ABSTRACT
This chapter reviews hypothetical relationships between sodium fluxes across the cell membrane and intracellular sodium concentration in vascular smooth muscle in the animal models of hypertension. It suggests that the inhibitor decreases norepinephrine uptake into cardiovascular adrenergic nerve terminals, thereby contributing to the hypertension. M. B. Pamnani et al. repeated the study in the rat with reduced renal mass-saline hypertension, another form of volume-expanded hypertension. Coexistence would drive the intracellular sodium concentration to higher levels, further increasing contractile activity of vascular smooth muscle. Membranes isolated from vascular smooth muscle form vesicles which in fact pump calcium; the problem is that the sarcolemma preparations often contain contaminant sarcoplasmic reticulum, which could account for this pumping. Efforts to determine whether chronic inhibition of the sodium-potassium pump in blood vessels affects the number of pump sites in the sarcolemma of the vascular smooth muscle cell should also be encouraged.
