Recent experimental evidence has provided important clues as to the role of electrolytes, particularly Ca, in the regulation of blood flow, renin secretion, and blood pressure. The smooth muscle cells of arterioles in general and the juxtaglomerular cells in the renal afferent arterioles have been shown to have Ca channels sensitive to voltage, hormones, and stretch. This paper reviews a model that utilizes these features along with a fundamental law of physics to point to some plausible explanations for some interesting experimental observations on renal blood flow, renin secretion, and hypertension. The chief features of the model are that in the steady state the arteriole must achieve a stable physical equilibrium in which the forces tending to distend the vessel (transmural pressure) counterbalance the forces tending to prevent distension (wall tension); the wall tension consists of a passive and an active component, the latter of which is sensitive to stretch of the vessel; and stretch activates the opening of stretch-sensitive Ca permeability channels that promote the influx of Ca to trigger active tension development. Thus Ca is the signal that couples stretch to contraction. This latter feature is the so-called myogenic response. Altered equilibrium may be initiated either by a rise in perfusion or tissue pressure to alter the distending force or by a rise in cytosolic Ca to increase active tension development and the constricting force. Several factors may initiate disequilibrium, some of which are discussed. Equilibrium is soon reestablished, however, at a new steady state. The model predicts curves for renal blood flow autoregulation and renin secretion in response to changes in renal perfusion pressure, tissue pressure, extracellular Ca, and blockers and promoters of Ca influx and Ca efflux. These predictions agree well with existing experimental evidence and suggest new experiments. The model provides a theoretical basis for explaining the steady-state blood pressure profile observed in renovascular hypertension and perhaps in other forms of hypertension as well. The model also provides a theoretical basis for understanding the volume-vasoconstriction approach used by some workers and the autoregulation approach used by others in explaining the mechanisms of hypertension.(ABSTRACT TRUNCATED AT 400 WORDS)