Dysfunction of Ca2+-pump of Vascular Muscle Membranes: An Important Etiological Factor in Hypertension

An increase in total peripheral resistance associated with sustained hypertension is thought to be contributed by the hyperresponsiveness of arteries, particularly at the level of small arteries and arterioles. Both structural and functional changes of blood vessels have long been recognized as contributing factors to the increased vascular responsiveness in animals with experimental hypertension [4]. Over the past decade, derangement of membrance functions in cardiovascular tissues has been repeatedly shown to be closely associated with the development of primary hypertension [13,14]. These membrane abnormalities included the handling (e.g., binding, active transport, exchange and/or passive flux) of ions (e.g., H+, Na+, K+, Cl−, and/or Ca2+), the interactions (e.g., affinity, density, and/or modulation) between membrane receptors and physiologically relevant vasoactive ligands (e.g, angiotensin II, catecholamines, and/or atrial natriuretic peptides), and the properties of membrane-associated anzymes (e.g., those responsible for ion transport, receptor coupling, signal transduction, or other unknown functions probably involving cellular proliferation). The nature of membrane abnormalities varied considerably depending on the mode and duration of hypertension, the vasculature selected, and the methodology employed.