Acute responses to arterial pressure and plasma renin activity to converting enzyme inhibition (SQ 20,881) in serially studied dogs with neonatally-induced coarctation hypertension.

Abstract

propriately "normal" (i.e., nonsuppressed) plasma renin activity (PRA) and normal renal function. 1 The abnormal renin/volume relationship in coarcted dogs is demonstrable at normal, low, and high steady-state sodium intakes.3 These observations are compatible with the hypothesis that coarctation hypertension is a renin-mediated process, initiated by balanced underperfusion of total renal mass via transient reninangiotensin excess, the latter generating volume expansion sufficient to normalize renal perfusion and thus PRA at a new steady state. 1To further assess the role of the renin-angiotensin system in coarctation hypertension, we serially examined acute arterial pressure and PRA responses to converting-enzyme inhibitor (CEI; SQ 20,881) in the same dogs during normal and low sodium intake. Concurrent study of littermate controls permitted quantitative analysis of normal CEI responses and comparision with results in coarcted dogs.

Canine neonatally induced coarctation hypertension in the second year. Variably hyperresponsive plasma renin activity.

“…Group 1 dogs were also included in 0-to 1-year studies reported previously. 16 " 18 Group 2 dogs, born in late 1978, contained three coarcted and three littermate control dogs drawn from two litters; Group 2 studies reported here were carried out in 1980. The technique of neonatal aortic banding and the littermate-control experimental design have been previously described.…”