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Amastatin

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Quentin J Pittman – 1st expert on this subject based on the ideXlab platform

  • vasopressin and Amastatin induce v1 receptor mediated suppression of excitatory transmission in the rat parabrachial nucleus
    Journal of Neurophysiology, 1999
    Co-Authors: Xihua Chen, Quentin J Pittman

    Abstract:

    We examined actions of arginine vasopressin (AVP) and Amastatin (an inhibitor of the aminopeptidase that cleaves AVP) on synaptic currents in slices of rat parabrachial nucleus using the nystatin-p…

  • Vasopressin and Amastatin Induce V1-Receptor-Mediated Suppression of Excitatory Transmission in the Rat Parabrachial Nucleus
    Journal of Neurophysiology, 1999
    Co-Authors: Xihua Chen, Quentin J Pittman

    Abstract:

    We examined actions of arginine vasopressin (AVP) and Amastatin (an inhibitor of the aminopeptidase that cleaves AVP) on synaptic currents in slices of rat parabrachial nucleus using the nystatin-perforated patch recording technique. AVP reversibly decreased the amplitude of the evoked, glutamate-mediated, excitatory postsynaptic current (EPSC) with an increase in paired-pulse ratio. No apparent changes in postsynaptic membrane properties were revealed by ramp protocols, and the inward current induced by a brief application of α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid was unchanged after AVP. The reduction induced by 1 μM AVP could be blocked by a V1 AVP receptor antagonist, [d(CH2)5 1-O-Me-Tyr2-Arg8]-vasopressin (Manning compound, 10 μM). Bath application of an aminopeptidase inhibitor, Amastatin (10 μM), reduced the evoked EPSC, and AVP induced further synaptic depression in the presence of Amastatin. Amastatin’s effects also could be antagonized by the Manning compound. Corticotropin-releasing hormone slightly increased the EPSC at 1 μM, and coapplication with AVP attenuated the AVP response. Pretreatment of slices with 1 μg/ml cholera toxin or 0.5 μg/ml pertussis toxin for 20 h did not significantly affect AVP’s synaptic action. The results suggest that AVP has suppressant effects on glutamatergic transmission by acting at V1 AVP receptors, possibly through a presynaptic mechanism involving a pertussis-toxin- and cholera-toxin-resistant pathway.

Carlo Alberto Maggi – 2nd expert on this subject based on the ideXlab platform

  • characterization of the tachykinin nk2 receptor in the human bronchus influence of Amastatin sensitive metabolic pathways
    British Journal of Pharmacology, 1994
    Co-Authors: M Astolfi, Carlo Alberto Maggi, Stefano Treggiari, Antonio Giachetti, Stefania Meini, Stefano Manzini

    Abstract:

    Abstract
    1. The aim of this study was to characterize the tachykinin NK2 receptor subtype mediating the spasmogenic response in the human isolated bronchus. The motor response to neurokinin A (NKA) and the selective NK2 agonist [beta Ala8]NKA(4-10), as well as the antagonistic effects of cyclic (L659,877) and linear (MEN 10376) peptide NK2 antagonists were assessed in the presence or absence of Amastatin (an inhibitor of aminopeptidases A and M). 2. NKA was more potent than [beta Ala8]NKA(4-10) in eliciting bronchoconstriction (pD2 being 7,43 and 6,87 respectively). In the presence of Amastatin (1 microM), the estimated affinity of [beta Ala8]NKA(4-10), but not that of NKA, was significantly increased to yield a pD2 of 7,44. 3. L659,877 and MEN 10376 inhibited [beta Ala8]NKA(4-10)-induced contraction with similar affinities; pA2 values were 5.7 +/- 0.22 and 6.3 +/- 0.32, respectively. Amastatin (1 microM) increased the potency of MEN 10376 to 7.28 +/- 0.46, whereas that of L659,877 was unaffected. 4. In the presence of Amastatin the pseudopeptide MDL 28,564 behaved as a partial agonist. 5. We conclude that the NK2 receptor subtype present in the human bronchus has properties similar to those described for the circular muscle of the human colon and thus may be classified as a ‘NK2A’ subtype. We show that the apparent potency of peptides, bearing N-terminal acidic residues, is influenced by an Amastatin-sensitive peptidase, possibly aminopeptidase A.

  • Characterization of the tachykinin NK2 receptor in the human bronchus: influence of Amastatin‐sensitive metabolic pathways
    British Journal of Pharmacology, 1994
    Co-Authors: M Astolfi, Carlo Alberto Maggi, Stefano Treggiari, Antonio Giachetti, Stefania Meini, Stefano Manzini

    Abstract:

