Biomedical subjects

A L Favaretto

Publications and source records attributed to A L Favaretto.

At least 37 records · Page 2Linked to original sources

PubMed1994

The male reproductive organs in experimental Chagas' disease. III. Plasma testosterone and accessory sex glands in the acute phase of the disease.

Male Wistar rats were injected i.p. with 2 x 10(5) trypomastigotes of the Bolivia strain. Fifteen days later, few parasite nests were observed in the fibromuscular layer surrounding the seminal vesicle acini of chagasic animals and no parasites were detected in the testis and ventral prostate. A significant decrease was observed in the absolute weight and fructose content of the seminal vesicle and ventral prostate of chagasic rats, which also presented a sharp decrease in plasma testosterone levels.

Animals↗

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

Morphometric evaluation of the rat testis, epididymis and vas deferens following chemical sympathectomy with guanethidine.

Selective chemical sympathectomy of the internal sex organs of adult male rats was undertaken by long term administration of low doses of guanethidine. The spermatogenic activity of the testis was unaffected by treatment. Examination of the vas deferens using morphometric methods revealed a marked increase in luminal area in contrast to a decrease in muscle layer area and in epithelial height. This is morphological evidence of sperm accumulation caused by a disorder in ductal contractile activity. No structural changes were observed in the epididymis. However, the concentration of spermatozoa in the sperm suspension stored in the cauda epididymidis was significantly increased in denervated rats. This result is discussed in terms of a sympathetic control of resorption mechanisms in the epididymis.

Animals↗

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↗

PubMed1993

[Traffic accidents in a metropolitan area of southern Brazil--victim and lesion characterization].

Casualties treated in a Emergency Hospital of Porto Alegre, Brazil, during the year 1988, for injuries received as a result of traffic accidents, are described by means of a retrospective study of the data provided by the Documentation and Statistics Sector of the hospital (n = 6.099). The results, similar to those described in the literature, draw special attention to the predominance of the male sex (69.2%), to the concentration of accidents involving individuals of between 20 and 39 years of age, inclusive, (52%) and to the frequency which the head is injured (49.6%) of the patients. Severe injuries such as bruises and fractures were found, respectively, in 61.5% and 24.2% of the patients. The data reveal, further, the large number and the seriousness of the injuries caused by accidents involving pedestrians which accounted for 32.7% of the total number of attendances related to traffic accidents, 57.2% of hospital internments; 54.6% of the victims of this kind of accident were under 9 years of age and 42.8% were over 60.

Accidents, Traffic↗

PubMed1993

Prepubertal development of rat prostate and seminal vesicle following chemical sympathectomy with guanethidine.

1. The internal genital organs of prepubertal, 21-day old male Wistar rats were sympathectomized by ip injection of guanethidine (G), at doses of 5 mg/kg per day (N = 10) or 10 mg/kg per day (N = 10), for 20 days. Controls (N = 10) received saline. 2. Plasma testosterone level (measured by radioimmunoassay) decreased significantly in sympathectomized rats from 4.11 +/- 0.57 to 1.76 +/- 0.37 ng/ml (5 mg/kg G) and to 1.17 +/- 0.26 ng/ml (10 mg/kg G). Plasma levels of luteinizing and follicle-stimulating hormones and of prolactin were unaltered. 3. Chemical denervation caused a significant decrease in ventral prostate wet weight from 74.3 +/- 5.5 to 59.3 +/- 4.7 mg (5 mg/kg G) and to 54.6 +/- 4.1 mg (10 mg/kg G) and in seminal vesicle wet weight from 36.5 +/- 6.8 to 31.7 +/- 5.2 mg (5 mg/kg G) and to 21.3 +/- 1.6 mg (10 mg/kg G). 4. The potential secretory activity of the prostate (measured in terms of fructose content) decreased significantly in guanethidine-treated rats from 0.38 +/- 0.02 to 0.30 +/- 0.02 mg/g (5 mg/kg G) and to 0.20 +/- 0.02 mg/g (10 mg/kg G). The seminal vesicle fructose content (0.33 +/- 0.04 mg/g for controls), however, was not altered by chemical denervation. 5. Our data suggested that sympathetic neurons may be involved in the control of LH receptors, at least in the prepubertal phase of sexual development. They may also be directly related to growth and secretory activity of the male accessory sex glands.

