Urocortin(UCN),a member of the corticotropin-releasing hormone(CRH)-related peptides,has been reported to play biologically diverse roles in several systems such as cardiovascular, reproductive, appetite, stress, inflammatory responses, etc. In heart, it was reported to have protective effects.On the other hand,it was also reported to have cardiac inotropic and hypertrophic effects and hence to cause cardiac remodeling.This paper will review the effects of UCN in cardiac system.

Urocortin(UCN),a newly isolated peptide,has been found to play an important role mainly in female reproductive system.In order to investigate the effect of UCN on T-type calcium currents(ICa,T), exploring the mechanisms of UCN s role in male reproductive system,especially in acrosome reaction,we directly measured the ICa,T in mouse spermatogenic cells exposed to UCN using standard whole-cell patch clamp recording technique.Our results showed that UCN reversibly inhibited the T-type Ca2+ currents in the cells in a concentration-dependent manner.The current density was inhibited by about 19% after exposure of the cells to UCN(0.1 lM)for 5 min,from the control value of 6.75±1.17 to 5.26±0.82 pA/pF.UCN up-shifted the current-voltage(I-V)curve.Frequency-dependence of UCN’s effects on ICa,T was also observed.Moreover,UCN at 0.1 lM did not markedly affect the activation of ICa,T but shifted the inactivation curve of ICa,T to the left.The inhibitory effect of UCN on the T-type Ca2+ current was not affected by Astressin,the CRF receptor blocker.Since T-type calcium channels are a key component in acrosome reaction,our data suggest that UCN might be a significant factor in male reproductive action and a potential contraceptive agent.

The newly isolated peptide,urocortin(UCN),is a member of the corticotropin-releasing factor(CRF)-related peptides that has been found to have potent cardiovascular protective effects.In order to investigate the effect of UCN on the viability of adult rat vascular smooth muscle cells(VSMC)and the relevant mechanisms,we exposed the VSMC to UCN to observe the change in cell viability using MTT assay and intracellular calcium concentration using confocal laser scanning microscope methods.Our results showed that UCN(10−7M)inhibited the viability of VSMC by about 26% (P<0.05, compared to control).The effect was concentration-dependent, but it was not dependent on the affecting time.Glybenclamide (Gly, 10−5M), the ATP-sensitive potassium channel(KATP channel)blocker,and astressin (10−6 M), a competitive antagonist of CRF receptors,had no influence on this inhibition.Bay K8644 (10−6 M), a special L-type calcium channel activator,increased the viability of VSMC. Pre-treatment of the cells with UCN diminished the effect of Bay K8644 (n=6, P<0.05). UCN was also observed to reduce the intracellular Ca2+ increase induced by KCl and Bay K8644. There was no significant difference in nitrite accumulation between UCN groups and the control.In conclusion,UCN reduced the viability of VSMC through L-type calcium channels.These interesting results might suggest that UCN may be a new vasoactive agent involved in hindering vascular remodeling in combination with previous reports about UCN's hypotensive effects.

Urocortin(UCN),a newly isolated peptide related to hypothalamic corticotrophin releasing factor(CRF)family,had been reported to play biologically diverse roles in several systems such as cardiovascular,reproductive,appetite,stress,and inflammatory responses,etc.It was thought previously to be an endogenous agonist,producing the several actions previously attributed to CRF. But, recently, it was shown to directly reduce L-type calcium currents of acute isolated cardiac myocytes and T-type calcium currents in mouse spermatogenic cells via inhibiting calcium channel instead of binding first to its CRF-R2 receptors.UCN could also reduce the intracellular calcium in vascular smooth muscle cells via inhibiting calcium channel directly.Furthermore,UCN could increase the gene expression of ATP-sensitive potassium channels(KATP)and activate sarcolemmal ATP-sensitive potassium current during normal or hypoxia,which could be inhibited by glibenclamide,a specific KATP blocker.This review will highlight the current novel findings on the ionic mechanisms by which UCN may exert its several actions.

This study investigated the activity of nitric oxide(NO)in the striatum(STR)for a further comprehension of the pathogenesis of Parkinson’s disease(PD).Microiontophoresis was used to observe the effects of sodium nitroprusside(SNP),l-glutamic acid(GLU)and γ-aminobutyric acid(GABA)on STR neurons’ firing rates.Itwas observed that 77.27%(51/66)of the tested STR neurons were excited by SNP.This excitatory effect could be antagonized by theNOsynthase(NOS)inhibitor,N(G)-nitro-l-arginine methyl ester(l-NAME).During the microiontophoresis of GLU,the excitatory firing of STR neurons was also attenuated by addition of l-NAME while SNP application could enhance the excitation of the neurons.On the other hand,in the presence of GABA,SNP still excited the tested STR neurons.These results demonstrated that NOergic,GLUergic and GABAergic co-existed in the same STR neurons.NOergic and GLUergic were excitatory whereas GABAergic was inhibitory on the firing activity in STR neurons.