Arterial resistance vessels in primary hypertension--evidence for altered cellular Ca2+ metabolism.

The role of intracellular free Ca2+ in arterial smooth muscle was investigated in aortic smooth muscle cells from spontaneously hypertensive and normotensive rats, as well as in porcine aortic smooth muscle. Intracellular free Ca2+ in aortic smooth muscle from spontaneously hypertensive rats was elevated. Incubation of porcine aortic smooth muscle with plasma from essential hypertensive and normotensive subjects revealed a humoral factor in subjects with essential hypertension, which increased intracellular free Ca2+. Cross-circulation experiments between spontaneously hypertensive and normotensive rats demonstrated a transmission of hypertension to the normotensive animals as a result of a circulating hypertensive factor possibly produced in the kidneys and adrenals. The experiments suggest that vasoconstriction in primary hypertension may be caused by a humoral factor that increases intracellular free Ca2+ in arterial smooth muscle.