TY - JOUR
T1 - In vitro determinants of plasma renin activity in serially-studied inbred dogs with neonatally induced coarctation hypertension
T2 - Renin reactivity, renin substrate, and renin concentration
AU - Bagby, Susan P.
AU - Mcdonald, Walter J.
AU - Gray, Daniel K.
N1 - Funding Information:
Supported by funds from: Medical Research Foundation of Oregon, NIH HL 19825, VA Career Development Program
PY - 1981
Y1 - 1981
N2 - 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.
AB - 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.
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U2 - 10.3109/10641968109033676
DO - 10.3109/10641968109033676
M3 - Article
C2 - 7018860
AN - SCOPUS:0019870190
SN - 1064-1963
VL - 3
SP - 455
EP - 475
JO - Clinical and Experimental Hypertension
JF - Clinical and Experimental Hypertension
IS - 3
ER -