Effects of synthetic atrial natriuretic factor on renal function and renin release

Abstract

Studies were performed in anesthetized dogs (n = 5) to determine the effects of synthetic atrial natriuretic factor on renal function and renin release. Intrarenal infusion of synthetic atrial natriuretic factor (ANF) (0.3 microgram X kg-1 X min-1) resulted in a transient increase in renal blood flow (126 +/- 8 to 148 +/- 11 ml/min). The duration of this transient vasodilation was 3.1 +/- 0.4 min. Continued infusion was followed by a slight decrease in renal blood flow (126 +/- 8 to 117 +/- 8 ml/min) and an increase in glomerular filtration rate (23.1 +/- 3.5 to 30.7 +/- 1.9 ml/min), with filtration fraction thus being increased (0.19 +/- 0.04 to 0.27 +/- 0.03). These hemodynamic alterations were associated with increases in fractional sodium excretion (0.6 +/- 0.2 to 5.8 +/- 0.8%), fractional potassium excretion (30.8 +/- 9.4 to 56.3 +/- 7.4%), fractional lithium excretion (32.2 +/- 7.1 to 60.3 +/- 5.7%), and fractional phosphate excretion (8.7 +/- 3.5 to 41.6 +/- 11.7%). Intrarenal infusion of synthetic ANF markedly suppressed renin secretion rate (295.5 +/- 84.6 to 17.2 +/- 10.6 ng/min) despite a slight reduction in arterial pressure (123 +/- 9 to 118 +/- 9 mmHg). Our studies demonstrate that synthetic ANF results in a marked natriuretic response that is in part mediated by an increase in glomerular filtration rate. The increase in fractional lithium and phosphate excretion suggests that this factor may also have an action on proximal tubule reabsorption. Further, these studies demonstrate that synthetic ANF markedly inhibits renin secretion.

Neutral Endopeptidase Inhibition Potentiates the Effects of Natriuretic Peptides in Renin Transgenic Rats.

“…CNP, given to anesthetized dogs had greater hemodynamic activity than ANP, but it was not natriuretic even when administered directly into the renal artery (46,48) . The observation of no change in sodium excretion is unique to this peptide when compared with ANP or BNP, which in previous studies produced marked natriuresis despite similar systemic hemodynamic changes (49). This is consistent with the report of Currie et al (49), who suggested that the renal hemodynamic and natriuretic actions of ANP are affected by the COON-terminal part of the peptide, which is absent in CNP.…”

“…The observation of no change in sodium excretion is unique to this peptide when compared with ANP or BNP, which in previous studies produced marked natriuresis despite similar systemic hemodynamic changes (49). This is consistent with the report of Currie et al (49), who suggested that the renal hemodynamic and natriuretic actions of ANP are affected by the COON-terminal part of the peptide, which is absent in CNP. In contrast, in the presence of NEP inhibition, CNP has a natriuretic action in dogs, which is due to inhibition of distal sodium reabsorption without increasing urinary cGMP excretion (50).…”

Distribution of atrial natriuretic factor receptors in dog kidney fractions

“…The mode of action of ANF on kidney function is still debated [7]. The hormone appears to enhance directly the glomerular filtration rate and both sodium and water filtration fractions [ 15,161. An inhibitory effect on tubular reabsorption has also been proposed [ 16,171. Specific high-affinity receptor sites have been documented in aorta [18], adrenal cortex [19], posterior lobe of the pituitary gland [14] and in kidney cortex [ 181.…”

The effects of atrial natriuretic peptide on renal function and the renin-aldosterone system in anesthetized rabbits.

“…Burnett et al 1984Burnett et al , 1986Maack et al 1984; Wakitani et al 1985; Kleinert et al 1986). But the mechanism by which atrial extract or atrial natriuretic peptide produces a natriuresis and diuresis is still unclear.…”