Osmotic and volaemic regulation of atrial and ventricular natriuretic peptide secretion in conscious eels

The effects of acute manipulation of plasma osmolality and blood volume on plasma atrial and ventricular natriuretic peptide (ANP and VNP) levels were examined in conscious freshwater eels, Anguilla japonica. A bolus injection of hypertonic NaCl (0·85 m and 1·7 m, 2·5 ml/kg body weight) through a catheter into the ventral aorta produced increases in plasma Na concentration and osmolality with parallel concentration-dependent, transient increases in plasma ANP and VNP levels. Plasma ANP and VNP levels also increased after injection of 1·7 m mannitol solution which produced an increase in plasma osmolality but a decrease in plasma Na concentration. However, injection of a 2·0 m solution of urea, which does not cause cellular dehydration in mammals, produced only small increases in plasma ANP and VNP levels, although plasma osmolality increased. A bolus injection of 10 or 25 ml/kg isotonic saline supplemented with 2% dextran for colloidal osmotic pressure, which theoretically increased blood volume by 29% or 71%, produced volume-dependent, transient increases in plasma ANP and VNP levels without changes in plasma Na concentration and osmolality. Similar volume expansion with dialysed eel plasma caused greater increases than with dextran-saline. However, these increases were much smaller than those after osmotic stimuli. These results indicate that secretion of ANP and VNP is regulated by two receptor mechanisms: osmoreceptors activated by cellular dehydration, not specifically by hypernatraemia, and volume or stretch receptors activated by hypervolaemia. The relative importance of the osmoreceptive mechanism is greater in eels than in mammals where volaemic regulation dominates over osmotic regulation for ANP secretion. Journal of Endocrinology (1996) 149, 441–447

Eel ventricular natriuretic peptide: isolation of a low molecular size form and characterization of plasma form by homologous radioimmunoassay

Ventricular natriuretic peptide (VNP) with 25 amino acid residues was isolated from the low molecular weight fraction of acid extracts of eel cardiac ventricles. No other short forms of VNP were recovered from the fraction. This peptide was named eel VNP(1–25) because it was a C-terminally truncated form of the previously isolated eel VNP(1–36) As observed before with eel VNP(1–36), eel VNP(1–25) had a much higher (146-fold) vasodepressor activity than human atrial natriuretic peptide (ANP) in eels, but was a third to a half as active in rats with respect to vasodepressor and natriuretic activities. Eel VNP(1–25) was generally less potent than eel VNP(1–36) for vasodepressor and natriuretic effects. A specific radioimmunoassay (RIA) has been developed for the measurement of eel VNP. The antiserum, raised against eel VNP(1–36), was highly specific and did not exhibit significant cross-reactivity with eel ANP and C-type natriuretic peptide, even though their amino acid sequences have more than 60% homology with that of eel VNP. The sensitivity of assay was 0·5 fmol/tube for eel VNP(1–36) with more than 99% confidence. Such high sensitivity permitted direct assaying of VNP with only a few microlitres of plasma. In fresh water eels, the concentration of VNP in the cardiac ventricle was higher than those in the atrium or brain and that of ANP in the ventricle. Thus, VNP seems to be a ventricular hormone. Although ANP is a major circulating hormone in mammals, the plasma concentration of VNP was threefold higher than that of ANP. The RIA coupled with gel-permeation chromatography revealed that a 14 kDa form, probably proVNP, and smaller forms (3–6 kDa) circulate in eel plasma. Reversephase high performance liquid chromatography identified both VNP(1–36) and VNP(1–25) in eel plasma; VNP(1–36) appeared to be a major form. Journal of Endocrinology (1994) 141, 81–89