Atrial natriuretic factor in mild to moderate chronic renal failure.

Abstract

SUMMARYThe relationship between kidney function and plasma immunoreactive atrial natriuretic factor (irANF) levels as well as the effects of synthetic human ANF-(99-126) were investigated in 13 patients with mild to moderate chronic renal failure. Under basal conditions, glomerular filtration rate averaged 39 ± 5 (SEM) ml/min/1.73 m 2 and blood pressure (BP) averaged 166/107 ± 7/2 mm Hg; 12 patients were hypertensive. Plasma irANF levels were significantly increased (98 ± 16 vs 42 ± 4 pg/ml in healthy control subjects; p< 0.001) and correlated (p< 0.05-0.005) inversely with hematocrit (r = -0.65) and positively with systolic BP (r = 0.75) or fractional sodium excretion (r = 0.75). Human ANF-(99-126) infusion for 45 minutes at 0.034 /ig/kg/min augmented (p< 0.05-0.01) diuresis and urinary sodium, chloride, calcium, phosphate, and magnesium excretion. During the subsequent 45 minutes of human ANF-(99-126) infusion at a rate of 0.077 /i.g/kg/min, diuresis and electrolyte excretion remained elevated (p<0.05-0.01). Glomerular filtration rate and effective renal plasma flow were not significantly modified, but filtration fraction rose progressively (p<0.01). Human ANF-(99-126) infusion decreased BP (p<0.05-0.01), produced bemoconcentration (hematocrit + 7%; p<0.01) without negative body fluid balance, and increased (p<0.01-0.001) plasma norepinephrine, insulin, and serum free fatty acids; plasma aldosterone and renin activity were unaltered during but rose after cessation of human ANF-(99-126) infusion. These findings indicate that circulating irANF increases in hypertensive patients with mild to moderate chronic renal failure and may support the homeostasis of sodium balance. Infused human ANF-(99-126) can acutely produce hemoconcentration, lower BP, induce sympathetic activation, stimulate plasma insulin, and augment the excretory function at least in part through tubular mechanisms. (Hypertension 11: 483-490, 1988)

Hypertensive Dysregulation and Its Modification by Calcium Channel Blockade in Nonoliguric Renal Failure

“…Regardless of the presence or absence of hypertension, the fractional excretion of so dium per functioning nephron rises progressively with decreasing glomerular filtration rate, thereby helping to avoid overhydration until oliguria occurs. The ANP sys tem may mediate this compensatory adaptation [30]. Circulating ANP levels were elevated in the present and previously studied patients with mild to marked chronic renal failure and shown [30] to correlate positively with fractional sodium excretion (r = +0.75; p < 0.005).…”

“…The ANP sys tem may mediate this compensatory adaptation [30]. Circulating ANP levels were elevated in the present and previously studied patients with mild to marked chronic renal failure and shown [30] to correlate positively with fractional sodium excretion (r = +0.75; p < 0.005). Moreover, the present findings demonstrate that the physiological response of plasma ANP to changes in pos ture or acute rises in arterial BP [31] remains intact in nonoliguric renal impairment.…”

Role of Atrial Natriuretic Peptide in the Control of Sodium Balance in Chronic Renal Failure

“…Reports by others [54,[61][62][63] showed that infusion of exogenous ANP in patients with chronic renal failure to provide plasma levels within the pathophysiological range was diuretic and natriuretic, thus confirming that the uremic nephron is highly responsive to circulating ANP.…”

Relationship between Renal Mass and Atrial Natriuretic Peptide Release

“…The latter is responsible for the increase in fractional sodium excretion [9-11. 13]It has been shown that serum ANP is in creased in chronic renal failure [14][15][16][17][18][19][20][21]. More over, a further rise occurs upon augmentation of extracellular volume in patients or experi mental animals with chronic renal failure [19.…”