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Talmir Augusto Faria Brizola Dos Santos – One of the best experts on this subject based on the ideXlab platform.

  • Subfornical organ mediates pressor effect of Angiotensin: Influence of nitric oxide synthase inhibitors, AT1 and AT2 Angiotensin Antagonist‘s receptors
    Journal of the American Society of Hypertension : JASH, 2008
    Co-Authors: Wilson Abrão Saad, Luiz Antonio De Arruda Camargo, Ismael Francisco Motta Siqueira Guarda, Talmir Augusto Faria Brizola Dos Santos

    Abstract:

    Abstract We investigated the influence of voltage-dependent calcium channels and nitric oxide (NO) on Angiotensin II (ANG II)-pressor effect injected into subfornical organ (SFO). The influence of NO on nifedipine antipressor action has also been studied by utilizing N W -nitro-L-arginine methyl ester (L-NAME) (20 μg × 0.2 μl −1 ) a nitric oxide synthase inhibitor (NOSI) and 7-nitroindazole (7-NIT) (20 μg × 0.2 μl −1 ), a specific neuronal nitric oxide synthase inhibitor (nNOSI). We have also investigated the role of losartan and PD123319, selective ANG II AT 1 and AT 2 receptor nonpeptide Antagonists, in the pressor effect of ANG II and in the effect of L-NAME and 7-NIT, injected into the SFO. Adult male Holtzman rats (220 to 280 g) were anesthetized with ketamine (80 mg/kg −1 of body weight) plus xylazine (7 mg/kg −1 of body weight), placed in a stereotaxic apparatus (David Kopf model for rats), and implanted with cannula into the SFO. Direct mean arterial blood pressure (MAP) was recorded in conscious rats in a test cage, without access to food or water. The previously implanted catheter into femoral artery was connected to a Statham (P23 Db) pressure transducer (Statham-Gould, Valley View, OH) coupled to a multichannel recorder (PowerLab Multirecord). MAP increased after ANG II injection. Pre-treatment with nifidipine (50 μg × 0.2 μl −1 or 100 μg × 0.2 μl −1 ) followed by 25 pmol × 0.2 μl −1 of ANG II, decreased ANG II-pressor effect. L-NAME and 7-NIT increased the elevation in MAP induced by ANG II, which was blocked by the prior injection of nifedipine. The AT 1 Angiotensin Antagonist losartan injected into the SFO blocked the effect of ANG II and the effects of L-NAME and 7-NIT while PD123319 did not. These results provide evidence that ANG II-pressor effect is influenced by nitrergic pathways that utilize L-type calcium channels in the SFO.

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Wilson Abrão Saad – One of the best experts on this subject based on the ideXlab platform.

  • Subfornical organ mediates pressor effect of Angiotensin: Influence of nitric oxide synthase inhibitors, AT1 and AT2 Angiotensin Antagonist‘s receptors
    Journal of the American Society of Hypertension : JASH, 2008
    Co-Authors: Wilson Abrão Saad, Luiz Antonio De Arruda Camargo, Ismael Francisco Motta Siqueira Guarda, Talmir Augusto Faria Brizola Dos Santos

    Abstract:

    Abstract We investigated the influence of voltage-dependent calcium channels and nitric oxide (NO) on Angiotensin II (ANG II)-pressor effect injected into subfornical organ (SFO). The influence of NO on nifedipine antipressor action has also been studied by utilizing N W -nitro-L-arginine methyl ester (L-NAME) (20 μg × 0.2 μl −1 ) a nitric oxide synthase inhibitor (NOSI) and 7-nitroindazole (7-NIT) (20 μg × 0.2 μl −1 ), a specific neuronal nitric oxide synthase inhibitor (nNOSI). We have also investigated the role of losartan and PD123319, selective ANG II AT 1 and AT 2 receptor nonpeptide Antagonists, in the pressor effect of ANG II and in the effect of L-NAME and 7-NIT, injected into the SFO. Adult male Holtzman rats (220 to 280 g) were anesthetized with ketamine (80 mg/kg −1 of body weight) plus xylazine (7 mg/kg −1 of body weight), placed in a stereotaxic apparatus (David Kopf model for rats), and implanted with cannula into the SFO. Direct mean arterial blood pressure (MAP) was recorded in conscious rats in a test cage, without access to food or water. The previously implanted catheter into femoral artery was connected to a Statham (P23 Db) pressure transducer (Statham-Gould, Valley View, OH) coupled to a multichannel recorder (PowerLab Multirecord). MAP increased after ANG II injection. Pre-treatment with nifidipine (50 μg × 0.2 μl −1 or 100 μg × 0.2 μl −1 ) followed by 25 pmol × 0.2 μl −1 of ANG II, decreased ANG II-pressor effect. L-NAME and 7-NIT increased the elevation in MAP induced by ANG II, which was blocked by the prior injection of nifedipine. The AT 1 Angiotensin Antagonist losartan injected into the SFO blocked the effect of ANG II and the effects of L-NAME and 7-NIT while PD123319 did not. These results provide evidence that ANG II-pressor effect is influenced by nitrergic pathways that utilize L-type calcium channels in the SFO.

