Atrial natriuretic peptide inhibits postural release of renin and vasopressin in humans

1988 ◽  
Vol 255 (3) ◽  
pp. R368-R372 ◽  
Author(s):  
T. D. Williams ◽  
K. P. Walsh ◽  
S. L. Lightman ◽  
R. Sutton
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Plasma Volume ◽  
Plasma Renin ◽  
The Other ◽  
Plasma Norepinephrine ◽  
Head Up Tilt ◽  
Plasma Arginine ◽  
Rate Infusion ◽  
Atrial Natriuretic

The effects of infusions of atrial natriuretic peptide (ANP) on the hormonal and hemodynamic responses to head-up tilt were investigated in six healthy adults. Head-up tilt at 45 degrees for 2 h during placebo saline infusion caused a 7% fall in blood volume accompanied by increases in plasma renin activity (PRA) and plasma arginine vasopressin (AVP) of 112 and 175%, respectively. Head-up tilt was repeated during an infusion of ANP producing a four- to sixfold increase in plasma ANP concentrations. This resulted in an 18% fall in plasma volume, yet despite this greater fall in plasma volume, PRA did not change. Two subjects experienced vasovagal symptoms toward the end of the ANP infusions accompanied by large increases in plasma AVP. In the other four subjects, plasma AVP remained unchanged during ANP infusions. Both procedures resulted in similar increases in plasma norepinephrine levels and in heart rate. Infusion of ANP prevents the posturally stimulated release of renin and AVP.

Passive heat exposure leads to delayed increase in plasma levels of atrial natriuretic peptide in humans

1991 ◽  
Vol 71 (2) ◽  
pp. 716-720 ◽  
Author(s):  
J. Leppaluoto ◽  
O. Arjamaa ◽  
O. Vuolteenaho ◽  
H. Ruskoaho
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Atrial Natriuretic Peptide ◽  
Systolic Blood Pressure ◽  
Natriuretic Peptide ◽  
Heat Exposure ◽  
Plasma Renin ◽  
Evaporative Water ◽  
Plasma Arginine ◽  
Atrial Natriuretic

The effects of passive heat exposure on atrial natriuretic peptide (ANP) were studied in six healthy men staying in a Finnish sauna at +92 degrees C for 20 min. Their rectal temperature increased by 0.4 degrees C, and evaporative water loss was 0.92 +/- 0.14 (SD) kg. Heart rate and systolic blood pressure increased significantly during the 20-min exposure. Serum osmolality and plasma arginine vasopressin levels increased during the exposure, then declined, and increased significantly again at 90–120 min. Plasma renin activity and aldosterone increased by two- to fourfold in 20 min. Plasma ANP levels rose from 13 +/- 7 to 39 +/- 15 ng/l at 60 min and to 41 +/- 13 ng/l at 120 min (P less than 0.01 for both). We conclude that transient increases in heart rate and systolic blood pressure or changes in blood volume as inferred from the weight loss do not contribute to the increased plasma ANP levels observed after the heat exposure. Instead, increased secretions of pressor hormones could explain the elevated plasma ANP levels observed after the thermal stress.

Effects of endogenous atrial natriuretic peptide released by rapid atrial pacing in dogs

1987 ◽  
Vol 253 (4) ◽  
pp. R599-R604 ◽  
Author(s):  
K. P. Walsh ◽  
T. D. Williams ◽  
R. Canepa-Anson ◽  
E. Pitts ◽  
S. L. Lightman ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Plasma Concentrations ◽  
Plasma Renin ◽  
Right Atrial ◽  
Plasma Norepinephrine ◽  
Atrial Pacing ◽  
Vascular Effects ◽  
Rebound Increase ◽  
Atrial Natriuretic

The relationships between the hemodynamic, renal, and endocrine changes induced by rapid atrial pacing were studied in seven chloralose-anesthetized greyhounds paced from the right atrial appendage for 60 min at 250 beats/min. Pacing increased mean pulmonary wedge pressure, decreased cardiac output, and decreased mean arterial pressure. Systemic vascular resistance did not change significantly. Coronary sinus atrial natriuretic peptide (ANP) concentrations rose maximally within 5 min of commencing pacing. The corresponding increase in arterial ANP concentrations during this time was only 44% of its maximum value after 30 min of pacing. Plasma concentrations of arginine vasopressin were unchanged. Plasma renin activity decreased during pacing and showed a marked rebound increase at 60 min postpacing. Plasma norepinephrine levels did not change significantly during pacing. Urine flow increased during the latter 30 min of pacing. There was no significant change in sodium clearance despite high sustained concentrations of ANP. The lack of significant natriuretic and systemic vasodilator effects in association with high arterial plasma concentrations of endogenous ANP, in the absence of antagonistic mechanisms, suggests that the natriuretic and vascular effects of ANP may not be its major physiological actions.

Atrial Natriuretic Peptide as a Regulator of Transvascular Fluid Balance

Physiology ◽  
1996 ◽  
Vol 11 (3) ◽  
pp. 138-143 ◽  
Author(s):  
EM Renkin ◽  
VL Tucker
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Plasma Volume ◽  
Fluid Balance ◽  
Interstitial Fluid ◽  
Fluid Volume ◽  
Interstitial Fluid Volume ◽  
Atrial Natriuretic

Unlike other natriuretics, which act via the kidneys to reduce interstitial fluid volume with little change in plasma volume, atrial natriuretic peptide has important extrarenal actions that enable it to reduce plasma volume preferentially.

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.

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.

Isoproterenol induces release of atrial natriuretic peptide from rat atrium in vitro

1992 ◽  
Vol 262 (1) ◽  
pp. H285-H292 ◽  
Author(s):  
G. Agnoletti ◽  
A. Rodella ◽  
A. Cornacchiari ◽  
A. F. Panzali ◽  
P. Harris ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Mechanical Stimulation ◽  
The Other ◽  
Mechanical Activity ◽  
Mechanical Function ◽  
Rat Atria ◽  
Rat Atrium ◽  
Atrial Natriuretic

To investigate the mechanism underlying the release of atrial natriuretic peptide (ANP) in in vitro condition, isolated, superfused rat atria were subjected to adrenergic, chronotropic, and mechanical stimulation. First administration of isoproterenol (Iso; either 10(-9) or 10(-6) M) caused a release of ANP, which was transient. Subsequent increments in concentration of Iso always resulted in a much lower release of ANP, despite the increased effects on the mechanical function of the atria. Stretching of the atria resulted in a transient release of ANP. Subsequent increments in stretching were followed by decreasing release of ANP. The total score of ANP in atrial tissue after Iso and stretching was not measurably depleted. Pacing the atria with increasing frequency did not induce release of ANP. Depolarization with 40 mM KCl abolished the release of ANP in response to Iso but not the release induced by stretch. In the presence of low external Ca2+, which abolished mechanical activity, both Iso and stretch could still induce release of ANP. Propranolol abolished the release of ANP by Iso but not that induced by stretching. Prazosin did not affect the release by either stretch or Iso. Stretching the atria 20 min after administration of Iso did not cause any further release of ANP. On the other hand, adding Iso 20 min after stretching induced a release of ANP. It is concluded that Iso and stretch cause a transient release from isolated strips of atria. The amount of ANP released is not related to the dose of Iso or to the load applied. Mechanisms involved in the release mediated by the two stimuli are different.(ABSTRACT TRUNCATED AT 250 WORDS)

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