Low-dose infusion of atrial natriuretic peptide in the conscious guinea pig increases blood flow to the placenta of growth-retarded fetuses

1. The effects of low dose infusion of atrial natriuretic peptide (ANP) were observed in a double-blind, placebo-controlled study in six fluid-loaded volunteers. After baseline observations, hourly increments of 0.4, 2 and 10 pmol min−1 kg−1 were infused with continuous observation of heart rate, blood pressure and cardiac output. Plasma ANP, aldosterone, and catecholamines, and urinary volume and sodium excretion, were estimated at half-hourly intervals. 2. ANP infusion resulted in an increase of 35, 98 and 207% in urinary sodium excretion and of 10, 20 and 71% in urinary volume when compared with placebo. Plasma ANP was markedly elevated above placebo levels only during infusion of 10 pmol of ANP min−1 kg−1. 3. No change in heart rate or blood pressure was noted during the study, but a significant fall in stroke volume index was observed during active treatment. Plasma levels of aldosterone and catecholamines were not significantly different on the 2 treatment days. 4. The potent natriuretic and diuretic effects of this peptide at plasma concentrations not significantly elevated from physiological suggest a hormonal role for ANP in the homoeostasis of salt and water balance.

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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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Interaction between atrial natriuretic peptide and vasoactive intestinal peptide in guinea pig cecal smooth muscle

Gastroenterology ◽

10.1016/0016-5085(95)90568-5 ◽

1995 ◽

Vol 109 (4) ◽

pp. 1105-1112 ◽

Cited By ~ 21

Author(s):

Hirotada Akiho ◽

Yoshiharu Chijiiwa ◽

Hiroaki Okabe ◽

Naohiko Harada ◽

Hajime Nawata

Keyword(s):

Smooth Muscle ◽

Guinea Pig ◽

Atrial Natriuretic Peptide ◽

Vasoactive Intestinal Peptide ◽

Natriuretic Peptide ◽

Atrial Natriuretic

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Direct effect of α-human atrial natriuretic peptide on human vasculature in vivo and in vitro

Clinical Science ◽

10.1042/cs0740207 ◽

1988 ◽

Vol 74 (2) ◽

pp. 207-211 ◽

Cited By ~ 28

Author(s):

A. Hughes ◽

S. Thom ◽

P. Goldberg ◽

G. Martin ◽

P. Sever

Keyword(s):

Blood Flow ◽

Atrial Natriuretic Peptide ◽

Natriuretic Peptide ◽

Forearm Blood Flow ◽

Renin Angiotensin System ◽

Organ Bath ◽

Human Atrial Natriuretic Peptide ◽

Atrial Natriuretic

1. The effect of a α-human atrial natriuretic peptide (1–28) (ANP) on human vasculature was investigated in vivo and in vitro. Possible involvement of vascular dopamine receptors and the renin-angiotensin system in the response to ANP was also studied in vivo. 2. Forearm blood blow was measured by venous occlusion plethysmography. Isolated human blood vessels were studied using conventional organ bath techniques. 3. ANP (0.1–1 μg/min, intra-arterially) produced a dose-dependent increase in forearm blood flow, corresponding to a 163% increase in net forearm blood flow in the study arm. This action of ANP was not antagonized by (R)-sulpiride (100 μg/min, intra-arterially), a selective vascular dopamine receptor antagonist, or 50 mg of oral captopril, an inhibitor of angiotensin-converting enzyme. 4. ANP (1 nmol/l–1 μmol/l) produced concentration-dependent relaxation of isolated human arteries, including brachial artery, but was without effect on isolated human saphenous vein. 5. ANP produces vasodilatation in vivo and relaxes isolated human arterial smooth muscle. This action of ANP may contribute to its reported hypotensive effects in vivo.

