The endogenous cytochemically assayable Na-K-ATPase inhibitor and its relation to hypertension

Acute volume expansion endows the plasma with the capacity to cause a natriuresis, to inhibit Na-K-ATPase and to stimulate vascular reactivity. These changes are due to a change in the concentration of two or more substances in the plasma. Atrial natriuretic peptides do not inhibit Na-K-ATPase and they decrease vascular reactivity. The search for the Na-K-ATPase inhibitor has been hampered by the lack of specificity of most assays which demonstrate the presence of many irrelevant Na-K-ATPase inhibitors. Cytochemical bioassays, however, appear to have a certain selectivity. They disclose the presence of a Na-K-ATPase inhibitor in the plasma, the concentration of which is controlled by salt intake but the only known substance so far tested, which these bioassays will detect, is ouabain. The hypothalamus contains the highest concentration of the cytochemically bioassayable inhibitory material and its content is also controlled by salt intake. The substance responsible for the cytochemically bioassayable inhibitory activity in the plasma and the hypothalamus share the same physico-chemical properties and on extraction appear in the same fraction. It is possible therefore, that the Na-K-ATPase inhibitor which is detectable by the cytochemical assays in the plasma and hypothalamus is the same. The concentration of cytochemically bioassayable Na-K-ATPase inhibitory activity is raised in the plasma of patients with essential hypertension, the SHR rat and the Milan hypertensive rat, as is the concentration of atrial natriuretic peptide.(ABSTRACT TRUNCATED AT 250 WORDS)