17 research outputs found

    Loss of orexinA-immunoreactive neurons in the LH after orexin-SAP treatment.

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    <p>A and B are low and high magnification photomicrographs of orexin-ir neurons in coronal sections of the brain in the blank-SAP-treated rat. C and D as A and B, but from the orexin-SAP-treated rat. Orexin neurons were significantly fewer after damage of the LH by orexin-SAP-treatment with a few residual ones indicated by black arrows. 3V: third ventricle, LH: lateral hypothalamus, F: Fornix.</p

    ASICs antagonist blocking acidification-induced increase of PND.

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    <p>A: Histological staining with neutral red: the sky blue spot was the injection site in the LH. Scale bar, 1 mm. B: Plot of the injection sites projected on Bregma −2.6 mm section: the solid dots were inside and the hollow ones outside of the LH. Scale bar, 1 mm. C: Unilateral microinjection of 0.1 µl ACSF (pH 6.5) into the LH increased raw PND (top) and iPND (bottom). Pre-treatment of amiloride (10 mM) or PcTX1 (10 nM) blocked the effect. Microinjection of ACSF (pH 7.4) served as the control. D: Group data show the effects of amiloride and PcTX1 on acidification-induced iPND (n = 6, *** P<0.001 relative to control, <sup>###</sup> P<0.001 relative to pH 6.5). E: Time course of iPND response to acidification of the LH. Please note that the response peaked at 20 min (n = 6, *** P<0.001 relative to pH 7.4). F: Responses of respiratory drive (PA/Ti). Note that amiloride and PcTX1 inhibited the acidification-induced effect (n = 6, <sup>#</sup> P<0.05 relative to pH 7.4, ** P<0.01 relative to pH 6.5). G: Inspiratory time (Ti) was increased by acidification but not statistically significant (<i>v.s.</i> pH 7.4).</p

    Co-expression of ASIC1 and OrexinA in the LH of adult SD rats.

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    <p>A representative confocal photomicrograph showing co-staining of orexinA and ASIC1 on neurons in the LH of an adult SD rat. <b>A:</b> OrexinA-ir neurons (green, FITC). <b>B:</b> ASIC1-ir neurons (red, cy3). <b>C:</b> Overlay of A and B.</p

    Schematic diagram showing the relationship between the renin-angiotensin system and stress-induced hypertension.

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    <p>ACE upregulation and/or ACE2 downregulation result in Ang II↑ and/or Ang-(1–7)↓. Ang, Angiotensin; ACE, angiotensin-converting enzyme; ACE2, angiotensin-converting enzyme homolog; AT<sub>1</sub>R, Ang II type 1 receptor; AT<sub>2</sub>R, Ang II type 2 receptor; SIH, stress-induced hypertension</p

    Chromatographic plots of amino acids in the RVLM following microinjection.

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    <p>ACSF in normal rats (A), Ang II in normal rat (B) or Ang II in SIH rat (C). The abscissa is retention time (min). The ordinate is absorbance. Asp, aspartate; Glu, Glutamate; Asn, asparagine; Gln, Glutamine; Gly, Glycine; Tau, taurine; GABA, γ-aminobutyric acid.</p

    Effects of microinjection of Ang II and Ang-(1–7) into the RVLM on HR.

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    *<p><i>P</i><0.05 compared with the artificial cerebrospinal fluid (ACSF) group; <sup>#</sup><i>P</i><0.05 compared with the normotensive animal (n = 8 in each group).</p

    Effects of microinjection of Ang-(1–7) or Ang779 into the RVLM on local release of amino acids.

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    *<p><i>P</i><0.05 compared with the ACSF group at the same time point; <sup>Δ</sup><i>P</i><0.05 compared with baseline (10 min prior to microinjection); <sup>#</sup><i>P</i><0.05 compared with the normotensive rats at the same time point. Amino acids (AA) were measured at baseline, 1<sup>st</sup>, 2<sup>nd</sup>, 3<sup>rd</sup> 10 min after administration of ACSF, Ang-(1–7) or Ang779, respectively (n = 8 in each group). Asp, aspartate; Glu, Glutamate; Gly, Glycine; Tau, taurine; GABA, γ-aminobutyric acid.</p
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