Fator natriurético atrial: ele é o responsável pela hiponatremia e natriurese em neurocirurgia? / Atrial natriuretic factor: is it responsible for hyponatremia and natriuresis in neurosurgery?

RESUMO Objetivo: Avaliar a presença de hiponatremia e natriurese, bem como suas associações com o fator natriurético atrial em pacientes de neurocirurgia. Métodos: Foram incluídos 30 pacientes submetidos à ressecção de tumor intracraniano e à clipagem de aneurisma cerebral. Os níveis plasmáticos e urinários de fator natriurético atrial foram medidos durante os períodos pré e pós-operatório. Resultados: Hiponatremia esteve presente em 63,33% dos pacientes, particularmente no primeiro dia pós-operatório. Observou-se natriurese em 93,33% dos pacientes, principalmente no segundo dia pós-operatório. Os níveis plasmáticos de fator natriurético atrial estavam aumentados em 92,60% dos pacientes em pelo menos um dos dias pós-operatórios, mas não houve associação estatisticamente significante entre fator natriurético atrial e sódio plasmático, e entre fator natriurético atrial e sódio urinário. Conclusão: Após neurocirurgia, na maior parte dos pacientes, estiveram presentes hiponatremia e natriurese; contudo, o fator natriurético atrial não pôde ser considerado diretamente responsável por tais alterações nos pacientes neurocirúrgicos. Provavelmente, há o envolvimento de outros fatores natriuréticos.

ABSTRACT Objective: To evaluate the presence of hyponatremia and natriuresis and their association with atrial natriuretic factor in neurosurgery patients. Methods: The study included 30 patients who had been submitted to intracranial tumor resection and cerebral aneurism clipping. Both plasma and urinary sodium and plasma atrial natriuretic factor were measured during the preoperative and postoperative time periods. Results: Hyponatremia was present in 63.33% of the patients, particularly on the first postoperative day. Natriuresis was present in 93.33% of the patients, particularly on the second postoperative day. Plasma atrial natriuretic factor was increased in 92.60% of the patients in at least one of the postoperative days; however, there was no statistically significant association between the atrial natriuretic factor and plasma sodium and between the atrial natriuretic factor and urinary sodium. Conclusion: Hyponatremia and natriuresis were present in most patients after neurosurgery; however, the atrial natriuretic factor cannot be considered to be directly responsible for these alterations in neurosurgery patients. Other natriuretic factors are likely to be involved.

Obesidad y excreción urinaria de sodio en niños y adolescentes / Obesity and urinary sodium excretion in children and adolescents

Background: Qbesity is a disease characterized by an abnormal accumulation body fat that results in neuroen-docrine changes that alter the homeostasis of sodium, producing an increased risk of hypertension in adulthood. objective: To evaluate the effect of obesity on urinary sodium excretion in children and adolescents. subjects and Methods: 266 male and female children in the age group of 5-15 years were studied: 154 obese (OB) with > 95th percentile of BMI, and 112 normal-weight patients (C) with percentile 5-85 of BMI, from the outpatient service of the Children Hospital, Posadas, Misiones, Argentina during the years 2008 -2009. The determinations of serum sodium (Na s) and 24-hour urine (Na ur) were performed using Ion Selective Electrode. The fractional excretion of sodium (FENa percent) was calculated. results: Na ur values (mEq/kg/day) and FENa percent reported significantly lower differences in the obese group compared to controls: OB Na ur 2.23 vs C Na ur 3.40 (p < 0.0001); OB FENa percent 0.59 vs C FENa percent 0.71 (p = 0.001). Conclusion: Results obtained in the present study showed that obese children have a significantly decreased urinary sodium excretion compared to normal weight children. This difference could be caused by renal retention of this ion.