Animals↗

PubMed1992

Carotid-aortic and renal baroreceptors mediate the atrial natriuretic peptide release induced by blood volume expansion.

Our previous studies have shown that stimulation of the anteroventral third ventricle (AV3V) region of the brain increases atrial natriuretic peptide (ANP) release, whereas lesions of the AV3V region or median eminence of the tuber cinereum block the release of ANP caused by blood volume expansion. These results suggest that participation of the central nervous system is critical to this response. The role of baroreceptors in the response was evaluated in the current research by studying the response of plasma ANP to blood volume expansion induced by intravenous injection of hypertonic saline solution (0.3 M NaCl, 2 ml/100 g of body weight, over 1 min) in conscious, freely moving male rats. Plasma samples were assayed for ANP by radioimmunoassay. In sham-operated rats, blood volume expansion induced a rapid increase in plasma ANP: the concentration peaked at 5 min and remained elevated at 15 min after saline injection. One week after deafferentation of the carotid-aortic baroreceptors, basal plasma ANP concentrations were highly significantly decreased on comparison with values of sham-operated rats; plasma ANP levels 5 min after blood volume expansion in the deafferented rats were greatly reduced. Unilateral right vagotomy reduced resting levels of plasma ANP but not the response to blood volume expansion; resting concentrations of plasma ANP and responses to expansion were normal in bilaterally vagotomized rats. In rats that had undergone renal deafferentation, resting levels of ANP were normal but the response to blood volume expansion was significantly suppressed. The evidence indicates that afferent impulses via the right vagus nerve may be important under basal conditions, but they are not required for the ANP release induced by blood volume expansion. In contrast, baroreceptor impulses from the carotid-aortic sinus regions and the kidney are important pathways involved in the neuroendocrine control of ANP release. The evidence from these experiments and our previous stimulation and lesion studies indicates that the ANP release in response to volume expansion is mediated by afferent baroreceptor input to the AV3V region, which mediates the increased ANP release via activation of the hypothalamic ANP neuronal system.

Afferent Pathways↗

PubMed1990

Morphometric and biochemical evaluation of rat prostate and seminal vesicle following chemical sympathectomy with guanethidine.

Selective chemical sympathectomy of the internal genital organs of adult male rats was undertaken by chronic treatment with low doses of guanethidine. Biochemical and morphometric methods revealed that removal of sympathetic innervation prevents fructose secretion in the prostate and seminal vesicle, in addition to promoting reduced efficiency of delivery by the latter.

Animals↗

PubMed1990

Effect of clonidine on growth and plasma somatomedin C levels of young rats.

To study the effects of clonidine on growth and plasma somatomedin C (SmC) levels, 42 male Wistar rats aged 28 days and weighing 75 to 105 g were given clonidine (1.5 micrograms/ml in drinking water), or filtered water alone and were weighed weekly. After 0, 4 and 8 weeks, the animals were sacrificed under ether anesthesia, their length was measured and blood was collected by cardiac puncture for measurement of SmC concentration. Growth and the weight/length ratio were lower, and plasma SmC levels (mean +/- SEM) were greater in the treated groups after 4 (616 +/- 44.7 vs 433.2 +/- 39.38 ng/ml, P less than 0.01) and 8 (595.2 +/- 28.3 vs 412.66 +/- 39.01 ng/ml, P less than 0.01) weeks of treatment, suggesting that clonidine treatment increased growth hormone secretion. In other experiments, treated animals showed increased food intake only during the first week of treatment and decreased epididymal fat weight after 3 weeks (1.412 +/- 0.0536 vs 1.6 +/- 0.1336 mg/100 g body weight, P less than 0.01). The results suggest that clonidine acts at the level of the central nervous system involving transitory modulation of food intake, as well as on the regulation of energy metabolism.

