Atrial natriuretic peptide: physiological release associated with natriuresis during negative pressure breathing in man

1989 ◽  
Vol 76 (4) ◽  
pp. 423-429 ◽  
Author(s):  
J. V. Anderson ◽  
D. L. Maxwell ◽  
N. N. Payne ◽  
J. D. H. Slater ◽  
S. R. Bloom
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Plasma Renin Activity ◽  
Natriuretic Peptide ◽  
Blood Volume ◽  
Negative Pressure ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Plasma Aldosterone Concentration ◽  
Negative Pressure Breathing

1. Negative pressure breathing was one of the first physiological tools used to study the renal effects of redistribution of the blood volume from the peripheries to the thorax. The recent discovery of a putative natriuretic hormone (atrial natriuretic peptide, ANP) in cardiac atrial tissue has rekindled interest in the effect of the cardiovascular system on renal function. We have therefore studied the effects of this physiological manoeuvre on plasma ANP concentrations and renal responses. 2. Plasma concentrations of ANP, plasma renin activity and plasma aldosterone concentration were measured during an 80 min period of negative pressure breathing at −12 cmH2O pressure in six hydrated normal subjects. Identical control studies were performed in the same subjects at at least 1 week apart. 3. Negative pressure breathing resulted in a natriuresis and diuresis which were associated with a significant rise in plasma ANP concentration. The natriuresis occurred despite an increase in plasma renin activity and in plasma aldosterone concentration. 4. These findings, under specific carefully controlled conditions, support the previously contentious postulate that negative pressure breathing enhances sodium excretion, in addition to its well-recognized diuretic effect. They add further weight to the hypothesis that expansion of the central blood volume is an important stimulus to the release of ANP from the heart (acting by way of atrial distension), and suggest that changes of plasma ANP concentration may have induced the natriuresis which occurred in the face of a modest activation of the sodium-retaining renin-aldosterone system.

Fluid-regulating hormones during exercise when central blood volume is increased by water immersion

1992 ◽  
Vol 262 (5) ◽  
pp. R779-R785 ◽  
Author(s):  
L. M. Sheldahl ◽  
F. E. Tristani ◽  
T. P. Connelly ◽  
S. G. Levandoski ◽  
M. M. Skelton ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Plasma Renin Activity ◽  
Natriuretic Peptide ◽  
Blood Volume ◽  
Arginine Vasopressin ◽  
Water Immersion ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Central Blood Volume

To examine the influence of an increase in central blood volume with head-out water immersion (WI) on fluid-regulating hormones during exercise, 10 healthy men underwent upright leg cycle exercise on land and with WI. Venous plasma renin activity and plasma venous concentrations of atrial natriuretic peptide, plasma aldosterone, and arginine vasopressin were determined at exercise intensities corresponding to approximately 40, 60, 80, and 100% peak oxygen consumption (VO2) and at minutes 1 and 5 of seated rest recovery within each environment. Peak VO2 did not differ on land and with WI. Atrial natriuretic peptide concentration was higher (P less than 0.05) and plasma renin activity was lower (P less than 0.05) in water than on land at 40% peak VO2 through minute 5 of recovery. Plasma aldosterone and arginine vasopressin concentrations were lower (P less than 0.05) in water at peak exercise and at minutes 1 and 5 of recovery. Osmolality and plasma sodium and potassium concentrations during exercise were similar in water and on land. The results indicate that WI alters the circulating levels of several hormones involved in fluid and electrolyte regulation during exercise. These hormonal alterations can best be explained by stimulation of low-pressure baroreceptors and atrial stretch due to increased central blood volume with head-out WI.

Atrial natriuretic peptide inhibits the effect of endogenous angiotensin II on plasma aldosterone in conscious sodium-depleted rats

1987 ◽  
Vol 72 (1) ◽  
pp. 31-35 ◽  
Author(s):  
Lynn Chartier ◽  
Ernesto L. Schiffrin
Keyword(s):  
Angiotensin Ii ◽  
Atrial Natriuretic Peptide ◽  
Plasma Renin Activity ◽  
Natriuretic Peptide ◽  
Adrenocorticotropic Hormone ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Aldosterone Secretion ◽  
Atrial Natriuretic

