Assessment of atrial natriuretic peptide resistance in cirrhosis with head-out water immersion and atrial natriuretic peptide infusion

1993 ◽  
Vol 71 (2) ◽  
pp. 157-164 ◽  
Author(s):  
Louis Legault ◽  
Leonard C. Warner ◽  
Wai Ming Leung ◽  
Alexander G. Logan ◽  
Laurence M. Blendis ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Collecting Duct ◽  
Water Immersion ◽  
Plasma Renin ◽  
Sodium Balance ◽  
Plasma Sodium ◽  
Sodium Retention ◽  
Serum Aldosterone ◽  
Atrial Natriuretic

The nature of sodium retention in cirrhosis complicated by ascites has been studied for the last 30 years. Resistance to the natriuretic action of atrial natriuretic peptide (ANP) may play a potential role in this sodium retention. To further evaluate this possibility, we studied 12 patients with biopsy-proven cirrhosis and ascites on 2 consecutive days after a 7-day period off diuretics while receiving a 20 mmol/day sodium restricted diet. Following a crossover design, patients underwent head-out water immersion (HWI) for 3 h and were infused with a α-human ANP for 2 h on 2 consecutive days. Blood and urine samples were collected hourly. Five patients displayed a natriuretic response to HWI, sufficient to achieve negative sodium balance, and these patients were termed responders. Each of these five patients also displayed a natriuretic response to ANP infusion. In contrast, the other seven patients (nonresponders) consistently failed to develop a natriuretic response to either maneuver. The two groups had similar elevations in plasma ANP concentrations, but at baseline differed in terms of plasma sodium, plasma renin activity, and serum aldosterone. Despite higher serum aldosterone concentrations, nonresponders excreted less potassium than responders during the peak effect of the interventions, suggesting greater sodium delivery to the aldosterone-sensitive nephron segment in responders. We conclude that the inability to mount an adequate sodium excretory response to HWI in patients with cirrhosis may be conveyed through increased antinatriuretic factors that decrease the sodium delivery to the medullary collecting duct and inhibit the natriuretic effect of ANP at that site.Key words: atrial natriuretic peptide, cirrhosis, ascites, sodium.

Natriuresis induced by mild hypernatremia in humans

2002 ◽  
Vol 282 (6) ◽  
pp. R1754-R1761 ◽  
Author(s):  
Lars Juel Andersen ◽  
Jens Lundbæk Andersen ◽  
Bettina Pump ◽  
Peter Bie
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Sodium Excretion ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Sodium Concentration ◽  
Plasma Sodium ◽  
Renal Sodium Excretion ◽  
Body Fluid Volume ◽  
Atrial Natriuretic

The hypothesis that increases in plasma sodium induce natriuresis independently of changes in body fluid volume was tested in six slightly dehydrated seated subjects on controlled sodium intake (150 mmol/day). NaCl (3.85 mmol/kg) was infused intravenously over 90 min as isotonic (Iso) or as hypertonic saline (Hyper, 855 mmol/l). After Hyper, plasma sodium increased by 3% (142.0 ± 0.6 to 146.2 ± 0.5 mmol/l). During Iso a small decrease occurred (142.3 ± 0.6 to 140.3 ± 0.7 mmol/l). Iso increased estimates of plasma volume significantly more than Hyper. However, renal sodium excretion increased significantly more with Hyper (291 ± 25 vs. 199 ± 24 μmol/min). This excess was not mediated by arterial pressure, which actually decreased slightly. Creatinine clearance did not change measurably. Plasma renin activity, ANG II, and aldosterone decreased very similarly in Iso and Hyper. Plasma atrial natriuretic peptide remained unchanged, whereas plasma vasopressin increased with Hyper (1.4 ± 0.4 to 3.1 ± 0.5 pg/ml) and decreased (1.3 ± 0.4 to 0.6 ± 0.1 pg/ml) after Iso. In conclusion, the natriuretic response to Hyper was 50% larger than to Iso, indicating that renal sodium excretion may be determined partly by plasma sodium concentration. The mechanism is uncertain but appears independent of changes in blood pressure, glomerular filtration rate, the renin system, and atrial natriuretic peptide.

Elevated levels of atrial natriuretic peptide during aldosterone escape

1987 ◽  
Vol 252 (5) ◽  
pp. R878-R882 ◽  
Author(s):  
J. P. Granger ◽  
J. C. Burnett ◽  
J. C. Romero ◽  
T. J. Opgenorth ◽  
J. Salazar ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Plasma Levels ◽  
Sodium Intake ◽  
Extracellular Fluid ◽  
Plasma Renin ◽  
Sodium Balance ◽  
Compensatory Mechanisms ◽  
Peak Value ◽  
Atrial Natriuretic

