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

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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Plasma Atrial Natriuretic Peptide, Plasma Renin Activity and Aldosterone during Treatment of Hyperthyroidism due to Graves' Disease

Hormone and Metabolic Research ◽

10.1055/s-2007-1009274 ◽

1989 ◽

Vol 21 (09) ◽

pp. 514-518 ◽

Cited By ~ 9

Author(s):

S. Shigematsu ◽

T. Iwasaki ◽

T. Aizawa ◽

M. Ishihara ◽

T. Shinoda ◽

...

Keyword(s):

Atrial Natriuretic Peptide ◽

Plasma Renin Activity ◽

Natriuretic Peptide ◽

Plasma Renin ◽

Renin Activity ◽

Graves Disease ◽

Plasma Atrial Natriuretic Peptide ◽

Atrial Natriuretic

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Plasma Atrial Natriuretic Peptide, Aldosterone, and Plasma Renin Activity Responses to Gradual Changes in Dietary Sodium Intake

American Journal of Hypertension ◽

10.1093/ajh/3.11.863 ◽

1990 ◽

Vol 3 (11) ◽

pp. 863-865 ◽

Cited By ~ 13

Author(s):

G. A. Sagnella ◽

N. D. Markandu ◽

M. G. Buckley ◽

M. A. Miller ◽

D. R. J. Singer ◽

...

Keyword(s):

Atrial Natriuretic Peptide ◽

Plasma Renin Activity ◽

Natriuretic Peptide ◽

Sodium Intake ◽

Plasma Renin ◽

Renin Activity ◽

Dietary Sodium ◽

Plasma Atrial Natriuretic Peptide ◽

Atrial Natriuretic

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

Clinical Science ◽

10.1042/cs0920255 ◽

1997 ◽

Vol 92 (3) ◽

pp. 255-260 ◽

Cited By ~ 13

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.

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

Clinical Science ◽

10.1042/cs0720031 ◽

1987 ◽

Vol 72 (1) ◽

pp. 31-35 ◽

Cited By ~ 17

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.

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