Renal function curve in patients with secondary forms of hypertension.

Abstract

SUMMARY The causative mechanisms of hypertension were investigated by studying the renal function (pressure-natriuresis) curve in patients with primary aldosteronism (JI = 6) and renovascular hypertension (n = 6). Before and after radical operation (removal of adenoma in primary aldosteronism and percutaneous transluminal angioplasty in renovascular hypertension), dietary NaCl intake was altered from 10 to 13 g/day in Week 1 to 1 to 3 g/day in Week 2. Mean arterial pressure (MAP) and urinary sodium excretion were measured on the last 3 days of each week. By restricting sodium intake before operation, MAP was reduced from 122 ± 7 to 113 ± 7 mm Hg (p<0.025) in primary aldosteronism but not in renovascular hypertension (130 ± 6 to 128 ± 5 mm Hg). The renal function curve was drawn by plotting urinary sodium excretion on the ordinate and MAP on the abscissa before and after operation. The slope of the curve was analyzed between the plotted points, and each curve was extrapolated to zero sodium excretion as an estimate of the degree of shift of the curve along the MAP axis. Before, as compared with after operation, the extrapolated v-intercept of the curve was shifted rightward in both primary aldosteronism (111 ± 7 vs 87 ± 4 mm Hg; p<0.025) and renovascular hypertension (128 ± 5 vs 95 ± 2 mm Hg; p<0.025) and the slope was depressed in primary aldosteronism (16 ± 1 vs 40 ±17 [mEq/day]7mm Hg; p < 0.025) but not in renovascular hypertension (130 ± 75 vs 40 ± 13 [mEq/day]/mm Hg). After operation, the renal function curves in primary aldosteronism and renovascular hypertension were normalized. The rightward shift of the curve in renovascular hypertension probably was due to an increase in renal vascular resistance caused by the stenotic renal vascular lesion as well as to increased resistance caused by stimulation of the reninangiotensin system. The rightward shift in primary aldosteronism presumably was due to enhancement of renal tubular sodium reabsorption by aldosterone; the depressed slope likely resulted from suppression of the renin-angiotensin feedback mechanism by the excess aldosterone and resultant volume expansion. Thus, an abnormal renal function curve seems to have played a major role in the genesis of each of these forms of secondary hypertension. (Hypertension 10: 11-15, 1987) KEY WORDS • arterial pressure-natriuresis relationship hypertension • primary aldosteronism pathogenesis • renovascular B ASED on the hypothesis of Guyton and colleagues, 1 -2 the renal function curve (pressurenatriuresis relationship) must always be affected in the genesis of hypertension regardless of the factors that initiate the hypertension process (if the From the Department of Medicine, National Cardiovascular Center, Osaka, Japan.Supported by a research grant for cardiovascular diseases (59C-8) from the Ministry of Health and Welfare.Presented in part at the 1 lth Scientific Meeting of the International Society of Hypertension, Heidelberg, West Germany, 1986. Address for reprints: Dr. Genjiro Kimura, Division of Nephrol...

Role of insulin resistance in the genesis of sodium sensitivity in essential hypertension

“…1,30,32 This sodiumvolume-BP state resembles, at least in part, the profile of primary aldosteronism, 30,32 a typical sodium sensitive form of hypertension due to an enhanced rate of tubule sodium reabsorption, while is in contrast to our report on diuretics. 31 From the above discussion, it is evident that enhanced tubular sodium reabsorption, instead of augmented glomerular filtration, is the primary event causing sodium sensitive type of hypertension.…”

“…Patients whose 24-h average of mean arterial pressure was lowered by more than 10% by sodium restriction were assigned to the sodium sensitive group based on Bartter's original definition, 3,4 the remaining patients were assigned to the non-sodium sensitive group. In addition, sodium sensitivity index was calculated as the ratio of the change in mean arterial pressure over the change in urinary sodium excretion rate induced by sodium restriction, which was the reciprocal of the slope of the pressure natriuresis curve, 1,2,10,15,16,[30][31][32] and which represented how much BP was affected by each mmol of sodium intake per day altered in the steady state. 1,2 Plasma glucose and insulin response during a standard oral glucose tolerance test (OGTT) were determined in all subjects on a regular sodium diet.…”

Relative Glomerular Hyperfiltration in Primary Aldosteronism

“…Kimura et al (7,19) demonstrated that dietary sodium restriction reduced MAP of PA patients. After removal of adenoma, the slope of the renal function curve (i.e., the linear regression of urinary sodium excretion on MAP) was enhanced, and its extrapolated x-intercept was shifted leftward.…”

Effect of chronic sodium loading on cardiovascular response in young blacks and whites.

“…Guyton and coworkers 3031 proposed that the kidney functions as a blood pressure regulator by its control of salt and water excretion in both the hypertensive and normotensive state. Kimura et al 32 used this concept in describing the change in slope on a renal function curve before and after corrective surgery in patients with primary hyperaldosteronism. After corrective surgery and removal of the stimulus for volume expansion, sodium excretion increased.…”