Search

Eels adapted to either freshwater or seawater were used in the investigation of the effects of atrial natriuretic peptide (ANP) on drinking and the levels of angiotensin II. Results reveal that ANP decreased both drinking rate and angiotensin II levels in eels although the magnitude of reduction was greater in freshwater-adapted eels. Whether the reduction in drinking rate was secondary to ANP or the reduction in angiotensin II levels was not established.

A peptide with bradykinin (BK)-like immunoreactivity was isolated from an incubate of heat-denatured eel plasma with porcine pancreatic kallikrein. The purified peptide had the following amino acid sequence: Arg-Arg-Pro-Pro-Gly-SerTrp-Pro-Leu-Arg. This decapeptide, named eel [[Arg.sup.0]]BK, was identical to two previously identified BK homologs from cod and trout. High conservation of the BK sequence among distant teleost species suggests an important function in this vertebrate group. Bolus intra-arterial injections of eel [[Arg.sup.0]]BK, BK, and [[Arg.sup.0]]-des-[Arg.sup.9]-BK (1-10 nmol/kg) caused significant (P [is less than] 0.05) inhibition of drinking in seawater-adapted eels. The potency of the inhibition was ranked in the following order: [[Arg.sup.0]]BK [is greater than] [[Arg.sup.0]]-des-[Arg.sup.9]-BK = BK. The BK peptides also produced an immediate, transient increase followed by a sustained increase in arterial blood pressure and an initial decrease followed by an increase in heart rate. Strong tachyphylaxis occurred for the cardiovascular effect but not for the antidipsogenic effect. The order of the potency of the cardiovascular actions, [[Arg.sup.0]]BK [is greater than] BK [is greater than] [[Arg.sup.0]]-des-[Arg.sup.9]-BK, was different from that of the antidipsogenic action. Slow infusions of eel [[Arg.sup.0]]BK in the dose range 1-1,000 pmol [multiplied by] [kg.sup.-1] [multiplied by] [min.sup.-1] produced concentration-dependent inhibition of drinking without changes in arterial pressure, plasma osmolality, and hematocrit. At the infusion rate of [is greater than] 100 pmol [multiplied by] [kg.sup.-1] [multiplied by] [min.sup.-1], plasma concentrations of angiotensin II, a potent dipsogenic hormone in eels, increased, suggesting an interaction of the kallikrein-kinin and reninangiotensin systems. In mammals, BK is dipsogenic and vasodepressor, so that our data demonstrate opposite effects on fluid and cardiovascular regulation of BK in the eel and suggest a new physiological role for the kallikrein-kinin system in teleost fish. kallikrein-kinin system; renin-angiotensin system; drinking behavior; cardiovascular effects; teleost fish

Role of the renin-angiotensin system in drinking of seawater-adapted eels Anguilla japonica: a reevaluation. Am J Physiol Regulatory Integrative Comp Physiol 279: R1105-R1111, 2000.--The role of ANG II, a potent dipsogenic hormone, in copious drinking of seawater eels was examined. SQ-14225 (SQ), an angiotensin-converting enzyme inhibitor, infused intra-arterially at 0.01-1 [micro]g [multiplied by] [kg.sup.-1] [multiplied by] [min.sup.-1], depressed drinking and arterial blood pressure in a dose-dependent manner. The inhibition was accompanied by a small decrease in plasma ANG II concentration, which became significant at 1 [micro]g [multiplied by] [kg.sup.-1] [multiplied by] [min.sup.-1]. After the infusate was changed back to the vehicle, the depression of drinking and arterial pressure continued for [is greater than] 2 h, although plasma ANG II concentration rebounded above the level before SQ infusion. By contrast, infusion of anti-ANG II serum (0.01-1 [micro]g [multiplied by] [kg.sup.-l] [multiplied by] [min.sup.-1]) did not suppress drinking and arterial pressure, although plasma ANG II concentration decreased to undetectable levels. Plasma atrial natriuretic peptide and plasma osmolality. which influence drinking rate in eels, did not change during; SQ or antiserum infusions. These results suggest that the renin-angiotensin system plays only a minor role in the, vigorous drinking observed in seawater eels. The results also suggest that the antidipsogenic and vasodepressor effects of SQ in seawater eels are not due solely to the inhibition of ANG II formation in plasma. converting enzyme inhibition by SQ-14225; immunoneutralization of angiotensin II; water intake; blood pressure; atrial natriuretic peptide

Presents information on a study which evaluated the role of endogenous renin-angiotensin system in copius drinking of seawater eels. Methodology; Effects of SQ-14225 and an anti-ANG II serum on drinking, plasma ANG II hormone, and blood pressure; Role of ANG II hormone in drinking of seawater fish.

Background/Aims: Lipocalin-type prostaglandin D synthase (L-PGDS), an enzyme converting prostaglandin H[sub 2] to prostaglandin D[sub 2] , occurs particularly in the cardiovascular system. Urinary L-PGDS excretion is increased in diabetes prior to overt proteinuria, suggesting that it is a predictor of renal injury. In this study, we tested the hypothesis that L-PGDS excretion reflects renal injury in primary glomerular diseases using Adriamycin-induced nephropathy in mice. Methods: Twenty 6-week-old ICR female mice were intravenously given a dose of 25 mg Adriamycin/kg body weight through the tail vein. 24-hour urine was collected every day, and blood samples were obtained. Results: The mice developed significant albuminuria from day 3 onward (p < 0.05), which was followed by overt proteinuria from day 4 (p < 0.05). Histological examination revealed focal mesangial expansion with partial tubular atrophy. Urinary L-PGDS excretion significantly increased from day 1 onward (p < 0.05), and apparently preceded the increase in urinary albumin excretions. Either serum L-PGDS or creatinine levels were not changed by administration of Adriamycin. However, serum creatinine levels were inversely correlated to urinary L-PGDS excretions (r = –0.88, p < 0.05). Immunohistochemistry showed that L-PGDS occurred in the tubules, but not in the glomeruli in Adriamycin mice and L-PGDS mRNA paralleled urinary L-PGDS excretion. Conclusion: Urinary L-PGDS excretion is increased in Adriamycin-induced nephropathy, and this precedes overt albuminuria. Copyright © 2004 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]