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J Antunes-Rodrigues

Publications and source records attributed to J Antunes-Rodrigues.

At least 55 records · Page 3Linked to original sources
PubMed1997

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.

Adrenal Glands↗
PubMed1997

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% NaCl, 12 ml/kg) in the morning (49.4 +/- 8 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.

Adrenal Glands↗
PubMed1996

Audiogenic and audiogenic-like seizures: locus of induction and seizure severity determine postictal prolactin patterns.

Audiogenic seizures (AS) are a model of generalized tonic-clonic seizures, evoked by high-intensity (110 dB) acoustic stimulation evaluated by means of behavioral severity indexes (SI). Postictal prolactin (PRL) is a marker of generalized seizures, both in animals and humans. Thus, in the present work we assayed postictal PRL in a) male Wistar AS susceptible (S, n = 5) and AS resistant (R, n = 13) rats made susceptible by specific midbrain lesions. b) In rats electrically stimulated in the central nucleus (CN) of the inferior colliculus (IC) (n = 20), or the cortical IC (CxIC, n = 18). In c) S rats pretreated with either bromocriptine (BRO; 4 mg/kg; SC), a PRL release inhibitor, or vehicle (V), 30 min before the electrical stimulation. Basal PRL was 2-10 ng/ml at time 0. In the S group, only animals with generalized seizures presented a postictal PRL elevation between 5 and 15 min (60-90 ng/ml; p < 0.05). R rats displayed a discrete PRL response lower than that of S animals. CxIC stimulation produced more severe seizures and greater postictal PRL enhancement than CNIC stimulation, always raising at 5-15 min (p < 0.01). BRO blocked the PRL increase even in the presence of higher seizure scores (p < 0.02). The positive correlation between seizure intensity (SI values), site of initiation (central or cortical IC nuclei), and postictal PRL patterns makes this a reliable model for studying the neurochemistry of the postictal phase and the interaction between hormones and epilepsy.

Acoustic Stimulation↗
PubMed1996

Characterization of the atrial natriuretic factor system in lungs of the toad Bufo paracnemis.

Blood pressure in the amphibian pulmonary circulation is relatively high because a single ventricle serves both the systemic and pulmonary circulation, creating a high degree of plasma filtration from pulmonary capillaries. Previous studies have shown that lung atrial natriuretic factor (ANF) may have an important physiological function in preventing edema in mammals. In this study, we report the presence of the complete ANF system in the lungs of the toad Bufo paracnemis. Radioimmunoassay of tissue homogenates revealed that toad lung ANF concentration was approximately twice as high (928.5 +/- 83.0 pg mg-1 protein) as that of lung tissue in mammals of a similar size. The amount of ANF was significantly higher in the left than in the right atrium (15.0 +/- 1.2 versus 1.9 +/- 0.8 ng mg-1 protein; N = 4, P < 0.001), while the ventricle contained 488.3 +/- 41.8 pg mg-1 protein. In extracts of both lungs and atria, high-performance liquid chromatography revealed two forms of the peptide; prohormone and a carboxy-terminal peptide of low molecular mass, which is the biologically active form of peptide. The presence of the prohormone suggests that ANF is synthesized in toad lungs and atria. Characterization of toad lung receptors by a competitive binding assay demonstrated three different subtypes of ANF receptors: the guanylyl cyclase (GC) receptors, GC-A and GC-B, as well as clearance (C) receptors. We conclude that the toad Bufo paracnemis has a well-developed complete ANF system in the lung, suggesting that it has a role in toad lung physiology.

Amino Acid Sequence↗
PubMed1996

Sodium balance of hyper- and hypo-natriophilic rats under basal conditions and during sodium deprivation.