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  • Research Article Subfornical organ mediates pressor effect of Angiotensin: Influence of nitric oxide synthase inhibitors, AT 1 and AT 2 Angiotensin Antagonist‘s receptors
    , 2008
    Co-Authors: Wilson Abrão Saad, Luiz Antonio De Arruda, Ismael Francisco, Motta Siqueira Guarda

    Abstract:

    We investigated the influence of voltage-dependent calcium channels and nitric oxide (NO) on Angiotensin II (ANG II)-pressor effect injected into subfornical organ (SFO). The influence of NO on nifedipine antipressor action has also been studied by utilizing N W -nitro-L-arginine methyl ester (L-NAME) (20 g 0.2 l 1 ) a nitric oxide synthase inhibitor (NOSI) and 7-nitroindazole (7-NIT) (20 g 0.2 l 1 ), a specific neuronal nitric oxide synthase inhibitor (nNOSI). We have also investigated the role of losartan and PD123319, selective ANG II AT1 and AT2 receptor nonpeptide Antagonists, in the pressor effect of ANG II and in the effect of L-NAME and 7-NIT, injected into the SFO. Adult male Holtzman rats (220 to 280 g) were anesthetized with ketamine (80 mg/kg 1 of body weight) plus xylazine (7 mg/kg 1 of body weight), placed in a stereotaxic apparatus (David Kopf model for rats), and implanted with cannula into the SFO. Direct mean arterial blood pressure (MAP) was recorded in conscious rats in a test cage, without access to food or water. The previously implanted catheter into femoral artery was connected to a Statham (P23 Db) pressure transducer (Statham-Gould, Valley View, OH) coupled to a multichannel recorder (PowerLab Multirecord). MAP increased after ANG II injection. Pre-treatment with nifidipine (50 g 0.2 l 1 or 100 g 0.2 l 1 ) followed by 25 pmol 0.2 l 1 of ANG II, decreased ANG II-pressor effect. L-NAME and 7-NIT increased the elevation in MAP induced by ANG II, which was blocked by the prior injection of nifedipine. The AT1 Angiotensin Antagonist losartan injected into the SFO blocked the effect of ANG II and the effects of L-NAME and 7-NIT while PD123319 did not. These results provide evidence that ANG II-pressor effect is influenced by nitrergic pathways that utilize L-type calcium channels in the SFO. J Am Soc Hypertens 2008;2(5): 326‐331. © 2008 American

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Keith M Kendrick – One of the best experts on this subject based on the ideXlab platform.

  • human extinction learning is accelerated by an Angiotensin Antagonist via ventromedial prefrontal cortex and its connections with basolateral amygdala
    Biological Psychiatry, 2019
    Co-Authors: Feng Zhou, Yayuan Geng, Fei Xin, Pan Feng, Congcong Liu, Weihua Zhao, Tingyong Feng, Adam J Guastella, Richard P Ebstein, Keith M Kendrick

    Abstract:

    Abstract Background Deficient extinction learning and threat adaptation in the ventromedial prefrontal cortex (vmPFC)-amygdala circuitry strongly impede the efficacy of exposure-based interventions in anxiety disorders. Recent animal models suggest a regulatory role of the renin-Angiotensin system in both these processes. Against this background, the present randomized placebo-controlled pharmacologic functional magnetic resonance imaging experiment aimed at determining the extinction enhancing potential of the Angiotensin II type 1 receptor Antagonist losartan (LT) in humans. Methods Seventy healthy male subjects underwent Pavlovian threat conditioning and received single-dose LT (50 mg) or placebo administration before extinction. Psychophysiological threat reactivity (skin conductance response) and neural activity during extinction served as primary outcomes. Psychophysiological interaction, voxelwise mediation, and novel multivariate pattern classification analyses were used to determine the underlying neural mechanisms. Results LT significantly accelerated the decline of the psychophysiological threat response during within-session extinction learning. On the neural level, the acceleration was accompanied and critically mediated by threat-specific enhancement of vmPFC activation. Furthermore, LT enhanced vmPFC-basolateral amygdala coupling and attenuated the neural threat expression, particularly in the vmPFC, during early extinction. Conclusions Overall the results indicate that LT facilitates within-session threat memory extinction by augmenting threat-specific encoding in the vmPFC and its regulatory control over the amygdala. The findings document a pivotal role of Angiotensin regulation of extinction learning in humans and suggest that adjunct LT administration has the potential to facilitate the efficacy of exposure-based interventions in anxiety disorders.

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  • human extinction learning is accelerated by an Angiotensin Antagonist via ventromedial prefrontal cortex and its connections with basolateral amygdala
    bioRxiv, 2019
    Co-Authors: Feng Zhou, Keith M Kendrick, Yayuan Geng, Pan Feng, Congcong Liu, Weihua Zhao, Tingyong Feng, Adam J Guastella, Benjamin Becker

    Abstract:

    Abstract Extinction is considered a core mechanism underlying exposure-based therapy in anxiety-related disorders. However, marked impairments in threat extinction learning coupled with impaired neuroplasticity in patients strongly impede the efficacy of exposure-based interventions. Recent translational research suggests a role of the renin-Angiotensin (RA) system in both these processes. However, the efficacy of pharmacological modulation of the RA system to enhance threat extinction in humans and the underlying neural mechanisms remain unclear. The present pre-registered, randomized placebo-controlled pharmacological neuroimaging trial demonstrates that pre-extinction administration of the Angiotensin II type 1 receptor Antagonist losartan accelerated attenuation of the psychophysiological threat response during extinction. On the neural level the acceleration of extinction was accompanied by threat-signal specific enhanced ventromedial prefrontal cortex (vmPFC) activation and its coupling with the basolateral amygdala. Multivoxel pattern analysis and voxel-wise mediation analysis further revealed that that losartan reduced the neural threat expression, particularly in the vmPFC, and confirmed that acceleration of extinction critically involved treatment-induced modulation of vmPFC activation. Overall the results provide the first evidence for a pivotal role of the RA system in extinction learning in humans and suggest that adjunct losartan administration can be leveraged to facilitate the efficacy of extinction-based therapies.

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