Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0241981 (loss of balance)
 452 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Endothelin is a 21-amino-acid, vasoactive peptide. Sequence analysis of cloned cDNAs for porcine and human endothelin precursors showed that endothelin-1 (ET-1) is produced in the endothelial cells. The peptide, endothelin (ET), was first identified as a potent vasoconstrictor. It is one of the most potent endogenous vascular smooth-muscle constrictors, ten times more potent than angiotensin II, vasopressin, and neuropeptide Y. Shortly after the discovery of this vasoconstrictor peptide, it was revealed that endothelin also possesses vasodilator properties at doses lower than those necessary to produce vasoconstriction. However, controversy still exists over the mechanism(s) of action; prostacyclin and endothelium-derived relaxing factor (EDRF) have mainly been implicated as the source of the initial vasodepressor effect. ET also elicits markedly different regional hemodynamic response patterns. There is a heterogeneity in the observed vasodilation or vasoconstriction, depending on species and on vascular beds studied in the same species. Endothelin has been implicated in a number of pathologic situations, including tissue ischemia and vasospasm. ET seems to be produced more actively around the site of endothelial damage; the loss of balance between its vasodilator- and vasoconstrictor-induced responses could contribute to its patho-physiologic properties. Experimental results strongly support the concept that ET could be important in controlling vascular tonus, both in the healthy and the diseased vessel.
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PMID:Endothelin: an endothelium-derived vasoactive peptide. 788 38

As an endogenous inhibitor of glutamate-mediated synaptic transmission in mammalian central nervous system, neuropeptide Y (NPY) plays a crucial role in regulating homeostasis of neuron excitability. Loss of balance between excitatory and inhibitory neurotransmission is thought to be a chief mechanism of epileptogenesis. The abnormal expression of NPY and its receptors observed following seizures have been demonstrated to be related to the production of epilepsy. The tremor rat (TRM) is a hereditary epileptic animal model. So far, there is no report concerning whether NPY and its receptors may be involved in TRM pathogenesis. In this study, we focused on the expression of NPY and its three receptor subtypes: Y1R, Y2R and Y5R in the TRM brain. We first found the expression of NPY in TRM hippocampus and temporal lobe cortex was increased compared with control (Wistar) rats. The mRNA and protein expression of Y1R was down-regulated in hippocampus but up-regulated in temporal lobe cortex, whereas Y2R expression was significantly increased in both areas. There was no significant change of Y5R expression in either area. The immunohistochemistry data showed that Y1R, Y2R, Y5R were present throughout CA1, CA3, dentate gyrus (DG) and the entorhinal cortex which is included in the temporal lobe cortex of TRM. In conclusion, our results showed the altered expression of NPY, Y1R and Y2R but not Y5R in hippocampus and temporal lobe cortex of TRM brain. This abnormal expression may be associated with the generation of epileptiform activity and provide a candidate target for treatment of genetic epilepsy.
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PMID:Altered expression of neuropeptide Y, Y1 and Y2 receptors, but not Y5 receptor, within hippocampus and temporal lobe cortex of tremor rats. 2444 22