Sodium and water balance was determined in two strains of Wistar rats selectively bred for high (hypernatriophilic, HR) or low salt preference (hyponatriophilic, HO) under basal conditions and during sodium deprivation. Male rats from each stain were selected for an average ingestion of 1.5% NaCl solution of more than (HR) or less than (HO) 4 ml 100 g body weight (-1) day (-1), during a 10-day period. HR rats (N = 17) presented markedly higher sodium intake under basal conditions (2.983 +/- 0.316 mEq 100 g body weight (-1) day (-1)) than HO rats (N = 12; 0.406 +/- 0.076 mEq 100 g body weight (-1) day (-1); Mann-Whitney test, P < 0.01). Water (HR: 8.6 +/- 0.57; HO: 7.7 +/- 0.32 ml 100 g body weight (-1) day (-1)) and sodium balances (HR: 0.936 +/- 0.153; HO: 0.873 +/- 0.078 mEq 100 g body weight (-1) day (-1)) were similar in both strains, despite a higher sodium and total fluid (HR: 16.3 +/- 1.06; HO: 10.8 +/- 0.49 ml 100 g body weight (-1) day (-1); P < 0.01) ingestion in HR rats. During sodium deprivation HR rats (N = 13) exhibited a sodium balance similar to that of HO rats (N = 13) (HR: -0.159 +/- 0.011; HO: -0.129 +/- 0.019 mEq 100 g body weight (-1) day (-1)), and, in addition, an adequate suppression of natriuresis (HR: 0.049 +/- 0.011; HO: 0.026 +/- 0.004 mEq 100 g body weight (-1) day (-1)). These data show that HR rats present hypernatriophilia as a primary trait, since their sodium-conserving mechanisms are intact. Therefore, these rats provide an adequate model to study factors that determine innate sodium preference.

Animals↗
PubMed1996

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 findings 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. Oxytocin 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.

Animals↗
PubMed1996

On the purinergic regulation of hormonal secretion from the anterior pituitary gland.

Purinergic regulation of hormonal secretion from the anterior pituitary may be characterized by effects with biphasic secretory response. This response may be started by activation of different subtypes of membrane prurinergic receptors (A1 and/or A2). A putative autocrine mechanism has been proposed to explain the action of adenosine on pituitary hormonal secretion. This mechanism may be dependent on adenosine degradation by the enzyme adenosine deaminase into the extracellular space. The regulation of AMPc and calcium levels in cytoplasm may be part of putative intracellular mechanisms involved in purinergic action. Additionally, hypophysiotrophic effects induced by hypothalamic substances may be modulated by adenosine. The mechanisms involved in this modulatory effects, however, remain elusive.

Pineal Gland↗
PubMed1995

Oxytocin mediates atrial natriuretic peptide release and natriuresis after volume expansion in the rat.

Our previous studies have shown that stimulation of the anterior ventral third ventricular region increases atrial natriuretic peptide (ANP) release, whereas lesions of this structure, the median eminence, or removal of the neural lobe of the pituitary block ANP release induced by blood volume expansion (BVE). These results indicate that participation of the central nervous system is crucial in these responses, possibly through mediation by neurohypophysial hormones. In the present research we investigated the possible role of oxytocin, one of the two principal neurohypophysial hormones, in the mediation of ANP release. Oxytocin (1-10 nmol) injected i.p. caused significant, dose-dependent increases in urinary osmolality, natriuresis, and kaliuresis. A delayed antidiuretic effect was also observed. Plasma ANP concentrations increased nearly 4-fold (P < 0.01) 20 min after i.p. oxytocin (10 nmol), but there was no change in plasma ANP values in control rats. When oxytocin (1 or 10 nmol) was injected i.v., it also induced a dose-related increase in plasma ANP at 5 min (P < 0.001). BVE by intra-atrial injection of isotonic saline induced a rapid (5 min postinjection) increase in plasma oxytocin and ANP concentrations and a concomitant decrease in plasma arginine vasopressin concentration. Results were similar with hypertonic volume expansion, except that this induced a transient (5 min) increase in plasma arginine vasopressin. The findings are consistent with the hypothesis that baroreceptor activation of the central nervous system by BVE stimulates the release of oxytocin from the neurohypophysis. This oxytocin then circulates to the right atrium to induce release of ANP, which circulates to the kidney and induces natriuresis and diuresis, which restore body fluid volume to normal levels.

Animals↗
PubMed1995

Reduced prolactin release during immobilization stress in thyrotoxic rats: role of the central serotoninergic system.

