anatibant has been researched along with icatibant* in 2 studies
2 other study(ies) available for anatibant and icatibant
Article | Year |
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The bradykinin B2 receptor antagonist icatibant (Hoe 140) blocks aminopeptidase N at micromolar concentrations: off-target alterations of signaling mediated by the bradykinin B1 and angiotensin receptors.
The N-terminal sequence of icatibant, a widely used peptide antagonist of the bradykinin B(2) receptors, is analogous to that of other known aminopeptidase N inhibitors. Icatibant competitively inhibited the hydrolysis of L-Ala-p-nitroanilide by recombinant aminopeptidase N (K(i) 9.1 microM). In the rabbit aorta, icatibant (10-30 microM) potentiated angiotensin III, but not angiotensin II (contraction mediated by angiotensin AT(1) receptors), and Lys-des-Arg(9)-bradykinin, but not des-Arg(9)-bradykinin (effects mediated by the bradykinin B(1) receptors), consistent with the known susceptibility of these agonists to aminopeptidase N. At concentrations possibly reached in vivo (e.g., in kidneys), icatibant alters physiological systems different from bradykinin B(2) receptors. Topics: Angiotensin II; Angiotensin III; Aniline Compounds; Animals; Aorta; Bradykinin; Bradykinin B2 Receptor Antagonists; CD13 Antigens; Dose-Response Relationship, Drug; In Vitro Techniques; Kallidin; Kinetics; Protease Inhibitors; Quinolines; Rabbits; Receptor, Bradykinin B1; Receptor, Bradykinin B2; Receptors, Angiotensin; Recombinant Proteins; Signal Transduction; Vasoconstriction; Vasoconstrictor Agents | 2006 |
Kinin and opioid receptors in the paratrigeminal nucleus modulate the somatosensory reflex to rat sciatic nerve stimulation.
The influence of kinin and opioid receptor blockade in the paratrigeminal nucleus (Pa5) on the somatosensory reflex (SSR) to sciatic nerve stimulation (SNS) was assessed in anaesthetized-paralyzed rats. SNS (square 1 ms pulses at 0.6 mA and 20 Hz for 10s) increased mean arterial pressure from 87+/-3 to 106+/-3 mmHg. Pressor responses to SNS were reduced 40-60% by HOE-140 and LF 16-0687 (B2 receptor antagonists; 20 and 100 pmol respectively), CTOP or nor-binaltorphimine (mu and kappa opioid receptor antagonists, respectively; 1 microg) but potentiated by naltrindole (delta opioid receptor antagonist) receptor antagonist microinjections into the contralateral (but not ipsilateral) Pa5. The SSR to sciatic nerve stimulation was not changed by B1 kinin receptor or NK1, NK2 and NK3 tachykinin receptor antagonists administered to the Pa5. Capsaicin pretreatment (40 mg/kg/day, 3 days) abolished the effects of the opioid receptor antagonists, but did not change the effect of kinin B2 receptor blockade on the SSR. Thus, the activity of B2 and opioid receptor-operated mechanisms in the Pa5 contribute to the SSR in the rat, suggesting a role for these endogenous peptides in the cardiovascular responses to SNS. Topics: Animals; Arteries; Blood Pressure; Bradykinin; Bradykinin Receptor Antagonists; Electric Stimulation; Evoked Potentials, Somatosensory; Male; Models, Biological; Naltrexone; Narcotic Antagonists; Quinolines; Rats; Rats, Wistar; Receptors, Bradykinin; Receptors, Opioid; Reflex, Abnormal; Sciatic Nerve; Somatostatin; Trigeminal Nuclei | 2005 |