovascular system, hormones, hormone substitutes, and hormone antagonists, circulatory and respiratory physiology
Abstract

Submitted by Guilherme Lemeszenski (guilherme@nead.unesp.br) on 2014-02-26T17:04:39Z No. of bitstreams: 0 Made available in DSpace on 2014-02-26T17:04:39Z (GMT). No. of bitstreams: 0 Previous issue date: 1991-11-01 Submitted by Vitor Silverio Rodrigues (vitorsrodrigues@reitoria.unesp.br) on 2014-05-20T15:26:16Z No. of bitstreams: 0 Made available in DSpace on 2014-05-20T15:26:16Z (GMT). No. of bitstreams: 0 Previous issue date: 1991-11-01 1. Intracerebroventricular (I.C.V.) infusion (60 ng h-1) of Isoleu5-angiotensin II (Isoleu5-AngII) and des-amine-angiotensin II (des-amine-AngII) in rats caused increased drinking behaviour and an increase in arterial blood pressure.2. Des-amine-AngII caused similar increases in heart rate and arterial blood pressure as AngII.3. Previous I.C.V. injection of the antagonists [Leu8]-AngII, des-amine-[Leu8]-AngII and octanoyl-[Leu8]-AngII prevented the increases in heart rate and blood pressure produced by I.C.V. infusion of AngII and caused partial reduction of the dipsogenic response.4. The three antagonists had no effect on the increase in arterial blood pressure and heart rate caused by des-amine-AngII. The drinking response was reduced by previous injection of [Leu8]-AngII and des-amine-[Leu8]-AngII but not by octanoyl-[Leu8]-AngII.5. In conclusion, Isoleu5-AngII and des-amine-AngII increase drinking behaviour, arterial blood pressure and heart rate when infused into the cerebral ventricle of rats. The study with the antagonists showed that des-amine-AngII probably binds more strongly to AngII-receptors. UNIV SAO PAULO,SCH MED,DEPT SURG,SAO PAULO,BRAZIL

Published
1991

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