Abnormality of the renin/body-fluid-volume relationship in serially-studied inbred dogs with neonatally-induced coarctation hypertension.

We have tested the steady-state predictions of the hypothesis that coarctation hypertension, if renin-mediated via total-renal underperfusion, will be characterized by a persistently abnormal renin/bodyfluid-volume relationship. In six inbred Labrador dogs with neonatally-induced thoracic aortic coarctation and in seven littermate controls, serial measurements of forelimb BP, plasma renin activity (PRA), extracellular (ECV), and plasma (PV) volumes ("Na and '"RISA spaces), and renal function (clearances of inulin and PAH) were performed during varied steady-state sodium intake over 1-12 months post-aortic-banding (PAB). In coarcted dogs, significant forelimb hypertension by indirect technique [p < 0.001) was confirmed by aorticarch pressures at 1 year PAB (182 ± 8/111 ± 8 mm Hg vs 131 ± 4/78 ± l,p < 0.001/ < 0.01). Significant increases in ECV (386 ± 4 cc/kg in coarcted, n = 80, vs 371 ± 3cc/kg in controls, n = 89,p < 0.01), in PV (49 ± 1 cc/kg, n = 76, vs 47 ± 1 cc/kg, n = 87, In controls, p < 0.025), and calculated blood volume (p < 0.025) in coarcted dogs averaged 4.1%, 4.1%, and 5.1% over littermate controls and were of similar magnitude during normal, low, and high sodium intake. Since PRA in coarcted animals was comparable to control values at each sodium intake (and thus in excess with reference to volume status), the renin/volume curve was displaced upward relative to that of normotensive controls. The maintenance of normal effective renal plasma flow and glomerular filtration rate in coarcted dogs over the first year PAB also fulfills the steady-state predictions for renin-mediated hypertension and suggests that the renal circulation is a major regulated variable in renin-angiotensin-volume homeostasls. We conclude that, during the first year PAB, neonatally-induced coarctation hypertension is characterized by an abnormal renin/volume relationship demonstrable during varied sodium intake and despite an apparently "normal" PRA. While available evidence supports the potential hypertensive impact of this quantitatively small abnormality, its renln-dependence remains to be documented. (Hypertension 2: 631-642, 1980)