Adult Wistar male rats in a thyrotoxic state T4 increases rats) induced by administration of T4 (350 micrograms/kg/day, i.p. for 7 days) as well as their euthyroid controls were submitted to immobilization stress during forty minutes. Prolactin (PRL) secretion during stress was significantly lower in T4 increases rats as compared to control animals. Treatment with MK 212, a serotoninergic agonist, entirely reverts this situation. The effect of MK 212 seems to be due to its interaction with 5-HT2 receptors since it is blocked by LY 53857, a selective 5-HT2 antagonist. Furthermore, the blockade of 5-HT2 receptors by LY 53857, a selective 5-HT2 antagonist, significantly diminishes prolactin (PRL) response to stress in euthyroid rats but has no effect in T4 increases animals. It is suggested that an increased concentration of thyroid hormone in plasma disrupts an endogenous serotoninergic brain input necessary to trigger stress-induced PRL rise.

Animals↗
PubMed1995

Is ovarian adrenergic innervation essential to gonadal function in adult rats?

We studied the relative importance of ovarian innervation during different phases of female rat sexual development, 30, 40, 45 and 60-day-old. Chemical sympathectomy was promoted by long term postnatal treatment with guanethidine (GD), an adrenergic neuron blocking agent. The sympathectomized rats exhibited delayed puberty and alterations in estrous cycle. Reduced circulating E2, LH and Prl levels at 30 days of age were observed, besides decreased steroidal secretory responsiveness to gonadotropins in vitro. On the other hand, normal pituitary secretory responsiveness to LHRH in vivo and plasma gonadotropin concentrations were observed in 60-day-old rats. These data reinforce the view that ovarian sympathetic innervation contributes to the regulation of the prepubertal development of the ovarian functions.

Animals↗
PubMed1994

Participation of the ascending serotonergic system in the stimulation of atrial natriuretic peptide release.

Results obtained in our laboratories have provided evidence for the participation of the hypothalamic atrial natriuretic peptide (ANP) neuronal system in the regulation of water and electrolyte homeostasis. The anterior ventral third ventricular (AV3V) region, a site of the perikarya of the ANP neurons, receives important afferent input from ascending serotoninergic axons. We hypothesized that the ascending serotoninergic tract might be involved in control of the liberation of ANP. Therefore, electrolytic lesions were produced in the mesencephalic dorsal raphé nucleus (DRN), the site of perikarya of serotonin (5-HT) neurons whose axons project to the AV3V region. Rats with sham lesions constituted the control group. In a second group of animals, the serotoninergic system was depleted of 5-HT by lateral ventricular administration of p-chlorophenylalanine (PCPA), an amino acid that causes depletion of 5-HT from the serotoninergic neurons. Control animals were injected with an equal amount of isotonic saline. The DRN lesions induced an increase of water intake and urine output beginning on the first day that lasted for 1 week after lesions were produced. There was a concomitant sodium retention that lasted for the same period of time. When water-loaded, DRN-lesioned and PCPA-injected animals showed diminished excretion of sodium, accompanied by a decrease in basal plasma ANP concentrations, and blockade of the increase in plasma ANP, which followed blood volume expansion by intraatrial injection of hypertonic saline. The results are interpreted to mean that ascending stimulatory serotoninergic input into the ANP neuronal system in the AV3V region produces a tonic stimulation of ANP release, which augments sodium excretion and inhibits water intake. Therefore, in the absence of this serotoninergic input following destruction of the serotoninergic neurons by DRN lesions or intraventricular injection of PCPA, an antinatriuretic effect is obtained that is associated with increased drinking, either because of sodium retention per se or removal of ANP-induced inhibition of release of the dipsogenic peptide, angiotensin II. The serotoninergic afferents also play an essential, stimulatory role in volume expansion-induced release of ANP and the ensuing natriuresis.

Animals↗
PubMed1994

Diuresis and natriuresis in non-seizing and in kindled rats from a genetically audiogenic susceptible strain.

