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

Abstract

SUMMARY In canine neonatally-induced coarctation hypertension, we reported abnormally elevated plasma renin activity (PRA) during sodium restriction in 2-year-old dogs, but found normal PRA responses to sodium restriction ± furosemide in coarcted dogs studied serially over the first year post aortic banding (PAB). To resolve this apparent discrepancy in PRA response, longitudinal studies were extended to 2 years PAB. In two separately-studied groups, each with three coarcted and three littermate controls, measurements of indirect forelimb blood pressure (BP) at 15 to 18 months, direct brachial arterial BP at 24 months, and serial measurement of PRA and extracellular volume (ECV, as 24 Na space) were made over a 15-to 24-month age range during three sodium-volume levels: ad libitum sodium intake (NS), low-sodium diet alone (LS), and low-sodium plus Lasix (LS/Lasix). While PRA in coarcted dogs of both groups was comparable to controls at NS and LS, PRA in Group 1 coarcted dogs significantly exceeded that of littermates during LS/Lasix in both 18-and 24-month studies. In contrast, PRA in Group 2 coarcted dogs was not hyperresponsive to LS/Lasix as compared to simultaneously-studied littermates. The hyperresponsive PRA in Group 1 coarcted dogs could not be attributed to larger absolute or relative ECV deficits. Overall, ECV in coarcted dogs of each group was higher on the average but was not statistically different from controls. Results indicate that the hyperresponsive PRA in this canine model is: 1) a variable feature, developing secondarily in the late established phase; 2) reproducible for a given animal; and 3) not attributed to exaggerated ECV deficits during the LS/Lasix protocol. (Hypertension 5: 328-335, 1983) KEY WORDS • extracellular volume • inbred dogs • littermate control T HE genesis and maintenance of hypertension in thoracic aortic coarctation requires the presence of a kidney located distal to the vascular stenosis.'" 4 Evidence supporting specific participation of the renin-angiotensin system is less definitive. In clinical coarctation hypertension, plasma renin activity (PRA) is consistently normal during unrestricted sodium intake 5 " 8 but, in some patients, may show an exag-

Chronic MK421 fails to modify evolution of hypertension in neonatally coarcted pups.

“…Our prior studies, using sodium-24 space of distribution, documented small but statistically significant and physiologically relevant extracellular fluid volume excess in coarcted dogs in a larger series spanning 2-12 months after banding 6 ; similar trends (not always significant) were apparent in smaller series in older dogs. 38 The present results using [ Early theories of coarctation hypertension included the view that the mechanical resistance of the stenotic site contributed significantly to the increased vascular resistance. 41 This concept was inappropriately discarded on the basis of results of infrarenal coarctation; thus, the absence of proximal hypertension after infrarenal aortic stenosis was seen as excluding a role for the stenotic resistance factor.…”