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  • Title: Pressor effects of noradrenaline injected into the lateral septal area of unanesthetized rats.
    Author: Scopinho AA, Resstel LB, Antunes-Rodrigues J, Corrêa FM.
    Journal: Brain Res; 2006 Nov 29; 1122(1):126-34. PubMed ID: 17011526.
    Abstract:
    The lateral septal area (LSA) is involved in central cardiovascular control. In the present study, we report on the cardiovascular effects of noradrenaline (NA) injection into the LSA of unanesthetized rats, as well as on local receptors and peripheral mechanisms involved in their mediation. Microinjections of NA (9, 15, 21, 27 or 45 nmol) caused long-lasting, dose-related pressor and bradycardic responses in unanesthetized rats. No responses were observed when the dose of 21 nmol of NA was microinjected into medial septal area or lateral ventricle suggesting a main action at the LSA. No changes were observed in arterial pressure and heart rate when NA was injected in the LSA of anesthetized rats. The effects of 21 nmol of NA were abolished by local pretreatment with 10 nmol of the specific alpha1-receptor antagonist WB 4101, but were not affected by pretreatment with 10 nmol of the specific alpha2-receptor antagonist RX 821002. The magnitude of pressor response to NA in the LSA was increased by i.v. pretreatment with the ganglion blocker pentolinium (10 mg/kg) and significantly reduced by i.v. pretreatment with the V1-vasopressin receptor antagonist dTyr (CH2)5(Me) AVP (50 microg/kg). No pressor response to NA was observed in hypophysectomized rats. The present observation of alpha1-adrenoceptor-mediated pressor responses after local injection of NA confirms earlier evidence of a LSA involvement in central cardiovascular control. Pretreatment with the alpha1-adrenoceptor antagonist WB-4101 did not affect baseline blood pressure or heart rate suggesting no tonic involvement of septal adrenergic mechanisms suggesting a modulatory LSA influence on cardiovascular control. Additionally, the blockade of the pressor response by the i.v. pretreatment with a V1-vasopressin antagonist indicates that noradrenergic LSA mechanisms modulate vasopressin release.
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