Introducción: La obesidad es una enfermedad caracterizada por el aumento de grasa corporal, que genera modificaciones neuroendocrinas involucrando alteraciones en la homeostasis del sodio, que podrían generar hipertensión arterial en la adultez. Objetivo: Evaluar el efecto de la obesidad sobre la excreción urinaria de sodio en niños y adolescentes. Pacientes y Método: Se estudiaron 266 niños de ambos sexos, entre 5 y 15 años: 154 obesos (OB) definidos como IMC percentil > 95, y 112 normopeso (C), IMC percentil 5-85, provenientes del Servicio de Consultorio Externo del Hospital de Pediatría-Posadas, Misiones, Argentina, durante los años 2008-2009. Las determinaciones de sodio en suero (Na s) y orina de 24 h (Na ur) se realizaron con electrodo ion selectivo. Se calculó la excreción fraccional de sodio (EFNa por ciento). Resultados: Los valores de Naur (mEq/ kg/día) y la EFNa por ciento significativamente menores en el grupo de obesos con respecto a los controles: Na ur QB 2,23 vs Na ur C 3,40 (p < 0,0001); EFNa por ciento OB 0,59 vs EFNa por ciento C 0,71 (p = 0,001). Conclusión: En el presente estudio los resultados mostraron que los niños y adolescentes obesos presentan una disminución significativa de la excreción urinaria de sodio respecto de los niños normopeso. Dicha diferencia podría estar generada por la retención renal de dicho ion.

Cerebral Salt Wasting Treated with Fludrocortisone in a 17-Year-Old Boy

Cerebral salt wasting is characterized by inappropriate natriuresis and volume contraction with associated cerebral pathology. It is distinct from the syndrome of inappropriate antidiuretic hormone secretion, which is characterized by inappropriate retention of free water. We report a patient with a porencephalic cyst who developed cerebral salt wasting. His initial treatment was supplementation of water and salt, which did not improve natriuresis or volume contraction. Fludrocortisone administration effectively managed the cerebral salt wasting.

Role of nitric oxide in the diuresis and natriuresis occurring in patients with obstructive sleep apnoea syndrome.

Objective. To determine whether nitric oxide (NO) has any role in the diuresis and natriuresis observed in patients with obstructive sleep apnoea syndrome (OSAS). Methods. We measured 12-hour urine volume in the day and in the night in patients with OSAS (n=20) and determined the concentrations of urinary sodium and nitrate. The frequency of urination in the night was also noted. The measurements were done again after two nights of continuous positive airway pressure (CPAP) therapy and after putting the patients on oral anti-oxidant treatment (vitamin C–100mg BD and vitamin E–400IU BD) for 45 days. Ten healthy normal subjects underwent the same protocol except the CPAP therapy. Results. In patients with OSAS, the night urine volume and sodium concentration were similar and the nitrate levels were higher compared to those in the day. After CPAP therapy, while the urine volume and sodium concentration decreased, the nitrate level became similar to that in the day. Such effects were not observed after anti-oxidant treatment. The frequency of urination was decreased in both the instances. The effects observed after CPAP therapy were similar to those observed in control subjects with or without anti-oxidant treatment. Conclusion. Renal NO promotes diuresis and natriuresis in patients with OSAS.

Actividad del sistema dopaminérgico renal en ratas con distinto contenido de sodio en la dieta / Activity of the renal dopaminergic system in rats

La dopamina (DA) renal modula la excreción de sodio y agua y la presión arterial por medio de receptores D1 (D1R) y D2 y es degradada por las enzimas monoamino-oxidasa (MAO) y catecol-O-metiltransferasa (COMT). Nuestro propósito es estudiar el patrón de excreción urinaria de DA (UDAV) y la actividad de MAO y COMT durante el consumo de dietas con distinto contenido de sodio.

Rol del riñón en la hipertensión sal-sensible / Role of the kidney in salt sensitive hypertension

An important proportion of patients with essential hypertension are salt sensitive, defined as those who experience signifcant blood pressure changes according to the amount of salt intake. They have a disturbance in the pressure induced natriuresis mechanism and their kidneys have functional and morphological alterations con-sistent with an acquired tubulointerstitial alteration, afferent arteriole damage and alteration of peritubular capillaries. All these alterations lead to disturbances in sodium load excretion under normal pressures. There is also an associated activation of kidney vasoconstrictor/salt retaining systems and a reduction in the vasodilator/ salt eliminating mechanisms. These alterations, that originate early in life, generate a new blood pressure level, that corrects natriuresis at the expense of a sustained hypertension.

Patterns of renal dopamine release to regulate diuresis and natriuresis during volume expansion: Role of renal monoamine-oxidase / Perfiles de secreción de dopamina renal en la expansión de volumen para regular diuresis y natriuresis: Rol de la monoaminoxidasa renal

Diuretic and natriuretic effects of renal dopamine (DA) are well established. However, in volume expansion the pattern of renal DA release into urine (U DA V) and the role of enzymes involved in DA synthesis/degradation have not yet been defined. The objective was to determine the pattern of U DA V during volume expansion and to characterize the involvement of monoamine-oxidase (MAO) and aromatic amino-acid decarboxylase (AADC) in this response. In this study male Wistar rats were expanded with NaCl 0.9% at a rate of 5% BWt per hour. At the beginning of expansion three groups received a single drug injection as follows: C (vehicle, Control), IMAO (MAO inhibitor Pargyline, 20 mg/kg BWt, i.v.) and BNZ (AADC inhibitor Benserazide, 25 mg/kg BWt, i.v.). Results revealed that in C rats U DA V (ng/30 min/100g BWt) increased in the first 30 min expansion from 11.5 ± 1.20 to 21.8 ± 3.10 (p < 0.05) and decreased thereafter. IMAO showed a similar pattern but significantly higher than C at 30 min expansion (32.5 ± 2.20, p < 0.05). IMAO greatly reduced MAO activity from 8.29 ± 0.35 to 1.1 ± 0.03 nmol/mg tissue/hour and significantly increased diuresis and natriuresis over controls. BNZ abolished the early U DA V peak to 3.2±0.72 (p < 0.01) and though, U DA V increased over C after 60 min expansion, natriuresis and diuresis were diminished by BNZ treatment. Results indicate that an increment in renal DA release into urine occurs early in expansion and in a peak-shaped way. In this response MAO plays a predominant role.

La dopamina (DA) intrarrenal ejerce efectos diuréticos y natriuréticos. Sin embargo, en los estado de expansión de volumen aún no está bien definido el patrón de liberación de dopamina renal hacia la orina y si cumplen un rol las enzimas involucradas en la síntesis o degradación de la amina. El objetivo del presente trabajo fue determinar el patrón de excreción urinaria de DA (U DA V) durante la expansión de volumen, caracterizando la participación de las enzimas monoaminooxidasa (MAO) y decarboxilasa de aminoácidos aromáticos (AADC) en esta respuesta. Para ello ratas Wistar macho fueron expandidas de volumen con NaCl 0.9% al 5% del peso corporal por hora durante dos horas y divididas en tres grupos, los que al comienzo de la expansión recibieron: C (vehículo, Control), IMAO (Pargilina, inhibidor de MAO, 20 mg/kg PC, i.v.) y BNZ (Benserazida, inhibidor de AADC, 25 mg/kg PC, i.v.). Se observó que en C la U DA V (ng/30min/100gPC) aumentó durante los primeros 30 minutos de expansión de 11.5 ± 1.20 a 21.8 ± 3.10 (p < 0.05), disminuyendo posteriormente. IMAO mostró un patrón de liberación similar pero significativamente mayor que C a los 30 min de expansión (32.5 ± 2.20, p < 0.05). En este grupo la actividad de MAO disminuyó de 8.29 ± 0.35 a 1.1 ± 0.03 nmol/mg tejido/hora y aumentaron la diuresis y natriuresis por sobre los controles. En BNZ, el pico de U DA V observado a los 30 min de la expansión disminuyó a 3.2 ± 0.72 (p < 0.01), aunque luego de 60 minutos fue mayor que en C. BNZ disminuyó tanto la diuresis como la natriuresis. Podemos concluir que al comienzo de la expansión de volumen se produce un pico de excreción de dopamina renal hacia la orina. La enzima MAO juega un rol fundamental en esta respuesta.

Influence of renal denervation on blood pressure, sodium and water excretion in acute total obstructive apnea in rats

Obstructive apnea (OA) can exert significant effects on renal sympathetic nerve activity (RSNA) and hemodynamic parameters. The present study focuses on the modulatory actions of RSNA on OA-induced sodium and water retention. The experiments were performed in renal-denervated rats (D; N = 9), which were compared to sham (S; N = 9) rats. Mean arterial pressure (MAP) and heart rate (HR) were assessed via an intrafemoral catheter. A catheter was inserted into the bladder for urinary measurements. OA episodes were induced via occlusion of the catheter inserted into the trachea. After an equilibration period, OA was induced for 20 s every 2 min and the changes in urine, MAP, HR and RSNA were recorded. Renal denervation did not alter resting MAP (S: 113 ± 4 vs D: 115 ± 4 mmHg) or HR (S: 340 ± 12 vs D: 368 ± 11 bpm). An OA episode resulted in decreased HR and MAP in both groups, but D rats showed exacerbated hypotension and attenuated bradycardia (S: -12 ± 1 mmHg and -16 ± 2 bpm vs D: -16 ± 1 mmHg and 9 ± 2 bpm; P < 0.01). The basal urinary parameters did not change during or after OA in S rats. However, D rats showed significant increases both during and after OA. Renal sympathetic nerve activity in S rats increased (34 ± 9 percent) during apnea episodes. These results indicate that renal denervation induces elevations of sodium content and urine volume and alters bradycardia and hypotension patterns during total OA in unconscious rats.

BTCI enhances guanylin-induced natriuresis and promotes renal glomerular and tubular effects

Guanylin and uroguanylin are small cysteine-rich peptides involved in the regulation of fluid and electrolyte homeostasis through binding and activation of guanylyl cyclases signaling molecules expressed in intestine and kidney. Guanylin is less potent than uroguanylin as a natriuretic agent and is degraded in vitro by chymotrypsin due to unique structural features in the bioactive moiety of the peptide. Thus, the aim of this study was to verify whether or not guanylin is degraded by chymotrypsin-like proteases present in the kidney brush-border membranes. The isolated perfused rat kidney assay was used in this regard. Guanylin (0.2 µM) induced no changes in kidney function. However, when pretreated by the black-eyed pea trypsin and chymotrypsin inhibitor (BTCI - 1.0 µM; guanylin - 0.2 µM) it promoted increases in urine flow (deltaUF of 0.25 ± 0.09 mL.g-1/min, P < 0.05) and Na+ excretion ( percent delta ENa+ of 18.20 ± 2.17, P < 0.05). BTCI (1.0 µM) also increased percentENa+ (from 22.8 ± 1.30 to 34.4 ± 3.48, P < 0.05, 90 minutes). Furthermore, BTCI (3.0 µM) induced increases in glomerular filtration rate (GFR; from 0.96 ± 0.02 to 1.28 0.02 mL.g-1/min, P < 0.05, 60 minutes). The present paper strongly suggests that chymotrypsin-like proteases play a role in renal metabolism of guanylin and describes for the first time renal effects induced by a member of the Bowman-Birk family of protease inhibitors.

Guanilina e uroguanilina são peptídeos pequenos, ricos em cisteína, envolvidos na regulação da homeostase de fluidos e eletrólitos através da ligação e ativação da guanilato ciclase expressa no intestino e nos rins. A guanilina é menos potente do que a uroguanilina como agente natriurético e é degradada in vitro pela quimiotripsina devido a características estruturais únicas no domínio bioativo do peptídeo. Portanto o objetivo deste trabalho foi verificar se a guanilina é degradada por proteases tipo quimiotripsina, presentes na membrana da borda em escova dos rins. Para esta investigação, foi usado o modelo do rim isolado de rato perfundido. A Guanilina (0,2 µM) não induziu mudanças na função renal. Entretanto, quando pré-tratada com inibidor de tripsina e de quimiotripsina de black-eyed pea (BTCI - 1,0 µM; guanilina - 0,2 µM) promoveu um aumento no fluxo urinário (deltaUF de 0,25 ± 0,09 mL.g-1/min, P < 0,05) e na excreção de Na+ ( por centoDENa+ de 18,20 ± 2,17, P < 0,05). BTCI (1,0 µM) também aumenta por centoENa+ (de 22,8 ± 1,30 a 34,4 ± 3,48, P < 0,0590 minutos). Além disto, BTCI (3,0 µM) induziu um aumento da taxa de filtração glomerular (GFR; de 0,96 ± 0,02 para 1,28 ± 0,02 mL.g-1/min, P < 0,05, 60 minutos). O presente trabalho sugere fortemente que proteases semelhantes à quimiotripsina desempenham um papel no metabolismo renal de guanilinas e descreve, pela primeira vez, os efeitos renais induzidos por um membro da família de inibidores de proteases do tipo Bowman-Birk.