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Atrial natriuretic peptide increases resistance to venous return in rats

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1987.252.5.h894 ◽

1987 ◽

Vol 252 (5) ◽

pp. H894-H899 ◽

Cited By ~ 4

Author(s):

Y. W. Chien ◽

E. D. Frohlich ◽

N. C. Trippodo

Keyword(s):

Blood Flow ◽

Cardiac Output ◽

Arterial Pressure ◽

Atrial Natriuretic Peptide ◽

Natriuretic Peptide ◽

Total Peripheral Resistance ◽

Venous Return ◽

Venous Pressure ◽

Peripheral Resistance ◽

Atrial Natriuretic

To examine mechanisms by which administration of atrial natriuretic peptide (ANP) decreases venous return, we compared the hemodynamic effects of ANP (0.5 microgram X min-1 X kg-1), furosemide (FU, 10 micrograms X min-1 X kg-1), and hexamethonium (HEX, 0.5 mg X min-1 X kg-1) with those of vehicle (VE) in anesthetized rats. Compared with VE, ANP reduced mean arterial pressure (106 +/- 4 vs. 92 +/- 3 mmHg; P less than 0.05), central venous pressure (0.3 +/- 0.3 vs. -0.7 +/- 0.2 mmHg; P less than 0.01), and cardiac index (215 +/- 12 vs. 174 +/- 10 ml X min-1 X kg-1; P less than 0.05) and increased calculated resistance to venous return (32 +/- 3 vs. 42 +/- 2 mmHg X ml-1 X min X g; P less than 0.01). Mean circulatory filling pressure, distribution of blood flow between splanchnic organs and skeletal muscles, and total peripheral resistance remained unchanged. FU increased urine output similar to that of ANP, yet produced no hemodynamic changes, dissociating diuresis, and decreased cardiac output. HEX lowered arterial pressure through a reduction in total peripheral resistance without altering cardiac output or resistance to venous return. The results confirm previous findings that ANP decreases cardiac output through a reduction in venous return and suggest that this results partly from increased resistance to venous return and not from venodilation or redistribution of blood flow.

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Mechanism for decrease in cardiac output with atrial natriuretic peptide in dogs

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1989.256.3.h760 ◽

1989 ◽

Vol 256 (3) ◽

pp. H760-H765 ◽

Cited By ~ 8

Author(s):

R. W. Lee ◽

S. Goldman

Keyword(s):

Blood Flow ◽

Cardiac Output ◽

Atrial Natriuretic Peptide ◽

Natriuretic Peptide ◽

Blood Volume ◽

Left Ventricular ◽

Right Atrial ◽

Total Blood Volume ◽

Total Blood ◽

Atrial Natriuretic

To examine the mechanism by which atrial natriuretic peptide (ANP) decreases cardiac output, we studied changes in the heart, peripheral circulation, and blood flow distribution in eight dogs. ANP was given as a bolus (3.0 micrograms/kg) followed by an infusion of 0.3 microgram.kg-1.min-1. ANP did not change heart rate, total peripheral vascular resistance, and the first derivative of left ventricular pressure but decreased mean aortic pressure from 91 +/- 4 to 76 +/- 3 mmHg (P less than 0.001) and cardiac output from 153 +/- 15 to 130 +/- 9 ml.kg-1.min-1 (P less than 0.02). Right atrial pressure and left ventricular end-diastolic pressure also decreased. Mean circulatory filling pressure decreased from 7.1 +/- 0.3 to 6.0 +/- 0.3 mmHg (P less than 0.001), but venous compliance and unstressed vascular volume did not change. Resistance to venous return increased from 0.056 +/- 0.008 to 0.063 +/- 0.010 mmHg.ml-1.kg.min (P less than 0.05). Arterial compliance increased from 0.060 +/- 0.003 to 0.072 +/- 0.004 ml.mmHg-1.kg-1 (P less than 0.02). Total blood volume and central blood volume decreased from 82.2 +/- 3.1 to 76.2 +/- 4.6 and from 19.8 +/- 0.8 to 17.6 +/- 0.6 ml/kg (P less than 0.02), respectively. Blood flow increased to the kidneys. We conclude that ANP decreases cardiac output by decreasing total blood volume. This results in a lower operating pressure and volume in the venous capacitance system with no significant venodilating effects. Cardiac factors and a redistribution of flow to the splanchnic organs are not important mechanisms to explain the decrease in cardiac output with ANP.

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