Evidence for an Involvement of the Renal Papilla in Hypertension

Several classic experiments support the view that the kidney exerts a nonexcretory antihypertensive function. Bilateral nephrectomy plus a sodium–volume load causes hypertension (Braun–Menendez and Von Euler, 1947; Grollman et al., 1949), while ureterovenous anastomosis (Grollman et al., 1949; Floyer, 1955; Muirhead, 1962) under similar circumstances prevents hypertension. Destruction of the renal papilla is attended by hypertension induced by sodium and volume (Muirhead et al., 1950, 1960a) on the one hand, and by aggravation of existing hypertension, on the other (Heptinstall et al., 1975). Unclipping of a one-kidney, one-clip hypertensive rat is followed by normalization of the arterial pressure within 24 hr or less (Byrom and Dodson, 1949; Floyer, 1955; Muirhead et al., 1976). Ureterovenous anastomosis plus unclipping is also attended by normalization of the arterial pressure (Floyer, 1955; Muirhead et al.., 1976), even though a longer time interval may be required. Indeed, ureterovenous anastomosis plus a saline load given intravenously (1.25-2.5% of the body weight) followed by unclipping is also attened by normalization of the arterial pressure, but additional time is needed (Muirhead and Brooks, 1980). Unclipping while an intravenous saline infusion equal to or greater than the urine loss is maintained is also attended by a normal pressure within 20 hr (Muirhead et al., 1976; Neubig and Hoobler, 1975). Thus, the recession of the arterial pressure in the ureterovenous experiment is not caused by substances entering the circulation via the ureter. Paired sham-operated controls for these manipulations had no change of the arterial pressure over the same time