Sensibilidade gustativa ao sal, natriúria e pressão arterial em indivíduos normotensos / Salt taste threshold, 24 hour natriuresis and blood pressure variation in normotensive individuals

OBJETIVO: O estudo avalia sensibilidade gustativa ao sal, excreção urinária de sódio e pressão arterial (PA) em normotensos. A hipótese foi de que limiar de sensibilidade gustativa ao sal (LSGS) aumentado se associasse a maior natriúria em 24 horas e níveis aumentados de PA. MÉTODOS: Foram avaliados 24 voluntários sem diagnóstico de HA. Para avaliar LSGS, usou-se soluções de cloreto de sódio (NaCl) em diferentes concentrações. Os voluntários foram submetidos à monitorização ambulatorial da pressão arterial (MAPA) de 24 horas e coleta de urina de 24 horas para dosagem de sódio (NaU). Para análise, foram agrupados de acordo com o LSGS, aumentado ou normal. RESULTADOS: Os grupos não diferiram para idade, índice de massa corporal (IMC), variáveis demográficas, uso de álcool, fumo e PA. NaU foi significativamente maior no grupo com LSGS aumentado. Utilizando-se o coeficiente de correlação de Pearson, com significância determinada pelo teste t, houve correlação de forte intensidade entre médias de PA sistólica e diastólica com IMC, de regular intensidade entre LSGS e NaU, assim como para PA sistólica e NaU. CONCLUSÃO: Natriúria de 24 horas foi maior em indivíduos com LSGS aumentado, sugerindo que esta maior avidez ao sal determine maior ingestão de sódio. Houve forte associação entre PA e IMC. Não foi evidenciada associação entre LSGS e PA, diferente do já documentado em pacientes com PA aumentada. Aumentando-se o número de pessoas, faixa etária e pacientes com níveis pressóricos aumentados, talvez se respondam outras perguntas a respeito da relação entre LSGS, natriúria e PA.

OBJECTIVE: The study evaluates salt taste sensibility, urinary sodium excretion and blood pressure (BP) in normotensive persons. The hypothesis was that a higher salt taste threshold (STT) can be associated to a higher 24 hour natriuresis and increased BP levels. METHODS: Twenty four not hypertensive volunteers were selected. To evaluate STT, different concentrations of sodium chloride were used. Individuals were submitted to 24 hour ambulatory blood pressure monitoring (ABPM) and the 24 hour urine was collected for sodium dosage. Patients were divided in two groups related to higher or normal STT. RESULTS: Both groups did not differ regarding age or body mass index (BMI). There was no difference between the groups regarding demographic variables, alcohol or tobacco use, and ABPM. Twenty-four hour natriuresis was significantly higher in the group with increased STT. Using Pearson´s correlation coefficient, with the significance determined by Student-t test, there was a strong correlation between 24 hour Systolic BP and BMI, Diastolic BP and BMI, and a regular correlation between STT with 24 hour natriuresis and Systolic BP with 24 hour natriuresis. CONCLUSION: Twenty four hour natriuresis was significantly higher in individuals with higher STT, suggesting that this avidity for salt is followed by higher ingestion of sodium. There was strong association between BP and BMI. The association between STT and BP levels was not confirmed. Increasing the number of persons, the age bracket, and of hypertensive patients may lead to a better understanding of the relations between STT, natriuresis and BP variation.

Efeito do bloqueio do hormônio antidiurético na natriurese associada à hemorragia intracerebroventricular experimental em ratos / Vasopressin V2 receptor antagonist effects in natriuresis after experimental intracerebroventricular hemorrage in rats

A hiponatremia é uma condição grave associada às lesões neurológicas, notadamente aos sangramentos no sistema nervoso central. Duas teorias têm sido apontadas como causadoras desta condição: a síndrome cerebral perdedora de sal e a síndrome da secreção inapropriada do hormônio antidiurético (HAD). Utilizou-se um bloqueador seletivo do receptor V2 renal do hormônio antidiurético em um modelo de sangramento intracerebroventricular...

