Atrial natriuretic factor plays a significant role in body fluid homeostasis.

Blaine, Edward H.

doi:10.1161/01.hyp.15.1.2

Cited by 83 publications

(27 citation statements)

References 20 publications

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“…The cardiac atria synthesize and store a peptide with natriuretic-diuretic and vasorelaxant properties, known as atriopeptin (AP) or atrial natriuretic factor [ANF-(99-126)], which is thought to participate in the regulation of blood volume and blood pressure (1,2). Raised plasma AP immunoreactivity (APir) levels have been reported in patients with congestive cardiac failure and the increase appears to correlate with the severity of the disease (3,4).…”

Section: Introductionmentioning

confidence: 99%

Maximizing the natriuretic effect of endogenous atriopeptin in a rat model of heart failure.

Wilkins

Settle

Stockmann

et al. 1990

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

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The effect of pharmacological manipulation of atriopeptin (AP) activity on sodium excretion and blood pressure was examined in the rat aortovenocaval (A-V) fistula model of cardiac failure. Introduction of an A-V shunt led to a marked and sustained elevation of plasma AP immunoreactivity and urinary cGMP levels. Further elevation ofplasma AP levels by infusion of exogenous peptide induced modest increases in urinary sodium and cGMP excretion and a decrease in blood pressure but these responses were significantly attenuated compared to sham-operated animals. In contrast, lowdose infusion of M+B 22948 (a cGMP phosphodiesterase inhibitor) or thiorphan [a neutral endopeptidase (membrane metallo-endopeptidase, EC 3.4.24.11) inhibitor] induced a natriuresis in A-V fistula rats, which exceeded that seen in control animals given these compounds and matched the peak natriuresis produced in sham-operated animals by high doses of AP. In the doses used, these compounds had little effect on blood pressure. The greater renal efficacy of M+B 22948 in A-V fistula rats is consistent with postreceptor facilitation of AP activity. The effect of thiorphan on sodium excretion was accompanied by a pronounced increase in urinary cGMP and AP iminunoreactivity excretion (and was attenuated by anti-AP monoclonal antibody) but could not be explained solely in terms of an increase in circulating AP levels. It is proposed that thiorphan allows filtered AP to reach renal tubule sites that are normally inaccessible to the peptide and are thus protected from down-regulation by high circulating AP levels. The implication of these observations for patients in cardiac failure is the potential for using pharmacological agents to maximize the response to endogenous AP without compromising cardiac function.The cardiac atria synthesize and store a peptide with natriuretic-diuretic and vasorelaxant properties, known as atriopeptin (AP) or atrial natriuretic factor ], which is thought to participate in the regulation of blood volume and blood pressure (1, 2). Raised plasma AP immunoreactivity (APir) levels have been reported in patients with congestive cardiac failure and the increase appears to correlate with the severity of the disease (3, 4). It is likely that the increase in plasma AP concentration represents a compensatory response, lessening cardiac workload by facilitating sodium and water excretion and reducing peripheral vascular resistance. This interpretation has stimulated studies to evaluate the therapeutic value of further increases in plasma AP levels in patients with heart failure. Studies in which the peptide has been infused have shown an enhancement of sodium and water excretion and an improvement in ventricular performance, as judged by changes in atrial and ventricular pressure and stroke volume (5-7). Unfortunately, the short half-life of the peptide, the necessity for parenteral administration, and occasional excessive drops in blood pressure limit the usefulness of the peptide itself as a therapeutic agent.An alternative...

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Section: Introductionmentioning

confidence: 99%

Maximizing the natriuretic effect of endogenous atriopeptin in a rat model of heart failure.

Wilkins

Settle

Stockmann

et al. 1990

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

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“…Several peptides directly regulate peripheral resistance such as angiotensin II [9], endothelin [10], vasopressin [11] and neuropeptide Y [12], which are vasoconstrictive, and atrial natriuretic peptide [13], calcitonin gene-related peptide (CGRP) [14], vasoactive intestinal peptide [15] and AM [7], which are vasodilators. Also there are volume regulating peptides such as atrial natriuretic peptide [16], vasopressin [17], and AM [18].…”

