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

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Abstract
Coarctation hypertension, if renin-mediated via total-renal underperfusion may be characterized by a persistently abnormal renin/body-fluid-volume relationship. In 6 inbred Labrador dogs with neonatally-induced thoracic aortic coaractation and in 7 littermate controls, serial measurements of forelimb BP, plasma renin activity (PRA), extracellular (ECV) and plasma (PV) volumes (24Na and 131RISA [radioiodinated serum albumin] spaces) and renal function (clearances of inulin and paraminohippurate) were performed during varied steady-state Na intake over 1-12 mo. post-aortic-banding (PAB). In coarcted dogs, significant forelimb hypertension by indirect technique (P < 0.001) was confirmed by aortic-arch pressures at 1 yr PAB (182 .+-. 8/111 .+-. 8 mm Hg vs. 131 .+-. 4/78 .+-. 2, P < 0.001 per < 0.01). Significant increases in ECV (386 .+-. 4 cm3/kg in coarcted, n = 80, vs. 371 .+-. cm3/kg in controls, n = 89, P < 0.01) in PV (49 .+-. 1 cm3/kg, n = 76, vs. 47 .+-. 1 cm3/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 Na intake. Since PRA in coarcted animals was comparable to control values at each Na intake (and 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 1st year PAB fulfills the steady-state predictions for renin-mediated hypertension and suggests that the renal circulation is a major regulated variable in renin-angiotensin-volume homeostasis. During the 1st yr PAB, neonatally-induced coarctation hypertension is characterized by an abnormal renin/volume relationship demonstrable during varied Na intake and despite an apparently normal PRA. Available evidence supports the potential hypertensive impact of this quantitatively small abnormality but its renin-dependence remains to be documented.