Avaliação da função renal de cães sadios e nefropatas crônicos sob diferentes bloqueios medicamentosos do sistema renina-angiotensina-aldosterona

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Influência do bloqueio de receptores do tipo 1 (AT1) sobre o perfil metabólico, endócrino e cardiovascular de ratos obesos

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Role of the lateral parabrachial nucleus in the control of sodium appetite

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

ANGIOTENSINERGIC AND CHOLINERGIC RECEPTORS OF THE SUBFORNICAL ORGAN MEDIATE SODIUM INTAKE INDUCED BY GABAergic ACTIVATION OF THE LATERAL PARABRACHIAL NUCLEUS

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

LESION OF THE COMMISSURAL NUCLEUS OF THE SOLITARY TRACT/A2 NORADRENERGIC NEURONS FACILITATES THE ACTIVATION OF ANGIOTENSINERGIC MECHANISMS IN RESPONSE TO HEMORRHAGE

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Healing Process of Autogenous Bone Graft in Spontaneously Hypertensive Rats Treated With Losartan: An Immunohistochemical and Histomorphometric Study

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Vias de sinalização endotelial α2, AT1, e AT2 sobre a reatividade da aorta de ratos após consumo de etanol e exposição ao estresse, isoladamente e em associação

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Fetal kidney programming by severe food restriction: effects on structure, hormonal receptor expression and urinary sodium excretion in rats

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

An update on the pharmacogenetics of treating hypertension

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Pressor mechanisms in adriamycin-induced nephropathy with hypertension in rats

We explored the role of angiotensin II and vasopressin in the maintenance of blood pressure during the nephrotic syndrome of adriamycin-induced nephropathy in rats. All 91 rats treated with adriamycin developed chronic renal failure with nephrotic syndrome, which was more pronounced in the normotensive rats than the 35% who became hypertensive. Angiotensin II blockade with DuP 753 produced a significantly greater hypotensive response in both the adriamycin-hypertensive (-16 +/- 3 mm Hg) and adriamycin-normotensive (-14 +/- 5 mm Hg) groups than the saline-treated controls (-5 +/- 1 mm Hg, P < .05). Vasopressin blockade with either a V1V2 inhibitor or a selective V1 inhibitor produced a hypotensive response in adriamycin-hypertensive rats only (by -16 +/- 4 and -17 +/- 2 mm Hg, respectively, P < .01), although the nonselective vasopressin inhibitor produced similar fluid loss and body weight reduction in all three groups. The data suggest that in adriamycin-induced nephropathy with nephrotic syndrome, angiotensin II contributes to blood pressure maintenance in both hypertensive and normotensive animals, whereas the pressor action of vasopressin contributes to elevated blood pressure in hypertensive animals only.

Effect of the gadolinium ion on body fluid regulation

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Importance of the central nucleus of the amygdala on sodium intake caused by deactivation of lateral parabrachial nucleus

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Mapping brain Fos immunoreactivity in response to water deprivation and partial rehydration: influence of sodium intake

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Losartan exerts no protective effects against acute pulmonary embolism-induced hemodynamic changes

The acute obstruction of pulmonary vessels by venous thrombi is a critical condition named acute pulmonary embolism (APE). During massive APE, severe pulmonary hypertension may lead to death secondary to right heart failure and circulatory shock. APE-induced pulmonary hypertension is aggravated by active pulmonary vasoconstriction. While blocking the effects of some vasoconstrictors exerts beneficial effects, no previous study has examined whether angiotensin II receptor blockers protect against the hemodynamic changes associated with APE. We examined the effects exerted by losartan on APE-induced hemodynamic changes. Hemodynamic evaluations were performed in non-embolized lambs treated with saline (n = 4) and in lambs that were embolized with silicon microspheres and treated with losartan (30 mg/kg followed by 1 mg/kg/h, n = 5) or saline (n = 7) infusions. The plasma and lung angiotensin-converting enzyme (ACE) activity were assessed using a fluorometric method. APE increased mean pulmonary arterial pressure (MPAP) and pulmonary vascular resistance index (PVRI) by 21 +/- 2 mmHg and 375 +/- 20 dyn s cm(-5) m(-2), respectively (P < 0.05). Losartan decreased MPAP significantly (by approximately 15%), without significant changes in PVRI and tended to decrease cardiac index (P > 0.05). Lung and plasma ACE activity were similar in both embolized and non-embolized animals. Our findings show evidence of lack of activation of the renin-angiotensin system during APE. The lack of significant effects of losartan on the pulmonary vascular resistance suggests that losartan does not protect against the hemodynamic changes found during APE.

The adipokine chemerin augments vascular reactivity to contractile stimuli via activation of the MEK-ERK1/2 pathway

Aims: Cytokines interfere with signaling pathways and mediators of vascular contraction. Endothelin-1 (ET-1) plays a major role on vascular dysfunction in conditions characterized by increased circulating levels of adipokines. In the present study we tested the hypothesis that the adipokine chemerin increases vascular contractile responses via activation of ET-1/ET-1 receptors-mediated pathways. Main methods: Male, 10-12 week-old Wistar rats were used. Endothelium-intact and endothelium-denuded aortic rings were incubated with chemerin (0.5 ng/mL or 5 ng/mL, for 1 or 24 h), and isometric contraction was recorded. Protein expression was determined by Western blotting. Key findings: Constrictor responses to phenylephrine (PE) and ET-1 were increased in vessels treated for 1 h with chemerin. Chemerin incubation for 24 h decreased PE contractile response whereas it increased the sensitivity to ET-1. Endothelium removal significantly potentiated chemerin effects on vascular contractile responses to PE and ET-1. Incubation with either an ERK1/2 inhibitor (PD98059) or ETA antagonist (BQ123) abolished chemerin effects on PE- and ET-1-induced vasoconstriction. Phosphorylation of MEK1/2 and ERK1/2 was significantly increased in vessels treated with chemerin for 1 and 24 h. Phosphorylation of these proteins was further increased in vessels incubated with ET-1 plus chemerin. ET-1 increased MEK1/2, ERK1/2 and MKP1 protein expression to values observed in vessels treated with chemerin. Significance: Chemerin increases contractile responses to PE and ET-1 via ERK1/2 activation. Our study contributes to a better understanding of the mechanisms by which the adipose tissue affects vascular function and, consequently, the vascular alterations present in obesity and related diseases. (c) 2012 Elsevier Inc. All rights reserved.