Atrial natriuretic peptide: Physiological release associated with natriuresis during water immersion in man

Anderson, J. V.; Millar, N. D.; O'Hare, J P; MacKenzie, Jane; Corrall, R. J. M.; Bloom, Stephen R.

doi:10.1042/cs0710319

Cited by 79 publications

(20 citation statements)

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“…A close relationship between plasma concentrations of ANP and right and left atrial pressures [8][9][10][11][12], as well as atrial dimensions [12], has been observed in humans. Acute alterations in atrial wall stress, induced by volume loading [8,11,13], headout-water-immersion [14], o1" physical exercise [15] were shown to induce rapid and pronounced changes in circulating ANP levels in humans.In patients with congestive heart failure, abnormal sodium and water retention is a well-known clinical phenomenon, which is primarily due to an increased activity of the sympathetic and renin-angiotensin systems and of vasopressin [16]. Since ANP is integTated into the homeostatic regulation of fluid and electrolyte balance [for review see 2, 3], a "relative" deficiency of circulating ANP in patients with congestive heart failure may be assumed.…”

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confidence: 99%

Plasma concentrations of atrial natriuretic peptide during physical exercise in patients with congestive heart failure

Haass

Dietz

Purgaj

et al. 1990

Cardiovasc Drug Ther

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Plasma concentrations of atrial natriuretic peptide (ANP) were measured in 25 patients with organic heart disease during physical exercise (baseline and maximum workload) in order to investigate if the responsiveness of stimulated release of ANP is still preserved in patients with heart failure and chronically elevated cardiac filling pressures. Since plasma concentrations of ANP are known to be positively correlated with mean right atrial pressures (RAP), the patients were divided into two groups according to their resting RAP; group I; those with normal RAP (less than or equal to 5 mmHg; n = 11); group II; those with elevated RAP (greater than 5 mmHg; n = 14). Under baseline conditions RAP (3.2 +/- 0.4 mmHg vs. 8.8 +/- 0.7 mmHg; p less than 0.01), pulmonary artery diastolic pressure (PADP; 9.5 +/- 0.9 mmHg vs. 17.9 +/- 1.8 pg/ml; p less than 0.01), and plasma ANP levels (128 +/- 19 pg/ml vs. 204 +/- 60 pg/ml; p less than 0.06) were significantly lower in group I than in group II. Both at rest and during maximum workload, plasma ANP concentrations were closely related to RAP, PADP, and mean pulmonary artery pressures in both groups. During exercise in all patients, RAP and PADP significantly increased, as well as plasma ANP concentrations. Similar increments in plasma ANP concentrations were accompanied by greater changes in RAP in group II than in group I. However, identical changes in PADP lead to identical increments in plasma ANP concentrations in both groups. In conclusion, the increments of plasma ANP concentrations during physical exercise were independent of the resting values of PADP, RAP, and plasma ANP concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

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mentioning

confidence: 99%

Plasma concentrations of atrial natriuretic peptide during physical exercise in patients with congestive heart failure

Haass

Dietz

Purgaj

et al. 1990

Cardiovasc Drug Ther

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“…Results derived from ani mal experiments predict ANP increases that are most likely mediated by a combination of atrial stretch and/or pressure [10], while in vitro studies independently elaborated atrial tension and rate of contraction in ANP release [11]. The latter observation is sup ported by the finding of increased ANP val ues in humans during exercise to levels seen in pathological hypervolemic states [12], Other maneuvers known to influence atrial stretch and venous return thereby causing ANP release are postural changes, such as head-down tilt, recumbency [12] and headout water immersion [13].…”

Section: Identification Release and Biological Effects Of Atrial Natmentioning

confidence: 98%

Cell Biology of Atrial Natriuretic Peptide

Huot

Tremblay²,

Hamet³

1991

J Vasc Res

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Atrial natriuretic peptide (ANP) exhibits a wide spectrum of cardiovascular, endocrine, metabolic and renal actions. cGMP is the major mediator of ANP at the cellular level and only tissues possessing paniculate guanylate cyclase appear to present ANP-induced actions. Three types of ANP receptors have recently been cloned. Two of them (A and B receptors) are homologous and contain guanylate cyclase catalytic domains. The C receptor could possibly regulate the metabolic fate of ANP. Data obtained by the radiation inactivation method suggest the presence of an inter- or intramolecular inhibitory component of nearly 90 kilodaltons that represses the catalytic activity of guanylate cyclase within its membrane environment. The mechanism of guanylate cyclase stimulation by ANP could involve this inhibitory component. Preliminary data suggest that the hyperresponsiveness of the particulate guanylate cyclase/cGMP system in hypertension occurs through modulation of the inhibitory component.

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“…1) [28][29][30] or water [31 ], an acute increase in sodium intake [28,32,33], a central shift of volume produced by the change from the upright to the supine position ( fig. 1) [30,33,34] or by immersion into water [35,36], a vaso constrictor hormone-induced acute increase in blood pressure (BP) and. hence, afterload ( fig.…”

Section: Regulation Of Plasma Anp In Normal Humansmentioning

confidence: 99%