1. Previous studies have shown that atrial natriuretic peptide (ANP) inhibits the secretion of aldosterone by isolated adrenal glomerulosa cells stimulated by angiotensin II, adrenocorticotropic hormone and potassium in vitro. We have also demonstrated that this inhibitory effect of ANP on plasma aldosterone induced by angiotensin II and adrenocorticotropic hormone can be reproduced in vivo in conscious unrestrained rats. In this study, we have investigated the effect of an intravenous infusion of ANP on plasma aldosterone in conscious unrestrained sodium-depleted rats. 2. During sodium depletion, the rise in plasma renin activity which determines an increment in the circulating concentration of angiotensin II was accompanied by a rise in aldosterone secretion as expected. ANP infused intravenously at a dose which increased the plasma concentration of the peptide three- to five-fold, produced a significant decrement in the concentration of aldosterone in plasma after an infusion period of 120 min. There was no significant effect of ANP on plasma renin activity and plasma corticosterone concentration. 3. Since the increase in plasma aldosterone levels in sodium-depleted rats is mainly dependent on the activation of the renin–angiotensin system, we conclude that ANP may modulate the effect of endogenous as well as exogenous angiotensin II on plasma aldosterone secretion.

Effect of Aging on Circadian Rhythm of Atrial Natriuretic Peptide, Plasma Renin Activity, and Plasma Aldosterone

1992 ◽  
Vol 47 (6) ◽  
pp. B214-B219 ◽  
Author(s):  
P. Cugini ◽  
P. Lucia ◽  
L. D. Palma ◽  
M. Re ◽  
R. Canova ◽  
...  
Keyword(s):  
Circadian Rhythm ◽  
Atrial Natriuretic Peptide ◽  
Plasma Renin Activity ◽  
Natriuretic Peptide ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Atrial Natriuretic

The effect of atrial natriuretic peptide on plasma renin activity, plasma aldosterone, and urinary dopamine in man

1986 ◽  
Vol 31 (2) ◽  
pp. 223-226 ◽  
Author(s):  
A. D. Struthers ◽  
J. V. Anderson ◽  
N. Payne ◽  
R. C. Causon ◽  
J. D. H. Slater ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Plasma Renin Activity ◽  
Natriuretic Peptide ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Urinary Dopamine ◽  
Atrial Natriuretic

Short-Term Effects of Atenolol and Nifedipine on Atrial Natriuretic Peptide, Plasma Renin Activity, and Plasma Aldosterone in Patients with Essential Hypertension

1991 ◽  
Vol 31 (3) ◽  
pp. 238-242 ◽  
Author(s):  
Domenico Colantonio ◽  
Raffaele Casale ◽  
Piergiorgio Desiati ◽  
Gildo Giandomenico ◽  
Valter Bucci ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Atrial Natriuretic Peptide ◽  
Plasma Renin Activity ◽  
Natriuretic Peptide ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Short Term ◽  
Short Term Effects ◽  
Atrial Natriuretic

Renin, aldosterone, electrolyte, and cortisol responses to hypoxic decompression

1977 ◽  
Vol 43 (3) ◽  
pp. 421-424 ◽  
Author(s):  
J. R. Sutton ◽  
G. W. Viol ◽  
G. W. Gray ◽  
M. McFadden ◽  
P. M. Keane
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Cortisol ◽  
Acute Mountain Sickness ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Plasma Sodium ◽  
Plasma Aldosterone Concentration ◽  
Urinary Potassium ◽  
Mountain Sickness

Responses of plasma renin activity, plasma aldosterone, plasma cortisol, and plasma electrolyte concentration and urinary electrolyte and aldosterone excretion were studied in four men during hypoxic decompression to a stimulated altitude of 4,760 m in a pressure chamber. Three of the four subjects developed significant acute mountain sickness. Plasma sodium and potassium concentrations were unchanged. No significant change in plasma renin activity was observed, but values tended to fall. Plasma aldosterone concentration was depressed while plasma cortisol was elevated and diurnal variation lost. Urinary sodium excretion was unchanged, but urinary potassium and aldosterone excretion were decreased. The decrease in plasma and urinary aldosterone and urinary potassium in the absence of change in plasma renin activity or plasma potassium is of uncertain origin. It is unlikely to be due to a decrease in adrenocorticotropin secretion since plasma cortisol rose during the same time. None of the changes could be causally implicated in the development of acute mountain sickness although the increase in plasma cortisol was greatest in the most ill.

Low-Dose Brain Natriuretic Peptide Infusion in Normal Men and the Influence of Endopeptidase Inhibition

1997 ◽  
Vol 92 (3) ◽  
pp. 255-260 ◽  
Author(s):  
C. M. Florkowski ◽  
A. M. Richards ◽  
E. A. Espiner ◽  
T. G. Yandle ◽  
E. Sybertz ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Plasma Renin Activity ◽  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Low Dose ◽  
Plasma Renin ◽  
Renin Activity ◽  
Plasma Brain Natriuretic Peptide ◽  
Normal Men ◽  
Atrial Natriuretic

