Ca2+ Movements in Vascular Smooth Muscle and their Alterations in Hypertension

This chapter outlines the limitations of calcium (Ca) flux studies. It presents evidence for increased Ca²⁺ permeability in vascular smooth muscle in hypertension. Increased Ca²⁺ permeability along with decreased Ca²⁺ extrusion may lead to increased cytoplasmic in vascular smooth muscle in hypertension. Contraction of vascular smooth muscle involves rapid fluctuations in the concentration of cytoplasmic calcium. These fluctuations in Ca²⁺ are controlled by two membrane systems, the sarcolemma and the sarcoplasmic reticulum. A number of different indicators have been used to estimate the involvement of intracellular Ca²⁺ release in vascular smooth muscle contraction. In 1979, two excitable Ca²⁺ channels were postulated to occur in smooth muscle, one receptor-operated and the other voltage-sensitive. In vascular smooth muscle, the contractile proteins are organized to form regular arrays of myosin and actin filaments. Studies of total arterial wall content of ⁴⁵Ca provide little information relevant to contractility in vascular smooth muscle, for the greatest portion of Ca²⁺ labeled is likely to be extracellular.