EFFECTS OF ONE-CLIP, ONE-KIDNEY HYPERTENSION IN CHRONICALLY CATHETERIZED PREGNANT EWES

1. Hypertension secondary to renal disease was studied in non-pregnant and pregnant ewes to determine whether there were any changes in arte rial pressure and the distribution of cardiac output and, in particula r, whether uteroplacental blood flow was affected. 2. In six non-pregn ant, chronically catheterized, uninephrectomized ewes, a reduction in renal blood flow (RBF) to 40-50% of control caused hypertension within 3 h. This was maintained for as long as RBF was reduced (72 h) and re turned to control 24 h after the occluder around the renal artery was released. When this experiment was repeated in 16 uninephrectomized pr egnant ewes (118-134 days gestation) hypertension occurred within 3 h and was sustained for as long as RBF was reduced (between 24 and 72 h) . Arterial pressure returned to control within 24-72 h of restoring RB F. 3. Compared with non-pregnant ewes, pregnant ewes had similar arter ial pressures, higher cardiac outputs (CO; P < 0.001) and heart rates (HR; P < 0.001), lower total peripheral resistances (TPR; P < 0.001) a nd similar blood flows to brain, ovary, pancreas, kidney and spleen. S plenic vascular resistance (VR) was greater (P = 0.006), gut blood dow was greater (P < 0.05) and gut VR was less (P < 0.05). Myoendometrial blood flow/g was greater (P < 0.005) and myoendometrial VR was less ( P = 0.006). 4. In pregnant sheep with renal clip hypertension, there w as no change in CO and HR, but TPR increased (P < 0.01), as did plasma renin activity. Gut, brain, pancreatic and myoendometrial VR were inc reased as long as RBF was reduced; in addition, myoendometrial VR rema ined high for the rest of the experiment. Placental blood dow was unch anged at 3 h; 24-72 h later it was reduced (P < 0.05) and remained low Placental VR was increased 24-72 h after RBF was restored when ewes w ere again normotensive. 5. Thus, one-clip, one-kidney renal hypertensi on in the pregnant ewe was due to increased TPR associated with a fall in uteroplacental blood flow that persisted even when RBF was restore d and ewes were normotensive. This reduction in uteroplacental blood f low could account for the high foetal morbidity and mortality that occ urs in pregnant women with renovascular hypertension.