Animals↗

PubMed1990

Spermatogenic and steroidogenic testicular function in hypothyroid pubertal rats.

The reproductive system of immature rats is held to be more influenced by thyroid dysfunction than that of adult animals. The effect of hypothyroidism on the spermatogenic process of the rat has not been reported previously. The objective of the present study was to investigate the spermatogenic and steroidogenic functions of pubertal hypothyroid rats. Hypothyroidism was induced by ad libitum ingestion of a 0.05% solution of propylthiouracil for 60 days, and confirmed by reduced plasma thyroxine levels in treated rats. Plasma testosterone level, the histological features of the testis and cauda epididymis and the concentration of spermatozoa stored in the cauda epididymis were unchanged by hypothyroidism.

Animals↗

PubMed1990

Pituitary-testicular axis in benznidazole-treated rats.

Benznidazole is used extensively throughout Latin America as an antiparasitic chemotherapeutic agent against chagasic infection. We have shown that rats chronically treated with 80 mg benznidazole kg-1 day-1 for 30 days present severe testicular atrophy and arrest of spermatogenesis. In the present experiments, plasma levels of testosterone (T), luteinizing hormone (LH), follicle stimulating hormone (FSH) and prolactin (Prl) were investigated in rats receiving 10, 40 and 80 mg benznidazole kg-1 day-1 for 30 days. No significant change in T, LH, or Prl levels was observed in treated rats (P greater than 0.05). Plasma FSH concentration, however, was markedly increased (P less than 0.05) by benznidazole treatment (40 and 80 mg kg-1 day-1) and remained high for 90 days after drug treatment was discontinued.

Animals↗

PubMed1990

Saturnism in the male rat: endocrine effects.

The effect of exposure to lead on endocrine function was studied in pubertal rats treated with 1.0 g/l lead acetate (PbAc) in drinking water for 20 days (subacute group) or 9 months (chronic group) in addition to iv injections of PbAc (0.1 mg/100 g body weight) every 10 (subacute group) or 15 days (chronic group). Although basal levels of testosterone were higher both in the plasma and in the testes of acutely intoxicated animals, the circulating levels of luteinizing hormone (LH) were not affected in either group, nor was the LHRH content of the median eminence. The density of [125I]LH/hCG binding sites in testicular homogenates was reduced by saturnism in both groups. However, the apparent affinity constant of the hormone-receptor complex significantly increased. These data can be viewed as the result of a mixture of specific lead toxicity (e.g., at the enzyme level) with other more general actions (e.g., at the level of the hypothalamus-pituitary-testicular axis).

Animals↗

PubMed1990

The effect of guanethidine-induced denervation of the peripheral sympathetic nervous system on the onset of puberty in female rats.

Intraperitoneal injection of guanethidine (50 mg kg-1 day-1) in newborn rats produces complete and permanent sympathectomy. The present study was performed to evaluate the effect of this form of denervation on the onset of puberty in female rats. Treatment began 7 days after birth and was maintained for 3 weeks. On the 45th day, animals were killed by decapitation and plasma LH and FSH levels were measured. Based on the day of vaginal opening (puberty index), the results show that guanethidine induces a delay in the onset of puberty. The concentrations of LH and FSH in the plasma were not statistically different from those in control rats.

Animals↗

PubMed1989

Role of the hypothalamus in the control of atrial natriuretic peptide release.

