Plasma Levels of Brain Natriuretic Peptide in Healthy Subjects and Patients with Essential Hypertension: Response to Posture

1993 ◽  
Vol 85 (4) ◽  
pp. 411-416 ◽  
Author(s):  
Giorgio La Villa ◽  
Silvio Vena ◽  
Alberto Conti ◽  
Caterina Fronzaroli ◽  
Aldo Brat ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Atrial Natriuretic Peptide ◽  
Plasma Renin Activity ◽  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Healthy Subjects ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Plasma Atrial Natriuretic Peptide ◽  
Atrial Natriuretic

1. To examine whether posture-induced changes in central volume affect brain natriuretic peptide secretion, plasma levels of human brain natriuretic peptide-32-like immunoreactivity (hBNP-32-li) were measured by radioimmunoassay in 11 healthy subjects and 20 patients with essential hypertension after 15 min supine, 15 min sitting and 15 min with the legs raised at 60°, together with plasma atrial natriuretic peptide concentration, plasma renin activity and plasma aldosterone concentration. 2. In the supine position, the plasma hBNP-32-li level was 1.57 + 0.10 fmol/ml in healthy subjects and significantly higher in hypertensive patients (2.39 +0.13 fmol/ml, P <0.001). In both groups, plasma hBNP-32-li level significantly (P <0.001) decreased when sitting (normotensive, 1.22 +0.08 fmol/ml; hypertensive, 1.85 +0.15 fmol/ml, P <0.001 versus normotensive) and increased again after leg raising (normotensive, 2.13+0.12 fmol/ml; P <0.002 versus resting; hypertensive, 2.84 + 0.16 fmol/min, P <0.001 versus resting, P <0.025 versus normotensive). 3. The plasma atrial natriuretic peptide concentration showed similar behaviour to the plasma hBNP-32-li, whereas plasma renin activity and plasma aldosterone concentration increased during sitting and decreased during leg raising in both healthy subjects and hypertensive patients, who had significantly higher plasma aldosterone levels when supine and sitting. 4. The plasma hBNP-32-li level, measured in all postural positions, was directly correlated with plasma atrial natriuretic peptide concentration (normotensive: r = 0.55, P <0.001; hypertensive: r = 0.69, P <0.001) and inversely correlated with plasma renin activity (r = −0.56, P <0.001 and r = −0.58, P <0.001). 5. We have shown that two physiological procedures, assumption of the sitting position and raising the legs to 60°, significantly affect the plasma hBNP-32-li level in healthy subjects. The response of the plasma hBNP-32-li level to postural changes is maintained in patients with essential hypertension, who have increased plasma levels of this hormone. The relevance of the observed modifications in the plasma hBNP-32-li level to the homoeostatic response to posture remains to be established.

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.

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.

scholarly journals Effects of insulin on plasma renin activity, plasma atrial natriuretic peptide and gody fluid volume in diabetes mellitus.

1990 ◽  
Vol 31 (5) ◽  
pp. 671-682 ◽  
Author(s):  
Tetsuya NAKAMURA ◽  
Shuichi ICHIKAWA ◽  
Tetsuo SAKAMAKI ◽  
Futao AIZAWA ◽  
Toshiaki KURASHINA ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Atrial Natriuretic Peptide ◽  
Plasma Renin Activity ◽  
Natriuretic Peptide ◽  
Plasma Renin ◽  
Fluid Volume ◽  
Renin Activity ◽  
Plasma Atrial Natriuretic Peptide ◽  
Atrial Natriuretic

scholarly journals Influence of Age, Posture and Intra-Individual Variation on Plasma Levels of Atrial Natriuretic Peptide

1989 ◽  
Vol 26 (6) ◽  
pp. 481-486 ◽  
Author(s):  
A C I T L Tan ◽  
P W C Kloppenborg ◽  
T J Benraad
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Individual Variation ◽  
Coefficient Of Variation ◽  
Healthy Subjects ◽  
Plasma Renin ◽  
Upright Position ◽  
Plasma Aldosterone ◽  
The Mean ◽  
Atrial Natriuretic

This paper describes some factors to which attention should be paid when atrial natriuretic peptide (ANP) values are to be interpreted. Changing from the supine to the sitting position decreased ANP levels, while no further decrease was observed when the upright position was assumed. On the other hand, plasma renin activity (PRA) increased only when changing from the sitting to the upright position. Returning to the supine position decreased PRA, while ANP did not change. Under these conditions plasma aldosterone levels did not differ in any of the four positions. No correlation was observed between the percentage changes of ANP, PRA and aldosterone. ANP values measured in 66 healthy subjects positively correlated with age ( r = 0·59, P < 0·01). To study intra-individual variation, ANP was sampled eight times within one hour. The mean, standard deviation and the coefficient of variation (CV) for each subject were calculated. The CV of 9 out of 15 subjects significantly exceeded the intra-assay coefficient of variation (7·0%), thereby indicating that ANP levels, like those of many other hormones, may exhibit endogenous fluctuations.

Plasma atrial natriuretic peptide during brief upright and supine exercise in humans

1989 ◽  
Vol 66 (5) ◽  
pp. 2159-2167 ◽  
Author(s):  
H. Perrault ◽  
M. Cantin ◽  
G. Thibault ◽  
G. R. Brisson ◽  
G. Brisson ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Plasma Renin Activity ◽  
Natriuretic Peptide ◽  
Maximal Exercise ◽  
Plasma Renin ◽  
Renin Activity ◽  
Plasma Atrial Natriuretic Peptide ◽  
Plasma Vasopressin ◽  
Exercise Induced ◽  
Atrial Natriuretic

The factors associated with the exercise-induced increase in plasma atrial natriuretic peptide (ANP) have not been clearly established. Thus the purpose of the study was to further document the stimulus for the exercise-induced release of ANP and to examine the role of ANP in the control of hydromineral balance during exercise. Eight healthy male volunteers (25.1 +/- 4.5 yr) were submitted to a graded cycling exercise in both the upright and supine positions. Venous blood was sampled at rest and at the end of each 5-min work load at 40, 60, and 80% maximal oxygen uptake (Vo2max), at maximal exercise, and during recovery through an indwelling catheter for the determination of plasma vasopressin, aldosterone, catecholamines, plasma renin activity, and ANP concentrations. Results indicate a significant increase in ANP (pg/ml) from rest to maximal exercise in the upright position [rest, 21.9 +/- 10.2; 40%, 24.7 +/- 12.6; 60%, 32.4 +/- 17*; 80%, 47.8 +/- 27.7*; 100% Vo2max, 65.9 +/- 34.5* (*P less than or equal to 0.05)]. Supine concentrations were significantly higher than upright at 40 (37.9 +/- 15.2), 60 (54.0 +/- 18.8), and 80% Vo2max (68.9 +/- 16.6). Plasma ANP during maximal exercise was similar in both positions. Plasma vasopressin, aldosterone, renin activity, and catecholamines increased with increasing exercise intensity in both positions, although lower values were systematically observed in the supine position. The association of higher plasma ANP and blunted plasma vasopressin, plasma renin activity, and norepinephrine concentrations during supine exercise suggests that ANP may exert modulatory effects on the control of the hydromineral hormonal system during exercise.

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