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confidence: 99%

Adrenomedullin and its Related Peptide

Shimosawa

Fujita

2005

Endocr J

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MORE than 100 years have passed since Riva-Rocci [1] modified the sphygmograph by Marey [2], Mahomed [3] and Von Basch [4] to make conventional blood pressure measurements possible. Two years after the method was established, existence of hypertensive agents, now known as renin, was reported [5]. Since then laboratory investigations as well as clinical and epidemiological studies in hypertension research have been advancing at an exponential rate [6]. Since the 1950s, several circulation-regulating peptides, both hypertensive and hypotensive, were discovered. Among them, a novel vasodilative peptide, adrenomedullin (AM) was isolated from pheochromocytoma tissue in 1993 [7]. Another processing site in a propeptide of AM was found and a new hypotensive peptide, named proadrenomedullin N-terminal 20 peptide (PAMP), was isolated from human plasma and urine [7,8].Blood circulates throughout the body by the pressure force generated by cardiac output and peripheral resistance. Each of these primary determinants of blood pressure is determined by the interaction of an exceedingly complex series of factors. Thus it is crucial to determine this complex of interactions in order to better understand the physiological role of these newly found factors. AM and PAMPAs mentioned above, AM, originally isolated from pheochromocytoma cell, is also produced and secreted in endothelial cells [7,19], and has been shown to exhibit hypotensive action by direct vasodilation via both the elevation of intracellular cAMP and alteration of calcium sensitivity in vascular smooth muscle cells [20]. Besides these actions, recent studies have shown that AM increases nitric oxide synthesis in endothelial cell by elevating intracellular calcium [21][22][23][24]. Studies on the physiological action of AM have also revealed that AM increases intracellular cAMP [22] [28]. Moreover, AM inhibits smooth muscle cell migration and proliferation [29, 30]. AM also shares a slight homology with CGRP and the above mentioned physiological effects are inhibited by CGRP antagonist CGRP(8-37) [21]. Together with the evidence that AM production is increased in failing heart [31, 32], it is speculated that

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“…None of our patients or controls had hypotensive episodes during the study. The increased basal BP in our patients would be expected to enhance the natriuretic response [32,33]. The low Aldo level together with non-elevated Ang II.…”

Section: Discussionmentioning

confidence: 77%

“…The low Aldo level together with non-elevated Ang II. AVP, and endothelin levels also would tend to increase the natriuretic response [33][34][35], Thus, the resistance to ANP could not be attributed to impaired renal perfusion, volume depletion, or increased activity of counterregulatory hormones.…”

Section: Discussionmentioning

confidence: 99%

Reduced Natriuretic Effect of Atrial Natriuretic Peptide in Nephrotic Syndrome: A Possible Role of Decreased Cyclic Guanosine Monophosphate

Jespersen¹,

Eiskjær²,

et al. 1995

Nephron

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To evaluate therapeutic and side effects, atrial natriuretic peptide (ANP) was administered as a pharmacological bolus dose (2 µg/kg body weight) to 7 patients with nephrotic syndrome and to 13 age- and gender-matched control subjects. The basal glomerular filtration rate was similar, but the blood pressure was slightly higher in the patients than in the controls. Injection of ANP induced a significant increase of sodium excretion in controls (from 0.21 to 0.52 mmol/min, medians, p < 0.01), but not in nephrotics (from 0.21 to 0.32 mmol/min). Urinary output and free water clearance after ANP had been given were also lower in the patients. The natriuretic effect was mediated through inhibition of distal tubular fractional sodium reabsorption, as estimated by the lithium clearance technique, and through an increase of glomerular filtration rate, both effects only significant in the healthy subjects. The blood pressure was reduced to the same extent in the two groups. Although similar levels of ANP were reached in the groups after injection, cyclic guanosine monophosphate (GMP)/ANP was less in the patients, both basally and after ANP injection, and the urinary excretion of cyclic GMP did not increase in the nephrotics (from 478 to 1,220 pmol/min, ns) as in the controls (from 389 to 2,500 pmol/min, p < 0.01). The urinary albumin excretion rate increased significantly in patients, whereas the prostaglandin E₂ excretion increased after ANP administration only in controls. Endothelin, angiotensin II, aldosterone, and arginine vasopressin were unchanged in the two groups. Basal aldosterone was lower and ANP higher in patients than in controls. In conclusion, the natriuretic effect of ANP was reduced in nephrotic patients. This could not be attributed to counterregulatory haemodynamic or hormonal factors, but probably to reduced second messenger cyclic GMP.

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Atrial natriuretic factor plays a significant role in body fluid homeostasis.

Cited by 83 publications

References 20 publications

Maximizing the natriuretic effect of endogenous atriopeptin in a rat model of heart failure.

Maximizing the natriuretic effect of endogenous atriopeptin in a rat model of heart failure.

Adrenomedullin and its Related Peptide

Reduced Natriuretic Effect of Atrial Natriuretic Peptide in Nephrotic Syndrome: A Possible Role of Decreased Cyclic Guanosine Monophosphate

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