Stimulation of the region antero-ventral to the third cerebral ventricle (AV3V) by a cholinergic drug, carbachol, and lesions of the AV3V have been demonstrated in previous studies to either augment or decrease sodium excretion, respectively. Atrial natriuretic peptide (ANP) dramatically increases renal sodium excretion and has been localized to brain areas previously shown to be involved in control of sodium excretion. Consequently, to evaluate a possible role of brain ANP in evoking the changes in renal sodium excretion that follow stimulations or lesions of the AV3V, we determined the effect of injection of carbachol into the AV3V of rats on the concentration of plasma ANP and its content in several neural tissues, the pituitary gland, lungs, and atria. Conversely, the effect of lesions in the AV3V on plasma ANP and the content of the polypeptide in the various organs was determined. Injection of carbachol into the AV3V produced the expected natriuresis, which was accompanied within 20 min by a dramatic rise in the plasma ANP concentration and a rise in ANP content in the medial basal hypothalamus, the neurohypophysis, and particularly the anterior hypophysis but without alterations in the content of ANP in the lungs or the right or left atrium. Conversely, there was a dramatic decline in plasma ANP at both 24 and 120 hr after the AV3V lesions had been placed. This was accompanied by a slight decline in the content of the peptide in the lungs. There was no change in its content in the right atrium at 24 hr after lesions, but there was a significant increase at 120 hr. There was a small decline in the content in the left atrium at 24 hr, followed by a rebound to slightly elevated levels at 120 hr. These small changes contrasted sharply with the dramatic decline in content of the peptide in the medial basal hypothalamus, median eminence, neurohypophysis, choroid plexus, anterior hypophysis, and olfactory bulb. These declines persisted or became greater at 120 hr; except in the olfactory bulb in which the decline was no longer significant. The dramatic increase in plasma ANP after carbachol stimulation of the AV3V that was accompanied by marked elevations in content of the peptide in basal hypothalamus and neuro- and adenohypophysis suggests that the natriuresis resulting from this stimulation is brought about at least in part by release of ANP from the brain. Conversely, the dramatic decline in plasma ANP after AV3V lesions was accompanied by very dramatic declines in content of ANP in these same structures, which suggests that the previously shown decrease in sodium excretion obtained after these lesions may be at least in part due to a decrease in release of ANP from the brain. In view of the much larger quantities of the peptide stored in the atria, it is still possible that changes in atrial release may contribute to the alterations in plasma ANP observed after stimulation or ablation of the AV3V region; however, these results suggest that the dramatic changes in plasma ANP that followed these manipulations may be due to altered release of the peptide from brain structures as well as the atria and lungs.

Animals↗

PubMed1989

Effect of adenosine on gonadotropin and prolactin secretion by hemipituitaries in vitro.

Incubation of hemipituitaries from male rats (200-220 g) with 10 nM to 1 microM adenosine induced a dose-dependent decrease of the release of luteinizing hormone (LH) and follicle stimulating hormone (FSH) into the medium, and increased prolactin (PRL) secretion. The effects of 10 nM adenosine were blocked by 100 nM caffeine, whereas 100 nM caffeine alone had no effect on the release of the hormones. Preincubation of hemipituitaries with 1 microM adenosine also inhibited 10 nM luteinizing hormone-releasing hormone (LHRH)-induced LH and FSH release by greater than 90%. These data indicate a regulatory role for adenosine in pituitary LH, FSH and PRL release, and also a possible modulatory effect of adenosine on the LHRH-LH and FSH system.

Adenosine↗

PubMed1989

Testes alterations in pubertal benznidazole-treated rats.

To determine the side effects of benznidazole, an antiparasitic chemotherapeutic agent against chagasic infection, rats were treated with 80 mg benznidazole kg-1 day-1, p.o., for 30 days, while controls received the vehicle. Treated animals developed severe testicular atrophy (0.25 +/- 0.02 g/100 g vs 0.44 +/- 0.02 g/100 g for the controls), though plasma testosterone level, relative weight of seminal vesicles and prostate were similar to those of the controls. Histological examination of the testes revealed a statistically significant alteration in the spermatogenic process with a marked decrease in the frequency of meiosis, number of tubular sections with mature spermatids and depletion of germinal epithelium.

Animals↗