Calcium is an essential factor in the function of many cells, including the contraction of muscle cells. When blood pressure is elevated, as in hypertension, it is known that the intracellular calcium is elevated in many cell types. Because of the central role of smooth muscle cells in arteries in controlling resistance to blood flow, and thus blood pressure, this cell has been extensively studied, and there is evidence that there is altered calcium-handling ability in smooth muscle in hypertension.

However, most of this evidence is from genetic models of hypertension, and, thus, it is unclear whether the altered calcium handling by smooth muscle cells is a cause, or a consequence, of hypertension. To address this issue, Simard and colleagues† measured the calcium-handling ability of smooth muscle cells isolated from a nongenetic model of hypertension. Using cellular electrophysiologic techniques, they measured how many calcium channels—the pores through which calcium flows into the smooth muscle cell—were in the membranes of cells from normal subjects and subjects who had hypertension induced. Calcium channel density was measured by how much calcium was conducted through an area of membrane. They studied calcium conductance, C, in the presence or absence of a drug that opens calcium channels widely, BayK 8644, B. They also measured the systolic blood pressure of each subject from which the smooth muscle cells were isolated. Is there any evidence that BayK 8644 changes the calcium conductance when accounting for the covariate, systolic blood pressure, P? (The data are in Table D-37, Appendix D.)