Escape from the sodium-retaining effects of aldosterone (ALDO) is thought to occur as a result of natriuretic compensatory mechanisms triggered by extracellular fluid volume expansion. The purpose of the present study was to determine whether increases in plasma levels of atrial natriuretic peptide occur during ALDO escape in conscious dogs (n = 6) maintained on a fixed sodium intake (60 meq/day). Infusion of ALDO at a rate of 15 micrograms X kg-1 X day-1 for 6 days decreased sodium excretion (UNaV) from 59.1 +/- 4.0 to 36.2 +/- 5.7 meq/day on day 1, and then UNaV gradually returned to control levels by day 5 of ALDO infusion. Net cumulative sodium balance progressively increased during ALDO infusion, reaching a peak value of 88.8 +/- 21.3 meq/day on day 5. Mean arterial pressure increased from 85 +/- 3 to 95 +/- 4 mmHg, and plasma renin activity decreased from 1.32 +/- 0.27 to 0.32 +/- 0.07 ng angiotensin (ANG) I X ml-1 X h-1 during ALDO infusion. Plasma levels of atrial natriuretic peptide averaged 67.5 +/- 8.9 pg/ml during control and increased to a peak value of 120 +/- 18 pg/ml by day 4 of ALDO infusion. Three to four days after ALDO infusion was stopped, plasma levels of atrial natriuretic peptide averaged 46 +/- 5 and 50 +/- 6 pg/ml, respectively. In summary, escape from the sodium-retaining effects of ALDO is associated with significant increases in the circulatory levels of atrial natriuretic peptide.

scholarly journals The role of atrial natriuretic peptide in the development of arterial hypertension in patients with hypothalamic puberty syndrome

1997 ◽  
Vol 43 (4) ◽  
pp. 21-22
Author(s):  
T. P. Krivchenko ◽  
N. I. Verbovaya
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Arterial Hypertension ◽  
Natriuretic Peptide ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Functional Relationships ◽  
Hypothalamic Syndrome ◽  
Serum Aldosterone ◽  
Atrial Natriuretic

Fifty-two youths with the hypothalamic syndrome of puberty and 13 normal subjects aged 13 to 24 were examined in order to elucidate the contribution of the depressor system factor atrial natriuretic peptide (ANP) to the development of arterial hypertension in such patients. The disease standing was 2 to 11 years. Plasma ANP, plasma renin activity, and serum aldosterone were radioimmunoassayed. The level of ANP was reliably decreased in patients with borderline arterial hypertension and directly correlated with changes of the renin-aldosterone system. This permitted a conclusion on the insufficient role of the depressor system in patients with the pubertal hypothalamic syndrome and contribution of ANP to the development of arterial hypertension and of disorders in the functional relationships between the renin-aldosterone system and ANP.

Role of insulin and atrial natriuretic peptide in sodium retention in insulin-treated IDDM patients during isotonic volume expansion

Diabetes ◽  
1990 ◽  
Vol 39 (3) ◽  
pp. 289-298 ◽  
Author(s):  
R. Trevisan ◽  
P. Fioretto ◽  
A. Semplicini ◽  
G. Opocher ◽  
F. Mantero ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Volume Expansion ◽  
Sodium Retention ◽  
Atrial Natriuretic

Effects of homologous atrial natriuretic peptide on drinking and plasma ANG II level in eels

1998 ◽  
Vol 275 (5) ◽  
pp. R1605-R1610 ◽  
Author(s):  
Takamasa Tsuchida ◽  
Yoshio Takei
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Direct Action ◽  
Sodium Concentration ◽  
Saline Infusion ◽  
Plasma Sodium ◽  
Ang Ii ◽  
Drinking Rate ◽  
Plasma Sodium Concentration ◽  
Atrial Natriuretic

The effects of eel atrial natriuretic peptide (ANP) on drinking were investigated in eels adapted to freshwater (FW) or seawater (SW) or in FW eels whose drinking was stimulated by a 2-ml hemorrhage. An intra-arterial infusion of ANP (0.3–3.0 pmol ⋅ kg−1 ⋅ min−1), which increased plasma ANP level 1.5- to 20-fold, inhibited drinking dose dependently in all groups of eels. The drinking rate recovered to the level before ANP infusion within 2 h after infusate was replaced by saline. The inhibition at 3.0 pmol ⋅ kg−1 ⋅ min−1was profound in FW eels and hemorrhaged FW eels, whereas significant drinking still remained after inhibition in SW eels. Plasma ANG II concentration also decreased dose dependently during ANP infusion and recovered to the initial level after saline infusion in all groups of eels. The decrease at 3.0 pmol ⋅ kg−1 ⋅ min−1was large in FW eels and hemorrhaged FW eels compared with that of SW eels. Thus the changes in drinking rate and plasma ANG II level were parallel during ANP infusion. Plasma sodium concentration and osmolality decreased during ANP infusion in SW and FW eels, and they were restored after saline infusion. In hemorrhaged FW eels, however, ANP infusion did not alter plasma sodium concentration and osmolality. Hematocrit did not change during ANP infusion in any group of eels. Collectively, ANP infusion at physiological doses decreased drinking rate and plasma ANG II concentration in parallel in both FW and SW eels. It remains undetermined whether the inhibition of drinking is caused by direct action of ANP or through inhibition of ANG II, which is known as a potent dipsogen in all vertebrate species, including eels.