Síndrome cerebral perdedor de sal / Cerebral salt losing syndrome

Se presenta escolar de 9 años, sexo masculino con una hemorragia subaracnoida secundario a malformación vascular dorsolumbar: Evoluciona con hipovolemia severa, natriuveris y tendencia a la hiponatremia lo que hace plantear Síndrome Cerebral Perdedor de Sal (SCPS). Se manejó con aporte extra de sodio y fármaco con propiedades mineralocorticoides (Fluorhidrocortisona) con lo cual se observa mejoría. Alrededor de 1988 se plantea por primera vez este síndrome, presentándose entre el 9 y el 33 por ciento de los pacientes con hemorragia subaracnoídea. Dado lo difícil que resulta precisar la causa de la hiponetremia en estos pacientes se expone las características clínicas, fisiopatológicas y manejode esta afección

La presión del intersticio renal en el control crónico de la presión arterial / The role of renal interstitial pressure on the chronic control of arterial blood pressure

Existe extensa evidencia de que el riñón participa en forma importante en la generación y mantenimiento de la hipertensión arterial. Esta evidencia proviene de modelos animales experimentales, de cepas de ratas con hipertensión genética y de estudios en humanos. Todos los genes identificados hasta la fecha en los que mutaciones puntuales producen alteraciones crónicas en la presión arterial, codifican para proteínas que participan en una vía común que tiene, con fin la reabsorción renal de sodio. La natriuresis de presión constituye el mecanismo de enlace entre la presión arterial y la excreción urinaria de sodio; en los últimos años hemos empleado a entender cómo se da la conexión entre presión arterial y natriuresis ya que se ha reconocido, la importancia de la presión del intersticio renal en este fenómeno. Parte del nuevo entendimiento de la fisiología de la excreción urinaria de sodio se debe al desarrollo de nuevas estrategias como la videomicroscopía y flujometría doppler-laser que permiten medir, con alto grado de certeza, los flujos sanguíneos de corteza y médula renales en forma independiente que, en combinación con estrategias ya conocidas como la implantación de cápsulas para determinación de la presión intersticial renal, muestran que la presión del intersticio renal es la responsable de la conexión entre la presión arterial sistémica y la natriuresis y por tanto, modula la presión arterial a largo plazo

El riñón y la causa de la hipertensión esencial / The kidney and the cause of essential hypertension

La hipertensión arterial esencial o primaria puede corregirse con el transplante de riñón de donante de presión normal. A su vez la hipertensión puede transmitirse con el trasplante del riñón de donante de familia con hipertensión esencial. Como se ha probado repetidas veces en la experimentación animal, la hipertensión o la presión normal siguen al injerto renal. Dos alteraciones funcionales principales se han observado en el riñón de pacientes hipertensos. La disminución de respuesta natriurética a la presión sanguínea renal se observa en todo tipo de hipertensión y aún antes del desarrollo de la hipertensión esencial. La vasoconstricción predomina en las nefronas yuxtamedulares y disminuye el flujo sanguíneo medular, la presión hidrostática intersticial desciende y facilita mayor reabsorción tubular de sodio y agua amortiguando la capacidad natriurética. Un defecto en la síntesis de óxido nítrico (NO) medular renal contribuye a la vasoconstricción y al aumento de la reabsorción tubular de sodio. Estos factores promueven un balance hidrosalino positivo que inicia los cambios circulatorios determinantes de la elevación crónica de la presión arterial. La relación causal entre flujo sanguíneo medular y nivel de presión arterial se ha probado con métodos que reducen selectivamente el flujo medular y producen hipertensión, mientras que aumentos exclusivos del flujo sanguíneo medular descienden la presión arterial

Aspectos reciente en la fisiopatología de la hipertensión arterial / New aspects in the physiopathology of arterial hypertension

En este trabajo analizamos los conocimientos recientes sobre los diversos mecanismos que se han relacionado con la fisiopatología de la hipertensión arterial esencial, su relación con el daño orgánico, principalmente aterosclerótico, las bases para tratamientos más específicos en el futuro, y la posibilidad de correcciones de tales alteraciones con los fármacos disponibles en la actualidad

Does plasma ANP participate in natriuresis induced by alpha-MSH?

