Theoretical assessment of the Ca2+ oscillations in the afferent arteriole smooth muscle cell of the rat kidney

Abstract

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[Formula: see text] between the cytosol and the sarcoplasmic reticulum, coupled to the stimulation of Ca[Formula: see text]-activated potassium and chloride channels, and to the modulation of voltage-gated L-type Ca[Formula: see text] 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[Formula: see text] signaling in an AA smooth muscle cell. The model represents detailed transmembrane ionic transport, intracellular Ca[Formula: see text] dynamics as well as kinetics of nitric oxide (NO) and superoxide (O[Formula: see text]) formation, diffusion and reaction. NO is an important factor in the maintenance of blood pressure and O[Formula: see text] 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 O[Formula: see text] on the behaviors of limit cycle oscillations.