Increased renin reactivity of plasma, suggesting an excess of circulating accelerators and/or deficit of inhibitors of the renin reaction, has been reported in a number of hypertensive states; however, its contribution to genesis and/or maintenance of hypertension is unknown. To longitudinally assess the evolution of plasma renin reactivity in relation to blood pressure in neonatally-induced coarctation hypertension, we have made serial observations in 6 coarcted dogs and in 7 littermate controls over 1-12 months post-aortic-banding during varied steady-state sodium intake. Measurements of renin reactivity (defined as the increment in angiotensin I-generation rate following addition of exogenous renin to plasma), renin substrate concentration (RS), and plasma renin activity (PRA), together with calculation of plasma renin concentration (PRC) (as PRC = PRA % renin reactivity) provided estimates of the three major determinants of PRA. RS values were adjusted for variability due to assay-control and to age via covariate analysis. Results indicate no difference in adjusted RS between coarcted and control dogs, thus obviating the influence of RS differences on renin reactivity results. Renin reactivity and PRC in coarcted dogs were also comparable to control values. Furthermore, responses of RS, renin reactivity and PRC to dietary sodium manipulation were similar in coarcted and control animals. We conclude that circulating modifiers of the renin reaction play no role in the genesis or in the first-year maintenance of neonatally-induced coarctation hypertension.
ASJC Scopus subject areas
- Internal Medicine