1. To assess the threshold dose for bioactivity of brain natriuretic peptide and the role of endopeptidase 24.11 in metabolism of brain natriuretic peptide at physiological plasma levels, we studied eight normal men receiving 2 h infusions of low-dose brain natriuretic peptide [0.25 and 0.5 pmol min−1 kg−1 with and without pretreatment with an endopeptidase inhibitor (SCH 32615, 250 mg intravenously)] in placebo-controlled studies. 2. Plasma brain natriuretic peptide increased 2-fold during the infusion of 0.25 pmol min−1 kg−1 (mean increment above control 3.9 pmol/l, P < 0.001), and tripled (P < 0.001) with 0.5 pmol min−1 kg−1. Plasma renin activity was inhibited by both doses (14.8%, P < 0.01, and 20%, P < 0.001, respectively). A significant natriuresis (56% increase in urine sodium/creatinine ratio, P < 0.02) occurred with the higher dose. Blood pressure, haematocrit, plasma cGMP, atrial natriuretic peptide and aldosterone were unaffected by either dose. 3. Compared with brain natriuretic peptide (0.5 pmol min−1 kg−1) alone, SCH 32615 pretreatment increased peak plasma brain natriuretic peptide (13.4±0.78 versus 12.4±0.86 pmol/l, P < 0.05), ANP (7.5±0.96 versus 5.9±0.4 pmol/l, P < 0.01) and cGMP (4.8 ± 1.7 versus 3.9 ± 1.4 nmol/l, P < 0.001). Plasma renin activity was further suppressed with SCH 32615 pretreatment (29% compared with 20%, P < 0.001). 4. Small acute increments in plasma brain natriuretic peptide (4 pmol/l) have significant biological effects in normal men without altering plasma atrial natriuretic peptide or cGMP.

scholarly journals Effects of Ramipril on the Aldosterone/Renin Ratio and the Aldosterone/Angiotensin II Ratio in Patients With Primary Aldosteronism

Hypertension ◽  
2020 ◽  
Vol 76 (2) ◽  
pp. 488-496 ◽  
Author(s):  
Zeng Guo ◽  
Marko Poglitsch ◽  
Diane Cowley ◽  
Oliver Domenig ◽  
Brett C. McWhinney ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Ace Inhibitors ◽  
Primary Aldosteronism ◽  
Characteristic Curve ◽  
False Negative ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Plasma Aldosterone Concentration

The aldosterone/renin ratio (ARR) is currently considered the most reliable approach for case detection of primary aldosteronism (PA). ACE (Angiotensin-converting enzyme) inhibitors are known to raise renin and lower aldosterone levels, thereby causing false-negative ARR results. Because ACE inhibitors lower angiotensin II levels, we hypothesized that the aldosterone/equilibrium angiotensin II (eqAngII) ratio (AA2R) would remain elevated in PA. Receiver operating characteristic curve analysis involving 60 patients with PA and 40 patients without PA revealed that the AA2R was not inferior to the ARR in screening for PA. When using liquid chromatography-tandem mass spectrometry to measure plasma aldosterone concentration, the predicted optimal AA2R cutoff for PA screening was 8.3 (pmol/L)/(pmol/L). We then compared the diagnostic performance of the AA2R with the ARR among 25 patients with PA administered ramipril (5 mg/day) for 2 weeks. Compared with basally, plasma levels of equilibrium angiotensin I (eqAngI) and direct renin concentration increased significantly ( P <0.01 or P <0.05) after ramipril treatment, whereas eqAngII and ACE activity (eqAngII/eqAngI) decreased significantly ( P <0.01). The changes of plasma renin activity and plasma aldosterone concentration in the current study were not significant. On day 14, 4 patients displayed false-negative results using ARR_direct renin concentration (plasma aldosterone concentration/direct renin concentration), 3 of whom also showed false-negative ARR_plasma renin activity (plasma aldosterone concentration/plasma renin activity). On day 15, 2 patients still demonstrated false-negative ARR_plasma renin activity, one of whom also showed a false-negative ARR_direct renin concentration. No false-negative AA2R results were observed on either day 14 or 15. In conclusion, compared with ARR which can be affected by ACE inhibitors causing false-negative screening results, the AA2R seems to be superior in detecting PA among subjects receiving ACE inhibitors.

[PP.35.07] PLASMA RENIN ACTIVITY/PLASMA ALDOSTERONE CONCENTRATION RATIO

2016 ◽  
Vol 34 ◽  
pp. e333-e334
Author(s):  
F. Giulietti ◽  
F. Spannella ◽  
E. Borioni ◽  
F.E. Lombardi ◽  
L. Landi ◽  
...  
Keyword(s):  
Plasma Renin Activity ◽  
Concentration Ratio ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Plasma Aldosterone Concentration
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