China
Africa
Explore chapters and articles related to this topic
Genetic Disorders of the Autonomic Nervous System
Published in David Robertson, Italo Biaggioni, Disorders of the Autonomic Nervous System, 2019
Clonidine acts on a2-adrenoreceptors or imidazoline receptors in the brainstem to reduce sympathetic outflow and lower blood pressure (Robertson et al., 1986b). It can also exert peripheral pressor effects by stimulation of vascular a?2-adrenoreceptors (Robertson et al., 1983). DBH-deficient patients have no fall in seated mean arterial pressure following the administration of clonidine, probably reflecting the fact that in these patients, blood pressure is not maintained by sympathetic tone. On the contrary, dramatic increases in blood pressure are seen with higher doses of this agent. It is noteworthy that heart rate decreases in DBH-deficient patients following the administration of clonidine, even though blood pressure does not fall, consistent with the postulated central parasympathetic component in clonidine-induced bradycardia.
Adrenoceptors: Classification and Distribution
Published in Kenneth J. Broadley, Autonomic Pharmacology, 2017
Further roles for imidazoline receptors are now emerging. Imidazolines, such as efaroxan (see Table 5.2), enhance the rate of insulin secretion from the islets of Langerhans, possibly through I2 receptors (Chan et al. 1994). Clonidine and the selective I1 imidazoline agonist, moxonidine (see Table 4.3), inhibit gastric acid secretion and reduce ethanol-induced gastric mucosal injury (Glavin & Smyth 1995). Moxonidine also induces sodium and water excretion when given centrally (Penner & Smyth 1994). However, peripheral administration of the α2-agonists, rilmenidine (I1) and guanabenz (I2), increased blood pressure and urine excretion via α2-adrenoceptors (Evans & Anderson 1995).
Responsiveness of α2-adrenoceptor/I1-imidazoline receptor in the rostral ventrolateral medulla to cardiovascular regulation is enhanced in conscious spontaneously hypertensive rat
Published in Clinical and Experimental Hypertension, 2019
Masanobu Yamazato, Minori Nakamoto, Atsushi Sakima, Yoriko Yamazato, Shuichi Takishita, Yusuke Ohya
Either α2-adrenoceptors (20) or non-adrenergic imidazoline binding site (hypothetical I1-imidazoline receptors) (21) or both (22) may mediate the sympathoinhibitory effect of clonidine and related drugs in the RVLM. However, previous studies (23–25) suggest that the functional dominance of imidazoline receptors in the RVLM I1-receptors has never been cloned or convincingly identified. In contrast, the importance of central α2A-receptors in the action of clonidine was studied in genetically engineered mice expressing mutated α2A-adrenoceptor, but with intact α2B and α2C adrenoceptor subtypes of α2-adrenoceptor; the study showed that impaired α2A-adrenoceptor is sufficient to eliminate the hypotensive effect of clonidine (26). In the present study, the hypotensive and bradycardic effects of clonidine microinjection into RVLM were abolished in WKY rats and significantly attenuated in SHRs with co-injection of 2-methoxyidazoxan—a selective α2-adrenoceptor antagonist. The findings of the present study in conjunction with previous reports (9,26,27) indicate that α2-adrenoceptors in the RVLM contribute to the action of clonidine in the RVLM. Furthermore, the same dose of efaroxan [an α2-antagonist with 40-fold greater affinity for I1-imidazoline receptors (28)] attenuated clonidine-induced hypotension. This finding indicates that I1-imidazoline receptors in the RVLM also contribute to the action of clonidine in the RVLM.
Trace amine-associated receptor 1: a multimodal therapeutic target for neuropsychiatric diseases
Published in Expert Opinion on Therapeutic Targets, 2018
Michael D. Schwartz, Juan J. Canales, Riccardo Zucchi, Stefano Espinoza, Ilya Sukhanov, Raul R. Gainetdinov
Hoffmann-La Roche investigators performed a large-scale effort to derivatize adrenergic ligands, which were screened for TAAR1 activation by cAMP assays in heterologous cells expressing TAAR1, and for specificity via radioligand binding experiments involving over a hundred different proteins. This effort yielded several full (e.g. RO5166017 and RO5256390) and partial (e.g. RO5203648 and RO5263397) TAAR1 agonists [11,13,14] that to date have been successfully used in experimental models of neurological diseases such as drug addiction, schizophrenia, and Parkinson’s disease. In general, the ‘RO compounds’ are over 100-fold selective for TAAR1 versus other aminergic receptors, but the Kis for some other receptors – namely α2 adrenergic, 5-HT2 5-HTergic, µ and κ opioid, and I1 imidazoline receptors – are in the nanomolar range, and so additional effects on different targets cannot be excluded in all cases.
Evaluation of plasma agmatine level and its metabolic pathway in patients with bipolar disorder during manic episode and remission period
Published in International Journal of Psychiatry in Clinical Practice, 2019
Emine Yılmaz, M. Ramazan Şekeroğlu, Ekrem Yılmaz, Erdem Çokluk
In another study investigating the anti-depressant effect of agmatine, this effect was proposed to be mediated by imidazoline receptors (Zeidan, Zomkowski, Rosa, Rodrigues, & Gabilan, 2007). Budni, Gadotti, Kaster, Santos, and Rodrigues (2007) have reported that agmatine could act through different potassium canals, effects of serotonin reuptake inhibitors (SSRI) are potentiated with agmatine. Taksande, Kotagale, Tripathi, Ugale, and Chopde (2009) have shown that SSRI could elevate cerebral agmatine levels and this effect could completely be blocked by d-arginine which is arginine decarboxylase inhibitor. However, the same effect could not be shown with receptor antagonists of imidazole.