Lucas, C. P.; Holzwarth, G.; Ocobock, R.; Sözen, T.; Stern, M.; Wood, P.; Haskell, W.; Farquhar, J.
January 1975
Angiology;Jan1975 Part 1, Vol. 26 Issue 1, p31
Academic Journal
Plasma renin activity (PRA), plasma renin reactivity (PRR) and plasma renin concentration (PRO were measured in 47 normotensive and 4 hypertensive subjects, none of whom were taking medication. There was a significant negative correlation between PRC and PRR of plasma. Contrary to previous reports, PRR was not increased in subjects with hypertension. The most significant finding was the negative correlation of PRC and PRA with blood pressure in normotensive subjects, but the lack of such a correlation in hypertensive subjects. This finding, plus the significantly higher PRC in hypertensive subjects, suggests a deficient suppression of renin release in hypertensive individuals. The renin-renin substrate reaction, as it occurs in the plasma, is illustrated below (Fig. 1). Renin, a proteolytic enzyme, released from the juxtaglomerular cells of the kidney, acts upon its α2 globulin tetradecapeptide renin substrate, splitting the leucyl-leucine bond, thus causing the release of angiotensin I (AI). AI, a decapeptide, is substrate for yet another enzymatic reaction, being converted in turn to angiotensin II (All), by the converting enzymes present in lung and plasma. This reaction sequence is undoubtedly oversimplified since it does not take into account a number of observations, the first of which was made in 1964 by Boucher and co-workers; namely that when equal amounts of purified renin were added in vitro to the plasma of different individuals, there were significant variations in the quantity of angiotensin generated.1 From this, as well as from later studies, the concept developed that plasma contained a renin inhibitor.2 These earlier observations were supported and extended by studies from Laragh's group, which reported that the plasma of patients on oral contraceptives produced exaggerated amounts of AI upon the addition of exogenous renin3,4, and these authors have referred to this phenomenon as the renin reactivity of plasma. Increased renin reactivity has since been reported in plasma of patients with essential hypertension,5,6,7 primary aldosteronism8 and renovascular hypertension.9 Thus, it has been thought that this phenomenon may play a role in the hypertensive process. If reactivity of plasma is increased in the above named situations (i.e., if there is exaggerated generation of AI upon the addition of purified renin). then it follows that in vivo AI generation or AI generation on incubation of plasma at 37° should also be increased relative to the amount of endogenous renin present. Thus the ratio of plasma renin activity (PRA) to plasma renin concentration (PRC) should be greater in women on oral contraceptives,9,10 as well as in people with the several varieties of hypertension mentioned above. The present report concerns itself, in part, with the measurement of the PRA: PRC ratio (which we use to express the reactivity of plasma) in normal and hypertensive subjects, as well as in subjects taking either estrogen-containing compounds or various antihypertensive medications. Our results confirm the observation that considerable variation in plasma reactivity does exist, and that there is increased reactivity in plasma of women on oral contraceptives or estrogen-containing compounds. Unexpected was the discovery that reactivity is inversely related to the concentration of renin. Our studies, however, failed to find increased reactivity in subjects with hypertension, and thus do not support the concept of an important role for a renin inhibitor or modifier in essential hypertension. Most important, however, was our discovery of a highly significant inverse correlation of both PRA and PRC with blood pressure in normal people. The lack of such a correlation, as well as the finding of elevated PRC in subjects with hypertension, suggests that the person with elevated blood pressure lacks the normal capacity to diminish renin secretion.


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