ABSTRACT
The cytosolic intracellular calcium concentration ([Ca(2+)](i)) is a major determining factor in the vascular smooth muscle tone. In the afferent arteriole it has been shown that agonists utilizing G-protein coupled receptors recruit Ca(2+) via release from intracellular stores and entry via pathways in the plasma membrane. The relative importances of entry vs. mobilization seem to differ between different agonists, species and preparations. The entry pathway might include different types of voltage sensitive Ca(2+) channels located in the plasmalemma such as dihydropyridine sensitive L-type channels, T-type channels and P/Q channels. A role for non-voltage sensitive entry pathways has also been suggested. The importance of voltage sensitive Ca(2+) channels in the control of the tone of the afferent arteriole (and thus in the control of renal function and whole body control of extracellular fluid volume and blood pressure) sheds light on the control of the membrane potential of afferent arteriolar smooth muscle cells. Thus, K(+) and Cl(-) channels are of importance in their role as major determinants of membrane potential. Some studies suggest a role for calcium-activated chloride (Cl(Ca)) channels in the renal vasoconstriction elicited by agonists. Other investigators have found evidence for several types of K(+) channels in the regulation of the afferent arteriolar tone. The available literature in this field regarding afferent arterioles is, however, relatively sparse and not conclusive. This review is an attempt to summarize the results obtained by others and ourselves in the field of agonist induced afferent arteriolar Ca(2+) recruitment, with special emphasis on the control of voltage sensitive Ca(2+) entry. Outline of the Manuscript: This manuscript is structured as follows: it begins with an introduction where the general role for [Ca(2+)](i) as a key factor in the regulation of the tone of vascular smooth muscles (VSMC) is detailed. In this section there is an emphasis is on observations that could be attributed to afferent arteriolar function. We then investigate the literature and describe our results regarding the relative roles for Ca(2+) entry and intracellular release in afferent arterioles in response to vasoactive agents, with the focus on noradrenalin (NA) and angiotensin II (Ang II). Finally, we examine the role of ion channels (i.e. K(+) and Cl(-) channels) for the membrane potential, and thus activation of voltage sensitive Ca(2+) channels.
