Search

The kallikrein-kinin and renin-angiotensin systems interact at multiple levels. In the present study, we tested the hypothesis that the B1 kinin receptor (B1R) contributes to vascular hypertrophy in angiotensin II (ANG II)–induced hypertension, through a mechanism involving reactive oxygen species (ROS) generation and extracellular signal-regulated kinase (ERK1/2) activation. Male Wistar rats were infused with vehicle (control rats), 400 ng/Kg/min ANG II (ANG II rats) or 400 ng/Kg/min ANG II plus B1 receptor antagonist, 350 ng/Kg/min des-Arg9-Leu8-bradykinin (ANGII+DAL rats), via osmotic mini-pumps (14 days) or received ANG II plus losartan (10 mg/Kg, 14 days, gavage - ANG II+LOS rats). After 14 days, ANG II rats exhibited increased systolic arterial pressure [(mmHg) 184±5.9 vs 115±2.3], aortic hypertrophy; increased ROS generation [2-hydroxyethidium/dihydroethidium (EOH/DHE): 21.8±2.7 vs 6.0±1.8] and ERK1/2 phosphorylation (% of control: 218.3±29.4 vs 100±0.25]. B1R expression was increased in aortas from ANG II and ANG II+DAL rats than in aortas from the ANG II+LOS and control groups. B1R antagonism reduced aorta hypertrophy, prevented ROS generation (EOH/DHE: 9.17±3.1) and ERK1/2 phosphorylation (137±20.7%) in ANG II rats. Cultured aortic vascular smooth muscle cells (VSMC) stimulated with low concentrations (0.1 nM) of ANG II plus B1R agonist exhibited increased ROS generation, ERK1/2 phosphorylation, proliferating-cell nuclear antigen expression and [H3]leucine incorporation. At this concentration, neither ANG II nor the B1R agonist produced any effects when tested individually. The ANG II/B1R agonist synergism was inhibited by losartan (AT1 blocker, 10 µM), B1R antagonist (10 µM) and Tiron (superoxide anion scavenger, 10 mM). These data suggest that B1R activation contributes to ANG II-induced aortic hypertrophy. This is associated with activation of redox-regulated ERK1/2 pathway that controls aortic smooth muscle cells growth. Our findings highlight an important cross-talk between the DABK and ANG II in the vascular system and contribute to a better understanding of the mechanisms involved in vascular remodeling in hypertension.

Concerning the structure of connective-muscular components the authors studied the walls of the terminal segments of the vertebral arteries as well as the basilar artery, utilizing the following staining methods: Azan modified by Heideinheim, Weigert's resorcin-fuchsin, and Weigert modified by van Gieson. It was established that wall of the vertebro-basilar system exhibits a mixed structure, muscular and elastic, by means of which the vessels are adjusted to the specific blood circulation conditions. Thus, vertebral arteries show in the most external layer of tunica media an evident external elastic lamina. In contrast, in the basilar artery the elastic tissue is localized mainly in the tunica media, and is distributed heterogeneously. In its caudal segment the elastic fibers are situated in the most internal layer of tunica media, and in the cranial segment the elastic component is homogenously distributed in the whole of tunica media. Os autores estudam a disposição dos componentes fibromusculares da parede das artérias vertebrais em seus segmentos terminais e a artéria basilar, usando os seguintes métodos de coloração: Azan modificado por Heidenheim, resorcina-fucsina de Weigert e Weigert modificado por van Gieson. O sistema vértebro-basilar apresentou em sua parede estrutura mista, muscular e elástica, pela qual os vasos se adaptam às condições circulatórias especificas daquela região. Besta forma, as artérias vertebrais apresentam na camada mais externa da túnica média uma lâmina elástica limitante externa evidente, ao contrário do encontrado na artéria basilar. Neste vaso, o tecido elástico se encontra principalmente na camada média, distribuindo-se de maneira heterogênea nos segmentos estudados, ou seja, no segmento caudal as fibras elásticas se dispõem predominantemente na camada mais interna da túnica média e, no segmento cranial, o componente elástico se dispõe homogeneamente em toda a camada média.

A fim de oferecer substrato anatômico que contribua para a interpretação clínica da cefaléia de origem cervical, estudo macro-mesoscópico do nervo occipital maior e da sua região de emergência subcutânea foi realizado. Observamos que, ao longo de sua estratigrafia, esse nervo descreve ângulos e mudanças de direção, que podem representar pontos críticos na etiologia da dor occipital; na região de sua emergência subcutânea forma, com a artéria e a veia occipital, feixe vásculo-nervoso envolvido por bainha de tecido conjuntivo fibroso, a qual mantém relações de continuidade e contigüidade com epimísio e perimísio adjacentes. A partir dos resultados encontrados, fazemos considerações anátomo-clínicas. In order to offer anatomical basis that aid for clinical interpretation of headache of cervical origin a macro-mesoscopic study of greater occipital nerve and its subcutaneous rise out site was accomplished. The authors observed that in its course this nerve delineates angles and direction shifts that can stand for critical points in etiology of occipital pain, so that in its subcutaneous rise out region both occipital artery and vein shape the vasculo-nervous bundle wrapped by sheath of fibrous connective tissue which has continuity and contiguity relation with the adjoining epimysium and perimysium. From our results, anatomo-clinical aspects are discussed.