The Effects of Low Dose Anp Infusion in Normal Man: Natriuretic and Negative Inotrope

Morice, Alyn H.; Pepke‐Zaba, Joanna; Loysen, Elena; Higgenbottam, T; Mj, Brown

doi:10.1042/cs072016pa

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“…After an 80-min equilibration (time -80 to 0 min), samples were collected continuously throughout a 12-min control period (time 0-12 min), a 10-min administration (time [12][13][14][15][16][17][18][19][20][21][22] no. V-9752, lot no.…”

Section: Methodsmentioning

confidence: 99%

“…Chronic ANF infusions in man and dog have transient effects on renal excretions of salt and water (7,8), challenging the concept that ANF is a blood volume regulatory hormone. ANF is released in the absence of atrial stretch in hypoxic hearts (9), hypoxic animals (10) and humans (11), and in pulmonary hypertension (12,13). Both endothelium-derived compounds (14) and neural factors (13) may be involved in this ANF release.…”

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Neural control of the endocrine rat heart.

Jiao

Baertschi²

1993

Proc. Natl. Acad. Sci. U.S.A.

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Although atrial stretch is the accepted stimulus for atrial natriuretic factor (ANF), in vivo studies suggest a stretch-independent, neurafly induced ANF release mechanism. Thus the hypothesis that cardiac nerves can stimulate ANF secretion was tested in the Langendorff-perfused, paced rat heart. Venom from the scorpion Centruroides sculpturatus was used to activate neuronal sodium channels, veratridine was added to activate sodium channels (predominantly in myocytes), and electrical stimulation was applied to the right atrial appendage. The efficacy of nerve stimulation was verified by measurements of increased neuropeptide Y in the effluent. ANF levels in the effluent increased by 120% over baseline with 0.5 IAM scorpion venom and by 88% with 0.5 ,uM veratridine (P < 0.01). Cardiac mechanics did not explain the large, concentration-dependent ANF response to the scorpion venom, since changes in the left ventricular developed pressure were small, opposite to those induced by veratridine, and unaffected by sympathectomy or adrenergic receptor blockade. Prior chemical sympathectomy and adrenergic receptor blockade almost abolished the ANF response to scorpion venom but hardly affected the ANF response to veratridine. Addition of 1FaM tetrodotoxin abolished all ANF responses. Electrical stimulation of the atrial appendage increased the ANF secretion by 60.2% (P < 0.02), in con,junction with neuropeptide Y, whereas control stimulations were ineffective. These studies unequivocally demonstrate that stimulation of cardiac sympathetic nerves potently stimulates ANF secretion.Atrial natriuretic factor (ANF), a potent natriuretic, diuretic, and vasorelaxant peptide (1), is thought to play an important role in the regulation of blood volume (2, 3). Atrial stretch (4) and blood volume expansion (5) stimulate ANF release, and ANF reduces the blood volume through increased renal excretions, inhibition offluid-retaining hormones, and loss of fluid to the interstitial space (2, 3). Quenching of circulating ANF with anti-ANF antibody reduces the renal response (diuresis) to acute volume expansion (6). However, doubts have been raised about this appealing concept in recent years. Chronic ANF infusions in man and dog have transient effects on renal excretions of salt and water (7,8), challenging the concept that ANF is a blood volume regulatory hormone. ANF is released in the absence of atrial stretch in hypoxic hearts (9), hypoxic animals (10) and humans (11), and in pulmonary hypertension (12,13). Both endothelium-derived compounds (14) and neural factors (13) may be involved in this ANF release.The evidence for a neural regulation of ANF is intriguing, but it has remained indirect and inconclusive. The ANF response to an unphysiological (20 ml/kg of body weight) volume expansion is blunted in pithed rats (15), but pithing inevitably alters baseline parameters (e.g., baseline ANF). Others found that the ANF response to a similar blood volume expansion is unaltered by autonomic denervation orThe publication costs of this...

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Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

Neural control of the endocrine rat heart.

Jiao

Baertschi²

1993

Proc. Natl. Acad. Sci. U.S.A.

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Atrial Natriuretic Factor in Human Pathophysiology

Crozier

Richards

Nicholls

et al. 1988

Clin Exp Pharma Physio

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1. Evidence from numerous experiments incorporating central blood volume expansion and changes in sodium status supports atrial stretch as the prime determinant of ANF release. 2. Plasma ANF levels are the result of both secretion and clearance of the peptide. Clearance is altered by a number of factors, including changes in posture in normal man and is probably impaired in disease states with diminished renal and hepatic blood flow. 3. In normal subjects an inverse relationship exists between plasma ANF values and renin-angiotensin-aldosterone system activity. This relationship is lost and replaced by a positive association in heart failure, presumably reflecting the abnormal concurrence of increased atrial stretch and diminished renal perfusion in this condition. Plasma ANF values rise with increasing severity of heart failure and fall with effective treatment. 4. Plasma ANF values are elevated in hypertension and cardiac tachyarrhythmias possibly reflecting raised central venous and atrial pressures. 5. A variety of other disorders may be associated with abnormal plasma ANF values including cirrhosis and the syndrome of inappropriate ADH secretion. 6. Evidence from low-dose infusions of ANF in normal volunteers suggests that the variations in plasma ANF seen in health and disease are sufficient to exert biological effects. 7. The advent of a specific antagonist is needed to provide further insight into the physiological and pathophysiological roles of ANF.

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The Effects of Low Dose Anp Infusion in Normal Man: Natriuretic and Negative Inotrope

Cited by 2 publications

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Neural control of the endocrine rat heart.

Neural control of the endocrine rat heart.

Atrial Natriuretic Factor in Human Pathophysiology

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