The afferent arteriole （AA） of rat kidney exhibits the myogenic response, in which the vessel constricts in response to an elevation in blood pressure and dilates in response to a pressure reduction. Additionally, t...The afferent arteriole （AA） of rat kidney exhibits the myogenic response, in which the vessel constricts in response to an elevation in blood pressure and dilates in response to a pressure reduction. Additionally, the AA exhibits spontaneous oscillations in vascular tone at physiological luminal pressures. These time-periodic oscillations stem from the dynamic exchange of Ca^2＋ between the cytosol and the sarcoplasmie reticulum, cou- pled to the stimulation of Ca^2＋-activated potassium and chloride channels, and to the modulation of voltage-gated L-type Ca^2＋ channels. The effects of physiological factors, including blood pressure and vasoactive substances, on AA vasomotion remain to be well characterized. In this paper, we analyze a mathematical model of Ca^2＋ signaling in an AA smooth muscle cell. The model represents detailed transmembrane ionic trans- port, intracellular Ca^2＋ dynamics as well as kinetics of nitric oxide （NO） and superoxide （O2^-） formation, diffusion and reaction. NO is an important factor in the maintenance of blood pressure and O2^- has been shown to contribute significantly to the functional alternations of blood vessels in hypertension. We perform a bifurcation analysis of the model equations to assess the effect of luminal pressure, NO and O2^- on the behaviors of limit cycle oscillations.展开更多
文摘The afferent arteriole （AA） of rat kidney exhibits the myogenic response, in which the vessel constricts in response to an elevation in blood pressure and dilates in response to a pressure reduction. Additionally, the AA exhibits spontaneous oscillations in vascular tone at physiological luminal pressures. These time-periodic oscillations stem from the dynamic exchange of Ca^2＋ between the cytosol and the sarcoplasmie reticulum, cou- pled to the stimulation of Ca^2＋-activated potassium and chloride channels, and to the modulation of voltage-gated L-type Ca^2＋ channels. The effects of physiological factors, including blood pressure and vasoactive substances, on AA vasomotion remain to be well characterized. In this paper, we analyze a mathematical model of Ca^2＋ signaling in an AA smooth muscle cell. The model represents detailed transmembrane ionic trans- port, intracellular Ca^2＋ dynamics as well as kinetics of nitric oxide （NO） and superoxide （O2^-） formation, diffusion and reaction. NO is an important factor in the maintenance of blood pressure and O2^- has been shown to contribute significantly to the functional alternations of blood vessels in hypertension. We perform a bifurcation analysis of the model equations to assess the effect of luminal pressure, NO and O2^- on the behaviors of limit cycle oscillations.
