The study identifies multiple forms of human plasma renin substrate in states of steroid excess and certain hypertensive diseases, which may account for altered renin reaction kinetics in these conditions.
Answers are grounded in this paper and cite their sources.
May explain discrepant renin kinetics in steroid excess or uremia; leaves open clinical assay impact and needs prospective validation.
The objective of this investigation was to determine whether heterogeneity of plasma renin substrate could be observed in states of steroid excess and various forms of hypertensive disease. In states of stimulated renin substrate production by estrogens or glucocorticoids, multiple forms of renin substrate were apparent when stimulation was excessive. Stimulation of substrate production caused by uremia associated with hypertension showed similar results. None, or only trace quantities of the additional forms of renin substrate were evident in subjects with normal or suppressed levels of plasma renin substrate. The additional forms of renin substrate could be distinguished from the normal form on the basis of cross-reactivity with a specific antiserum to the normal form, electrophoretic mobility, and kinetic rate constants. Differences in rate constants of the various forms of plasma renin substrate may account for the altered rate of the renin reaction associated with several states of hypertension. In plasma of patients with renovascular hypertension, significant quantities of a protein which cross-reacted with the antiserum but could not generate angiotensin I were observed.
No takes yet. Share an insight, caveat, or question.
Eggena et al. (1978) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: