Recep tors

The effect on the blood pressure by these compounds can be explained by an action on central a-re-ceptors. But from the aforementioned facts it can be assumed that the sedation and reduction in salivation are dependent also on an influence on central a-recep-tors. 

The issue, however, has proved to be far from settled, because Soutar et al. have reported that in FH heterozygotes with an identical underlying LDL-recep-tor mutation, Lp(a) levels were similar to those of their unaffected family members (G16, S41). 

Simons FE Is antihistamine (Hj-recep-tor antagonist) therapy useful in clinical asthma Clin Exp Allergy 1999 29 (suppl3) 98-104. 

As described above, ondansetron has potent and highly selective antagonist properties at the 5-HT3-receptor [7]. The selectivity of action of ondansetron for the 5-HT3 receptor has been demonstrated using a number of in vitro preparations which respond to activation of a number of different neurotransmitter receptors. The selectivity ratio for ondansetron on 5-HT3-recep-tors compared with other receptor types is greater than 1000. In animals and in man, ondansetron has no overt actions on cardiovascular parameters and there are no effects on normal behaviour [7]. 

Hellen, E. H. and Axelrod, D. (1991) Kinetics of epidermal growth factor/recep-tor binding on cells measured by total internal reflection/fluorescence recovery after photobleaching. J. Fluorescence 1,113-128. 

Due to its equally high affinity for all a-and p-receptors, epinephrine does not permit selective activation of a particular receptor subtype. Like most catecholamines, it is also unsuitable for oral administration (catechol is a trivial name for o-hydroxyphenol). Norepinephrine differs from epinephrine by its high affinity for a-receptors and low affinity for P2-receptors. In contrast, isoproterenol has high affinity for p-recep-tors, but virtually none for a-receptors (A). 

Pentazocine is an antagonist at p-recep-tors and an agonist at K-receptors (A). 

Immunoglobulin M (IgM), a membrane protein on the surface of B lymphocytes, serves to bind free antigens to the B cells. By contrast, T cell receptors only bind antigens when they are presented by another cell as a complex with an MHC protein (see below). Interaction between MHC-bound antigens and T cell receptors is supported by co-recep-tors. This group includes CDS, a membrane protein that is typical in cytotoxic T cells. T helper cells use CD4 as a co-receptor instead (not shown). The abbreviation CD stands for cluster of differentiation. It is the term for a large group of proteins that are all located on the cell surface and can therefore be identified by antibodies. In addition to CD4 and CDS, there are many other co-receptors on immune cells (not shown). 

There are differences between the receptors on nerves (presynaptic receptors) and those on effector cells (postsynaptic receptors). Furthermore, some a-agonists and antagonists exhibit selectivity for one of these receptor types. Terminology classifies receptors as either i or tt2. i-Receptors are those whose stimulation has traditionally been associated with the postsynaptic a-receptors of smooth muscle, while a2-receptors are those originally associated with the presynaptic a-re-ceptors of peripheral nerves. However, the designation of receptors as either or 2 cannot be categorized strictly by anatomical location (i.e., presynaptic or postsynaptic), since evidence now indicates that az-recep-tors occupy, in addition to peripheral nerves, a variety of sites including smooth muscle, adrenal medullary cells, the brain, and melanocytes. 

Greibrokk, T., G. Lofroth, L. Nilsson, R. Toftgard, J. Carlstedt-Duke, and J. Gustafsson, Nitroarenes Mutagenicity in the Ames Salmonella./Microsome Assay and Affinity to the TCDD-Recep-tor Protein, in Toxicity of Nitroaromatic Compounds (D. E. Rick-ert, Ed.), pp. 166-183, Hemisphere Publishing, Washington, DC, 1985. 

It is a potent opioid analgesic. Chemically it is N-phenyl-N-propanamide. It interacts predominantly with opioid p-recep-tor in human brain, spinal cord and other tissues. It exerts its principle pharmacologic effects on the CNS. It is 80-100 times more potent than morphine, both in analgesia and respiratory depression. 

Figure 3.38 Schematic representation of receptor (R)-ligand (L) binding to form a recep-tor/ligand complex (C).

Gross, W., and Lohse, M. J. (1991). Mechanism of activation of A2 adenosine recep-tors.2. A restricted collision-coupling model of receptor-effector interaction. Mol. Pharmacol. 39, 524—530. 

Ariens, E. J., Rodrigues de Miranda, J.F., Simonis, A. M., The pharmacon-recep-tor-effector concept a basis for understanding the transmission of information in biological systems. In The Receptors, O Brien, R. D. (ed.). Plenum Press, New York, 1979, pp. 33-91. 

Von Willebrand M, Jascur T, Bonnefoy-Berard N, Yano H, Altman A, Matsuda Y, Mustelin T. Inhibition of phosphatidylinositol 3-kinase blocks T cell antigen recep-tor/CD3-induced activation of the mitogen-activated kinase Erk2. Eur J Biochem 1996 235 828-35. 

Black JW, Duncan WA, Durant CJ, Ganellin CR, Parsons EM. Definition and antagonism ofhistamine H2-recep-tors. Nature, 1972 236, 385-390. 

Four different QSAR were derived for the inhibition of DHFR from rat liver, human leukemia, mouse L1210, and bovine liver by 2,4-diamino, 5-Y, 6-Z-quinazolines (Fig. 1.3) (202, 213-215). A comparison of their QSAR presents an interesting study on the importance of spanned space in delineating enz37me-recep-tor interactions. 

Inhibitory Signaling from Recep tor Trio NgR-Lingol-p75NTR... 

Rotshenker S (2003) Microglia and macrophage activatiorr and tire regulation of complemerrt-recep tor-3 (CR3/MAC-l)-mediated myelirr phagocytosis hr hrjury and disease. J Mol Neurosci 21 65—72. 

---