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Calcium handling by vascular myocytes in hypertension
Braz. j. med. biol. res ; 30(3): 315-23, Mar. 1997. ilus
Artigo em Inglês | LILACS | ID: lil-191343
RESUMO
Calcium ions (Ca2+) trigger the contraction of vascular myocytes and the level of free intracellular Ca2+ within the myocyte is precisely regulated by sequestration and extrusion mechanisms. Extensive evidence indicates that a defect in the regulation of intracellular Ca2+ plays a role in the augmented vascular reactivity characteristic of clinical and experimental hypertension. For example, arteries from spontaneously hypertensive rats (SHR) have an increased contractile sensitivity to extracellular Ca2+ and intracellular Ca2+ levels are elevated in aortic smooth muscle cells of SHR. We hypothesize that these changes are due to an increase in membrane Ca2+ channel density and possibly function in vascular myocytes from hypertensive animals. Several observations using various experimental approaches support this

hypothesis:

1) the contractile activity in response to depolarizing stimuli is increased in arteries from hypertensive animals demonstrating increased voltage-dependent Ca2+ channel activity in hypertension; 2) Ca2+ channel agonists such as Bay K 8644 produce contractions in isolated arterial segments from hypertensive rats and minimal contraction in those from normotensive rats; 3) intracellular Ca2+ concentration is abnormally increased in vascular myocytes from hypertensive animals following treatment with Ca2+ channel agonists and depolarizing interventions, and 4) using the voltage-clamp technique, the inward Ca2+ current in arterial myocytes from hypertensive rats is nearly twice as large as that from myocytes of normotensive rats. We suggest that an alteration in Ca2+ channel function and/or an increase in Ca2+ channel density, resulting from increased channel synthesis or reduced turnover, underlies the increased vascular reactivity characteristic of hypertension.
Assuntos
Texto completo: DisponíveL Índice: LILACS (Américas) Assunto principal: Resistência Vascular / Éster Metílico do Ácido 3-Piridinacarboxílico, 1,4-Di-Hidro-2,6-Dimetil-5-Nitro-4-(2-(Trifluormetil)fenil) / Canais de Cálcio / Cálcio / Hipertensão / Músculo Liso Vascular Limite: Animais Idioma: Inglês Revista: Braz. j. med. biol. res Assunto da revista: Biologia / Medicina Ano de publicação: 1997 Tipo de documento: Artigo / Congresso e conferência

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Texto completo: DisponíveL Índice: LILACS (Américas) Assunto principal: Resistência Vascular / Éster Metílico do Ácido 3-Piridinacarboxílico, 1,4-Di-Hidro-2,6-Dimetil-5-Nitro-4-(2-(Trifluormetil)fenil) / Canais de Cálcio / Cálcio / Hipertensão / Músculo Liso Vascular Limite: Animais Idioma: Inglês Revista: Braz. j. med. biol. res Assunto da revista: Biologia / Medicina Ano de publicação: 1997 Tipo de documento: Artigo / Congresso e conferência