Alpha-Melanocyte-stimulating hormone (alpha-MSH;0.6 and 3 nmol) microinjected into the anteroventral region of the third ventricle (AV3V) induced a significant increase in diuresis without modifying natriuresis or kaliuresis. Intraperitoneal (ip) injection of alpha-MSH (3 and 9.6 nmol) induced a significant increase urinary sodium, potassium and water excretion. Intraperitoneal (3 and 4.8 nmol) or iv (3 and 9.6 nmol) administration of alpha-MSH did not induce any significant changes in plasma atrial natriuretic peptide (ANP), suggesting that the natriuresis, kaliuresis and diuresis induced by the systemic action of alpha-MSH can be dissociated from the increase in plasma ANP. These preliminary results suggest that alpha-MSH may be involved in a gamma-MSH-independent mechanism of regulation of hydromineral metabolism.

ANP as a neuroendocrine modulator of body fluid homeostasis

The role played by the central nervous system (CNS) in the control of body fluid homeostasis has been demonstrated by several authors. The AV3V plays a key role in central control of sodium excretion since its cholinergic, adrenergic, angiotensinergic and osmotic stimulation enhances and its destruction blocks sodium excretion in rats and goats. Cholinergic stimulation of the AV3V induced an increase in plasma ANP as well as a marked elevation in content of the peptide in medial basal hypothalamus, neuro and adenohypophysis. On the other hand, a decline in plasma ANP after AV3V lesions was accompanied by dramatic declines in content of ANP in these same structures. Our previous work has also indicated the essential role of the AV3V region and its ANPergic neurons in the control of ANP release in response to volume expansion (BVE) and indicated that alpha-adrenergic and muscarinic receptors are critical in mediating these responses. Lesions of the AV3V region, or of the median eminence or posterior lobe of pituitary gland blocked the increase in plasma ANP concentration in response to BVE. That this effect is related to blockage of the activity of the brain ANPergic neurons is supported by fyndings in sheep and in rats that the injection of the antiserum directed against ANP into the AV3V region at least partially blocked the BVE-induced release of ANP. We and others have also previously shown that denervation of baroreceptors inhibits ANP release induced by BVE. Activation of the ANP neurons also cause release of ANP from the anterior and neural lobe of pituitary gland. ANP neurons may activate oxytocinergic neurons in the supraoptic and paraventricular, which projects to neural lobe. Oxytocin would circulate to the atria and may directly activate release of ANP from the atrial myocytes, since i.v. or i.p. injection of oxytocin increases sodium excretion as well as elevates plasma ANP. Oxytoxin is present in the neural lobe in large quantity, which could reach the atria myocytes in high concentration and release ANP that circulate to the kidneys and evokes natriuresis to return circulating blood volume to normal.

Sensibilidad a la sal en sujetos normotensos: proyecto piloto (resrultados preliminares) / Sensivity a the salt in subject normoten: pilot proyect (preliminary result)

En una muestra de sujetos normotensos, no obesos, con historia familiar de Hipertensión Arterial, se evaluaron las respuestas de presión arterial, frecuencia cardíaca, peso corporal, diuresis, natriuresis, kaliuresis y otros parámetros bioquímicos en relación a cambios en el consumo dietético de cloruro de sodio. Se introduce el concepto operacional de sensibilidad a la sal. en dieta hipersódica se observó elevación de cifras de presión arterial en relación a valores basales en sujetos sal-resistentes con historia familiar de Hipertensión Arterial quienes además mostraron menor diuresis que los sujetos contrarreguladores. Se encontró que la excreción urinaria de sodio y potasio del subgrupo sal-resistentes es diferente del resto de la población normotensa. Se propone un método de despistaje para identificar sujetos en riesgo de desarrollar Hipertensión Arterial de acuerdo a su sensibilidad a la sal