Péptidos natriuréticos atriales / Atraial natriuretic peptides

Se realiza una revisión bibliográfica sobre los péptidos natriuréticos atriales. Se revisa su fisiología, se destaca su importancia en la regulación hídrica del organismo, así como sus alteraciones y su papel terapeútico en diversas condiciones.

Water and creatinine clearance in thyrotoxicosis

In thyrotoxicosis, changes in urine output and serum creatinine [Cr] concentration has been related to increased glomerular filtration rate [GFR]. The aim of this study is to clarify the mechanism of these changes. Forty-one thyrotoxic patients, 9 male and 32 female with the age range of 16-62 years were selected and body weight, 24-h urine output, serum and urine Cr concentration, and GFR were measured in the thyrotoxic state and two months after treatment. The data was analyzed by student 't' test and paired 't' test. The following parameters were measured and are compared in thyrotoxic and euthyroid states respectively. Body weight: 58.4 +/- 10.6 Kg and 61.6 +/- 10.4 Kg after receiving anti-thyroid therapy [p<0.001]. 24-h urine output: 1430 +/- 420 ml, and 1165 +/- 450 ml [p <0.001]. Serum creatinine concentration: 0.7 +/- 0.11 mg/dl, and 0.84 +/- 0.13 mg/dl [p<0.001]. 24-h urine creatinine concentration: 906 +/- 225 mg/l and 1081 +/- 285 mg/l [p<0.001]. The change in GFR was not statistically significant, being 90.1 ml/min before therapy and 89.5 ml/min in the euthyroid state. Increased urine output and decreased serum creatinine concentration in thyrotoxicosis is not GFR related

Release of plasma atrial natriuretic peptide after volume expansion is not related to pituitary-adrenal axis diurnal variation in normal subjects

The existence of a circadian rhythm of atrial natriuretic peptide (ANP) in humans is controversial. We studied the plasma ANP response to isotonic blood volume expansion in the morning and in the afternoon and its relationship with adrenocorticotropic hormone (ACTH)-cortisol diurnal variation in seven normal subjects. Basal plasma ANP level was similar in the morning (19.6 + 2.4 pg/ml) and in the afternoon (21.8 + 4.8 pg/ml). The ANP peak obtained with saline infusion (0.9 percent NaCl, 12 ml/Kg) in the morning (49.4 + pg/ml) did not differ from that obtained in the afternoon (60.3 + 10.1 pg/ml). There was no correlation between the individual mean cortisol and ACTH levels and the ANP peak obtained with saline infusion. These data indicate no diurnal variation in plasma ANP secretion induced by blood volume expansion and no relationship between plasma ANP peak and ACTH-cortisol diurnal variation.

Neuroendocrine regulation of salt and water metabolism

Neurons which release atrial natriuretic peptide (ANPergic neurons) have their cell bodies in the paraventricular nucleus and in a region extending rostrally and ventrally to the anteroventral third ventricular (AV3V) region with axons which project to the median eminence and neural lobe of the pituitary gland. These neurons act to inhibit water and salt intake by blocking the action of angiotensin II. They also act, after their release into hypophyseal portal vessels, to inhibit stress-induced ACTH release, to augment prolactin release, and to inhibit the release of LHRH and growth hormone-releasing hormone. Stimulation of neurons in the AV3V region causes natriuresis and an increase in circulating ANP, whereas lesions in the AV3V region and caudally in the median eminence or neural lobe decrease resting ANP release and the response to blood volume expansion. The ANP neurons play a crucial role in blood volume expansion-induced release of ANP and natriuresis since this response can be blocked by intraventricular (3V) injection of antisera directed against the peptide. Blood volume expansion activates baroreceptor input via the carotid, aortic and renal baroreceptors, which provides stimulation of noradrenergic neurons in the locus coeruleus and possibly also serotonergic neurons in the raphe nuclei. These project to the hypotlalamus to activate cholinergic neurons which then stimulate the ANPergic neurons. The ANP neurons stimulate the oxytocinergic neurons in the paraventricular and supraoptic nuclei to release oxytocin from the neural lobe which circulates to the atria to stimulate the release of ANP. ANP causes a rapid reduction in effective circulating blood volume by releasing cyclic GMP which dilates peripheral vessels and also acts within the heart slow its rate and atrial force of contraction. The released ANP circulates to the kidney where it acts through cyclic GMP to produce natriuresis and a return to normal blood volume.

Atrial natriuretic peptide and feeding activity patterns in rats

This review presents historical data about atrial natriuretic peptide (ANP) from its discovery as an atrial natriuretic factor (ANF) to its role as an atrial natriuretic hormone (ANH). As a hormone, ANP can interact with the hypothalamic-pituitary-adrenal axis (HPA-A) and is related to feeding activity patterns in the rat. Food restriction proved to be an interesting model to investigate this relationship. The role of ANP must be understood within a context of peripheral and central interactions involving different peptides and pathways.

effect of arm and leg cycling on plasma ANP in males

The effect of both arm and leg cycling on the level of plasma atrial natriuretic peptide in males was studied. This study included ten normal subjects with age ranged 19-35 years. The results showed significant rise of atrial natriuretic peptide after both arm and leg cycling. This rise was significantly higher with arm cycling than with leg cycling. The study concluded that arm and leg cycling increased the atrial natriuretic peptide level that might be beneficial in acute and chronic diseases that need natriuresis

Atrial natriuretic peptide in children with nephrotic syndrome

Plasma levels of atrial natriuretic peptide [ANP] were measured using a specific and sensitive radioimmunoassay in 40 children with nephrotic syndrome [NS]. Nine patients were steroid resistant and the remaining had primary steroid responsive NS. Renal biopsy was performed to four steroid resistant nephrotic patients and revealed membranoproliferative glomerulo nephritis [MPGN] in three patients and lupus nephritis in one patient. Plasma levels of ANP were also measured in 18 healthy children as a control group. High plasma concentrations of ANP were detected in nephrotic patients during active stage of the disease [edema and heavy proteinuria] irrespective to the underlying renal pathology or to the response to steroid therapy. Plasma ANP values in nephrotic patients correlated negatively with serum albumin and with serum creatinine clearance