Audiogenic seizures are evoked by acoustic stimulation in susceptible (S) but not in resistant (R) rats. Repeated audiogenic seizures recruit limbic areas, a model called audiogenic kindling. In order to evaluate excretory patterns (urinary volume, Na+ and K+ excretion), S and R animals were non-stimulated, submitted to one (acute) or 10 (kindled) stimulations or to two aqueous overloads (5% b.w.). Non-stimulated S animals displayed a significant increase (p < 0.05) in Na+ excretion at 60, 80, 100 and 120 min. Acutely stimulated S animals showed greater natriuresis than non-stimulated animals at 40, 60, 80 and 100 min. Kindled S animals displayed the greatest natriuresis (p < 0.005) at 40, 60, 80, 100 and 120 min and the highest diuretic response (p < 0.05) at 40, 60 and 80 min. Abnormalities of the endogenous hydroelectrolytic profile of non-stimulated S animals and their overt expression in kindled rats may be related to alterations in neuroendocrine systems regulating hydroelectrolytic balance, in addition to the long-lasting effects of kindled seizures.

Acoustic Stimulation↗
PubMed1994

Hypothalamic control of water and salt intake and excretion.

This article provides a personal and historical review of research concerning the hypothalamic control of water and salt intake and excretion. The following major points will be considered: 1. Electrical, osmotic, cholinergic, alpha-adrenergic and peptidergic stimulation of the hypothalamus. 2. Determination of the pathways involved in these neuroendocrine responses. 3. The participation of ANP in the control of thirst and salt excretion. 4. The participation of the brain ANPergic neuronal system in ANP release. 5. The role of hypothalamic ANPergic neurons and of sinoaortic and renal baroreceptors in the regulation of volume expansion-induced release of ANP. 6. Effects of the brain ANP system on other hormones.

Angiotensin II↗
PubMed1993

Essential role of hypothalamic muscarinic and alpha-adrenergic receptors in atrial natriuretic peptide release induced by blood volume expansion.

Expansion of the blood volume induces natriuresis, which tends to return the blood volume to normal. This response is mediated at least in part by the release of atrial natriuretic peptide (ANP) into the circulation. Previous experiments have shown the participation of the anterior ventral third ventricular (AV3V) region of the hypothalamus in the ANP release that follows volume expansion. When injected into the AV3V region, the cholinergic drug carbachol induces natriuresis and the release of ANP. In the present experiments, microinjection of norepinephrine into the AV3V region induced natriuresis and an increase in plasma ANP. To determine whether cholinergic and alpha-adrenergic pathways are crucial to the volume expansion-induced release of ANP, certain receptor-blocking drugs were injected into the AV3V region of conscious rats. Thirty minutes later blood volume was expanded by intravenous injection of 2.0 ml/100 g of body weight of hypertonic saline (0.3 M NaCl). Microinjection of isotonic saline (2 microliters) into AV3V region of control animals 30 min prior to volume expansion had no effect on the 3-fold increase in plasma ANP concentrations measured 5 min after volume expansion. In contrast, although the receptor-blocking drugs did not alter the initial concentrations of plasma ANP 30 min later, just prior to volume expansion, blockade of muscarinic cholinergic receptors by intraventricular injection of 5 nmol (2 microliters) of atropine sulfate or methylatropine markedly reduced the response to volume expansion but did not obliterate it. Microinjection of the alpha receptor blocker phentolamine (5 nmol) into the AV3V 30 min prior to volume expansion also markedly suppressed the ANP response. Intraperitoneal (i.p.) injection of methylatropine (0.01 mmol/100 g of body weight), which does not cross the blood-brain barrier, also did not affect the basal levels of ANP 30 min after i.p. injection. But, in striking contrast with the blockade of the response to volume expansion induced by intraventricular injection of methylatropine, the response to volume expansion was markedly enhanced by i.p. injection of methylatropine. The results therefore indicate that hypothalamic muscarinic and alpha-adrenergic synapses are essential to release of ANP in response to volume expansion. These results are consistent with a hypothetical pathway for physiological control of ANP release which involves distension of baroreceptors within the right atria, carotid and aortic sinuses, and kidney which alters afferent input to brain stem noradrenergic neurons with axons projecting to the AV3V region. There they activate cholinergic interneurons by an alpha 1-adrenergic synapse. The cholinergic neurons in turn stimulate ANP neurons in this brain region via muscarinic receptors. The stimulation of these neurons activates efferent pathways which induce the release of ANP.

Animals↗
PubMed1993

Circadian variations of plasma atrial natriuretic peptide and corticosterone in rats with continuous or restricted access to food.

