Barium removes the ouabain-induced increase in the rod response to light.

The mass receptor potential of the excised, superfused retina of the bullfrog was isolated with aspartate. Rods were selectively stimulated by using very dim flashes of light. In the presence of 0.1 mM ouabain, the amplitude of the receptor response was found first to increase transiently and, subsequently, to decrease progressively. The ouabain-induced transient increase in receptor response was completely eliminated by 0.4 mM barium chloride. However, barium did not affect the rate at which the response decayed in the presence of ouabain. The ability of barium to remove the ouabain-induced transient increase in the amplitude of the receptor response is discussed in terms of reducing the coupling ratio of the postulated electrogenic sodium-potassium pump of rods.

Pathophysiology of experimental renovascular hypertension.

The genesis of renovascular hypertension follows a continuum from an acute to a chronic phase. Reduction in renal perfusion initiates renin release and angiotensin-mediated systemic vasoconstriction. Aldosterone secretion, sodium and water retention, and expansion of the extracellular volume ensue. Sustained hypertension is further maintained by interacting physiologic mechanisms including increased angiotensin II sensitivity, vasopressin, ouabain-like substance, the sympathetic nervous system, CNS mechanisms, autoregulation, and structural changes.

Evidence for the presence of 'ouabain like' compound in human cerebrospinal fluid.

Material extracted and partially purified from human cerebrospinal fluid (CSF) is capable of: a, inhibiting [3H]ouabain binding to rat brain synaptosomes; b, inhibiting the activity of purified pig kidney Na+,K+-ATPase; and c, inhibiting ouabain sensitive induced 86Rb influx to tissue cultured fibroblasts. These results demonstrate the existence of an 'ouabain like' compound (OLC) in human CSF, and are consistent with the hypothesis of the function of this compound as a neuromodulator.

An endogenous ouabain-like factor associated with hypertensive pregnant women.

Levels of a ouabain-like factor (OLF) were measured in amniotic fluid from 49 undigitalized third trimester pregnant women by means of its cross-reactivity in a digoxin RIA and its inhibition of ouabain-sensitive [Na,K]ATPase. The results from these 2 assays were significantly correlated (P less than 0.05). Of the women included in this study, 25 had blood pressures considered normal for their gestational age, while 24 had developed during their current pregnancy blood pressures judged to be elevated. When levels of OLF in the amniotic fluids from the normotensive and hypertensive pregnant women were compared, significantly higher levels were present in the hypertensive group for both assays (P less than 0.002). Further, there was a significant correlation between the diastolic blood pressures of these women at the time of amniocentesis and the amniotic fluid OLF levels determined by either assay (P less than 0.002). These results are consistent with OLF having a role in hypertensive complications of pregnancy.

Humoral factors and the sodium-potassium pump in low renin hypertension.

Recent studies suggest that sodium dependent low renin hypertension results in part from the release of a ouabain-like factor, perhaps natriuretic hormone, from the brain. This humoral factor inhibits Na+, K+-ATPase and hence the active pumping of sodium and potassium in the muscle cells of blood vessels and heart. The pump suppression causes increased contractile activity and hence increased arterial blood pressure. In the muscle cells of the blood vessels, the increased contractile activity appears to be related to membrane depolarization.