    Abstract
    1. The aim of this study was to characterize the tachykinin NK2 receptor subtype mediating the spasmogenic response in the human isolated bronchus. The motor response to neurokinin A (NKA) and the selective NK2 agonist [beta Ala8]NKA(4-10), as well as the antagonistic effects of cyclic (L659,877) and linear (MEN 10376) peptide NK2 antagonists were assessed in the presence or absence of Amastatin (an inhibitor of aminopeptidases A and M). 2. NKA was more potent than [beta Ala8]NKA(4-10) in eliciting bronchoconstriction (pD2 being 7,43 and 6,87 respectively). In the presence of Amastatin (1 microM), the estimated affinity of [beta Ala8]NKA(4-10), but not that of NKA, was significantly increased to yield a pD2 of 7,44. 3. L659,877 and MEN 10376 inhibited [beta Ala8]NKA(4-10)-induced contraction with similar affinities; pA2 values were 5.7 +/- 0.22 and 6.3 +/- 0.32, respectively. Amastatin (1 microM) increased the potency of MEN 10376 to 7.28 +/- 0.46, whereas that of L659,877 was unaffected. 4. In the presence of Amastatin the pseudopeptide MDL 28,564 behaved as a partial agonist. 5. We conclude that the NK2 receptor subtype present in the human bronchus has properties similar to those described for the circular muscle of the human colon and thus may be classified as a ‘NK2A’ subtype. We show that the apparent potency of peptides, bearing N-terminal acidic residues, is influenced by an Amastatin-sensitive peptidase, possibly aminopeptidase A.

  • Characterization of the tachykinin neurokinin-2 receptor in the human urinary bladder by means of selective receptor antagonists and peptidase inhibitors.
    Journal of Pharmacology and Experimental Therapeutics, 1993
    Co-Authors: S. Giuliani, Riccardo Patacchini, Antonio Giachetti, Gabriele Barbanti, Damiano Turini, Paolo Rovero, Laura Quartara, Carlo Alberto Maggi

    Abstract:

    The tachykinin (NK2) receptor-mediating contraction of the human isolated bladder to NKA was investigated by studying the affinities of eight structurally different receptor-selective antagonists (linear peptides, cyclic peptides and pseudopeptides, nonpeptide NK2 receptor antagonists). The affinities of the antagonists were compared to those measured for the same ligands at the NK2 receptors previously characterized in the rabbit pulmonary artery and hamster trachea. In the presence of a cocktail of peptidase inhibitors (bestatin captopril and thiorphan, 1 microM each) no significant correlation was found between pA2 values measured in the human bladder vs. those measured in the other two NK2 receptor-bearing preparation. In the presence of the aminopeptidase inhibitor Amastatin, however, pA2 values of linear antagonists bearing an N-terminal Asp residue MEN 10,207 and MEN 10,376 were significantly enhanced and these pA2 values were used for analysis; a significant correlation was found between pA2 values measured in the human urinary bladder and rabbit pulmonary artery. The pseudopeptide analog of NKA (4-10), MDL 28,564 which also bears a N-terminal Asp residue behaved as an agonist and its action was enhanced by Amastatin. We conclude that the NK2 receptor-mediating contraction of the human urinary bladder smooth muscle is similar to that previously characterized in the rabbit pulmonary artery (NK2A receptor category); in the human bladder smooth muscle an Amastatin-sensitive peptidase (possibly aminopeptidase A) limits biological activity of linear peptide derivatives of NKA bearing a N-terminal Asp residue.

Xihua Chen – 3rd expert on this subject based on the ideXlab platform

  • vasopressin and Amastatin induce v1 receptor mediated suppression of excitatory transmission in the rat parabrachial nucleus
    Journal of Neurophysiology, 1999
    Co-Authors: Xihua Chen, Quentin J Pittman

    Abstract:

    We examined actions of arginine vasopressin (AVP) and Amastatin (an inhibitor of the aminopeptidase that cleaves AVP) on synaptic currents in slices of rat parabrachial nucleus using the nystatin-p…

  • Vasopressin and Amastatin Induce V1-Receptor-Mediated Suppression of Excitatory Transmission in the Rat Parabrachial Nucleus
    Journal of Neurophysiology, 1999
    Co-Authors: Xihua Chen, Quentin J Pittman

    Abstract:

    We examined actions of arginine vasopressin (AVP) and Amastatin (an inhibitor of the aminopeptidase that cleaves AVP) on synaptic currents in slices of rat parabrachial nucleus using the nystatin-perforated patch recording technique. AVP reversibly decreased the amplitude of the evoked, glutamate-mediated, excitatory postsynaptic current (EPSC) with an increase in paired-pulse ratio. No apparent changes in postsynaptic membrane properties were revealed by ramp protocols, and the inward current induced by a brief application of α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid was unchanged after AVP. The reduction induced by 1 μM AVP could be blocked by a V1 AVP receptor antagonist, [d(CH2)5 1-O-Me-Tyr2-Arg8]-vasopressin (Manning compound, 10 μM). Bath application of an aminopeptidase inhibitor, Amastatin (10 μM), reduced the evoked EPSC, and AVP induced further synaptic depression in the presence of Amastatin. Amastatin’s effects also could be antagonized by the Manning compound. Corticotropin-releasing hormone slightly increased the EPSC at 1 μM, and coapplication with AVP attenuated the AVP response. Pretreatment of slices with 1 μg/ml cholera toxin or 0.5 μg/ml pertussis toxin for 20 h did not significantly affect AVP’s synaptic action. The results suggest that AVP has suppressant effects on glutamatergic transmission by acting at V1 AVP receptors, possibly through a presynaptic mechanism involving a pertussis-toxin- and cholera-toxin-resistant pathway.