Increased blood pressure (BP) in genetic hypertension is usually caused by high activity of sympathetic nervous system (SNS) which is enhanced by central angiotensin II but lowered by central nitric oxide (NO). We have therefore evaluated NO synthase (NOS) activity as well as neuronal NOS (nNOS), inducible NOS (iNOS) and endothelial NOS (eNOS) protein expression in brainstem and midbrain of adult spontaneously hypertensive rats (SHR) characterized by enhanced sympathetic vasoconstriction. We also studied possible participation of brain NO in antihypertensive effects of chronic captopril treatment of adult SHR. NOS activity was increased in midbrain of SHR compared to Wistar-Kyoto (WKY) rats. This could be ascribed to enhanced iNOS expression, whereas nNOS expression was unchanged and eNOS expression was reduced in this brain region. In contrast, no significant changes of NOS activity were found in brainstem of SHR in which nNOS and iNOS expression was unchanged, but eNOS expression was increased. Chronic captopril administration lowered BP of adult SHR mainly by attenuation of sympathetic tone, whereas the reduction of angiotensin II-dependent vasoconstriction and the decrease of residual BP (amelioration of structural remodeling of resistance vessels) were less important. This treatment did not affect significantly either NOS activity or expression of any NOS isoform in the two brain regions. Our data do not support the hypothesis that altered brain NO formation contributes to sympathetic hyperactivity and high BP of adult SHR with established hypertension.

• MeSH
• kaptopril farmakologie   MeSH
• krevní tlak účinky léků   fyziologie   MeSH
• krysa rodu Rattus MeSH
• mozek účinky léků   enzymologie   MeSH
• NG-nitroargininmethylester farmakologie   MeSH
• pentoliniumtartrát farmakologie   MeSH
• potkani inbrední SHR MeSH
• potkani inbrední WKY MeSH
• renin-angiotensin systém účinky léků   MeSH
• sympatický nervový systém účinky léků   MeSH
• synthasa oxidu dusnatého, typ I metabolismus   MeSH
• synthasa oxidu dusnatého, typ II metabolismus   MeSH
• synthasa oxidu dusnatého, typ III metabolismus   MeSH
• synthasa oxidu dusnatého antagonisté a inhibitory   metabolismus   MeSH
• tělesná hmotnost účinky léků   MeSH
• velikost orgánu účinky léků   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• kaptopril MeSH
• NG-nitroargininmethylester MeSH
• pentoliniumtartrát MeSH
• synthasa oxidu dusnatého, typ I MeSH
• synthasa oxidu dusnatého, typ II MeSH
• synthasa oxidu dusnatého, typ III MeSH
• synthasa oxidu dusnatého MeSH

The proliferative activity in the subependymal layer of lateral brain ventricles in adulthood is known. We were interested in the reaction of this layer to ibotenic acid lesions, which simulate neurodegenerative processes in Huntington's disease. Animals with a unilateral ibotenic acid lesion were compared with sham-lesioned animals and control animals with intact brains at 5 and 13 weeks after surgery. Five weeks after surgery, increased proliferation was found in most GFAP-positive astrocytes and to a lesser extent in CNPase-positive oligodendrocytes in comparison with controls. Interestingly, a slight increase in proliferation was found as well in the contralateral non-lesioned hemispheres. Moderate elevation of cell proliferation was found after induction of sham-lesions as well. The intensity of the reaction in the subependymal layer decreased in the following 8 weeks. Only a few scattered cells that originated from the subependymal layer had migrated over a short distance to adjacent brain tissue. We conclude that the reaction of the subependymal layer is (a) non-specific, as it is a response to any type of lesion, and (b) slowly decreases in time.

• MeSH
• 2',3'-cyklické nukleotidfosfodiesterasy analýza   MeSH
• agonisté excitačních aminokyselin toxicita   MeSH
• antigen Ki-67 analýza   MeSH
• astrocyty chemie   účinky léků   patologie   MeSH
• bromodeoxyuridin analýza   MeSH
• ependym chemie   účinky léků   patologie   MeSH
• gliový fibrilární kyselý protein analýza   MeSH
• imunohistochemie MeSH
• krysa rodu Rattus MeSH
• kyselina ibotenová toxicita   MeSH
• oligodendroglie chemie   účinky léků   patologie   MeSH
• potkani Long-Evans MeSH
• proliferační antigen buněčného jádra analýza   MeSH
• ventriculi laterales chemie   účinky léků   patologie   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• 2',3'-cyklické nukleotidfosfodiesterasy MeSH
• agonisté excitačních aminokyselin MeSH
• antigen Ki-67 MeSH
• bromodeoxyuridin MeSH
• gliový fibrilární kyselý protein MeSH
• kyselina ibotenová MeSH
• proliferační antigen buněčného jádra MeSH

The neurotoxic lesion of the rat brain, induced by stereotaxic infusion of the ibotenic (IA) or kainic (KA) acids, is a commonly used model of Huntington's disease (HD) in animal studies. Neurodegenerative process in HD develops for 10-20 years. However, the majority of studies related to the animal models of HD deal with only the several weeks surviving animals. For that reason, a detailed description of the development of histopathological changes in the striatum in the rat brain is presented in this study. Intrastriatal instillation of both, the IA or the KA causes the partial necrosis of the striatum, accompanied by a rarefaction of the neuropil. Owing to a rather low number of subsequently in situ proliferating glial cells, predominantly astrocytes, the whole process results in a shrinkage of the striatum compensated by an enlargement of the lateral brain ventricles. Although, the fully developed IA lesion is envisaged at 1 week and KA lesion at 3-4 weeks after the injection of neurotoxic acids, the degenerative process within the striatum develops in a rather long time -- at least 6 months. The only morphological observation that doesn't correlate to the findings from the HD patients, is the needle-track area, which is repaired by a conspicuous glial or glial-fibrotic scar. There is no substantial difference in the histopathological characteristics of both the neurotoxic acids used in our studies. However, if the IA must be applied into 3-4 sites in each hemisphere in comparison with only one injection of the KA, the use of KA is, from the morphological point of view, more suitable in relation to the number of artificial needle-track areas.

• MeSH
• corpus striatum účinky léků   patologie   MeSH
• Huntingtonova nemoc chemicky indukované   patologie   MeSH
• krysa rodu Rattus MeSH
• kyselina ibotenová MeSH
• kyselina kainová MeSH
• modely nemocí na zvířatech * MeSH
• neurotoxiny MeSH
• potkani Long-Evans MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• zvířata MeSH
• Publikační typ
• anglický abstrakt MeSH
• časopisecké články MeSH
• Názvy látek
• kyselina ibotenová MeSH
• kyselina kainová MeSH
• neurotoxiny MeSH