In the present study plasma Atrial Natriuretic Peptide (ANP) and Corticosterone (B) levels were determined in 2 groups of Wistar rats, a Control group (C) with free access to food, and a Food Shift group (FS) with access to food only from 0900 to 1100 h for 2 weeks. Blood samples were collected by decapitation at 4 hour intervals. ANOVA indicated that B varied over time in both groups (F (6.46) = 10.14, p < 0.0001 for C and F (6.5) = 5.10, p = 0.0005 for FS). There was also time variation in plasma ANP levels in both groups (F (6.54) = 3.78, p = 0.003 for C and F (6.48) = 2.73, p = 0.02 for FS group). Plasma B presented circadian variations from 78 +/- 17 nmol/l (mean +/- SEM) at 0800 h to 339 +/- 79 nmol/l at 2000 h. The day peak plasma ANP level (pmol/l) was also attained at 2000 h (68 +/- 19). This value was higher than all others measured throughout the day. The restricted feeding regimen resulted in a 12 hour shift of peak B values (395 +/- 39 vs 125 +/- 24). The FS rats presented the highest ANP level at 0800 h. The present study indicates similar circadian variations of plasma ANP and B in rats on an ad lib or restricted feeding regimen. ANP and B secretion may occur in anticipation of the feeding period or day activity.

Analysis of Variance↗
PubMed1993

Brain atrial natriuretic peptide neurons play an essential role in volume expansion-induced release of atrial natriuretic peptide and natriuresis.

The brain atrial natriuretic peptide (ANP) neuronal system appears to be involved in the increase in plasma ANP which follows blood volume expansion in the rat. To determine if this neuronal system is essential to the natriuresis and increase in plasma ANP which follow volume expansion, highly specific antiserum against ANP (ANP-AB) and/or normal rabbit serum as a control was microinjected into the third cerebral ventricle (3V) of conscious rats, and the effect on the natriuresis and increase in plasma ANP induced by intravenous injection of 2 ml/100 g body weight of 0.3 M NaCl was examined. Although there was no effect of ANP-AB on initial levels of plasma ANP or natriuresis 3 h after 3V injection, the natriuresis in response to blood volume expansion was significantly inhibited. The increase in plasma ANP which followed volume expansion was also significantly reduced at 5 min but recovered at 15 min. The results indicate that the brain ANP neuronal system plays an essential role in the mediation of volume expansion-induced increase in plasma ANP and natriuresis. The failure to block these responses completely may be due to the use of an inadequate dose of antiserum or other brain mechanisms may be able to mediate these responses.

Animals↗
PubMed1993

Possible role of endothelin acting within the hypothalamus to induce the release of atrial natriuretic peptide and natriuresis.

Since endothelin has been localized in neurons in areas involved in water and electrolyte metabolism, areas which also contain atrial natriuretic peptide (ANP) neurons, we determined whether endothelin would release ANP and induce natriuresis. Endothelin-3 (ET-3) in doses ranging from 38 to 760 pmol was microinjected into the third ventricle (3V) of conscious, water-loaded male rats, and the effect on natriuresis and plasma ANP was determined. ET-3 evoked a dose-related natriuresis beginning within 20 min of injection. Even the lowest dose tested (38 pmol) was effective. At a dose of 95 pmol, it produced a rapid increase of plasma ANP within 5 min peaking at 20 min. A slight kaliuresis and antidiuresis was observed at the 2 highest doses of 380 and 760 pmol. The urinary changes following 3V injection of ET-3 were similar to those evoked by ANP, except for the antidiuresis with increased sodium concentration which followed injection of the 2 higher doses. These results suggest that these 2 higher doses also released vasopressin. Alternatively, activation of the sympathetic nervous system by these higher doses may have decreased glomerular filtration rate and been in part responsible for the antidiuresis. The results with 3V injection of ET-3 contrasted sharply with those obtained following intravenous injection of the 95-pmol dose injected intraventricularly. This intravenous dose of ANP induced a transient decrease in sodium and potassium excretion and urine volume, maximal at 20 min, and had no effect on plasma ANP concentrations at 5 or 20 min after injection.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