Effects of Physiological Increments in Human α-Atrial Natriuretic Peptide and Human Brain Natriuretic Peptide in Normal Male Subjects

1994 ◽  
Vol 86 (6) ◽  
pp. 723-730 ◽  
Author(s):  
B. M. Y. Cheung ◽  
J. E. C. Dickerson ◽  
M. J. Ashby ◽  
M. J. Brown ◽  
J. Brown
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Human Brain ◽  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Physiological Role ◽  
Sodium Balance ◽  
Urinary Flow ◽  
Male Subjects ◽  
The Brain ◽  
Atrial Natriuretic

1. Brain natriuretic peptide, closely related to atrial natriuretic peptide in structure, may be an important circulating hormone. Its physiological role is unclear. First, we studied the effects of incremental infusions of brain natriuretic peptide in six healthy men on plasma brain natriuretic peptide levels and the pharmacokinetics of brain natriuretic peptide. Synthetic human brain natriuretic peptide-32 was infused intravenously, at an initial rate of 0.4 pmol min−1 kg−1, doubling every 15 min until the dose rate reached 6.4 pmol min−1 kg−1, at which rate the infusion was maintained for 30 min. 2. The brain natriuretic peptide infusion raised the brain natriuretic peptide-like immunoreactivity from 1.4 ± 0.5 pmol/l to 21.4 ± 7.6 pmol/l. Brain natriuretic peptide-like immunoreactivity after the end of infusion was consistent with a bi-exponential decay, with half-lives of 2.1 min and 37 min. 3. Next, we studied the effects of low-dose infusion of brain natriuretic peptide to mimic physiological increments in the circulating levels in comparison with atrial natriuretic peptide. Six dehydrated male subjects received intravenous infusions of atrial natriuretic peptide and brain natriuretic peptide, separately and in combination, in a randomized double-blind, placebo-controlled, four-part cross-over design. Atrial natriuretic peptide and brain natriuretic peptide were given at the rate of 0.75 and 0.4 pmol min−1 kg−1, respectively, for 3 h. The control infusion consisted of the vehicle. 4. Analysis of variance showed that atrial natriuretic peptide and atrial natriuretic peptide plus brain natriuretic peptide, but not brain natriuretic peptide alone, increased urinary flow and decreased urinary osmolality significantly. However, urinary sodium excretion was significantly increased by atrial natriuretic peptide, brain natriuretic peptide and atrial natriuretic peptide plus brain natriuretic peptide. 5. None of the four infusates significantly altered the blood pressure, heart rate or glomerular filtration rate. 6. This study showed, for the first time, that physiological increments in brain natriuretic peptide, like those in atrial natriuretic peptide, are natriuretic. Although atrial natriuretic peptide and brain natriuretic peptide do not appear to interact synergistically, they are likely to act in concert in the physiological regulation of sodium balance.

Effect of physical exercise in hypobaric conditions on atrial natriuretic peptide secretion

1992 ◽  
Vol 263 (3) ◽  
pp. R647-R652 ◽  
Author(s):  
O. Vuolteenaho ◽  
P. Koistinen ◽  
V. Martikkala ◽  
T. Takala ◽  
J. Leppaluoto
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Sea Level ◽  
Natriuretic Peptide ◽  
Plasma Renin ◽  
Amino Terminal ◽  
Significant Difference ◽  
Elimination Mechanism ◽  
Peptide Secretion ◽  
Ergometer Test ◽  
Atrial Natriuretic

To evaluate the role of atrial natriuretic peptide (ANP) in exercise-related cardiovascular and hormonal adjustments in hypobaric conditions, 14 young athletes performed a maximal ergometer test in a hypobaric chamber adjusted to simulate the altitudes of sea level and 3,000 m. Plasma immunoreactive ANP levels rose from 5.89 to 35.1 pmol/l at sea level and rose significantly less (P less than 0.05), from 5.36 to 22.3 pmol/l, at simulated 3,000 m. Plasma immunoreactive amino-terminal peptide of proANP (NT-proANP) levels increased to the same extent at sea level and at simulated 3,000 m (from 240 to 481 pmol/l and from 257 to 539 pmol/l, respectively). Plasma immunoreactive aldosterone increased significantly less at simulated 3,000 m (P less than 0.05), but the changes in plasma renin were similar in both conditions. Plasma immunoreactive endothelin-1 and serum erythropoietin levels remained unchanged. In conclusion, we found a blunted ANP response to maximal exercise of ANP in acute hypobaric exposure compared with that in normobaric conditions, but no significant difference in the NT-proANP responses between the two conditions. The divergence may be due to stimulation of the elimination mechanism of ANP.

Sign in / Sign up

Export Citation Format

Share Document