Biomedical subjects

J Antunes-Rodrigues

Publications and source records attributed to J Antunes-Rodrigues.

At least 73 records · Page 4Linked to original sources

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↗

PubMed1992

Alterations in the water intake caused by central inhibition of angiotensin-converting enzyme in the rat.

In the present study we investigated the effects of central (i.c.v.) and subcutaneous (s.c.) injections of a 2 micrograms dose of lisinopryl, an inhibitor of angiotensin I(ANGI)-converting enzyme (CE), on water intake. I.c.v. but not s.c. injection of lisinopryl abolished drinking in response to s.c. isoprenaline (100 micrograms/kg) and significantly reduced drinking in response to 24 h water deprivation or s.c. polyethylene glycol (30% w/v, 10 ml/kg). Lisinopryl had no effect on water intake induced by cellular dehydration (s.c. injection of hypertonic saline (2 M NaCl)). These results are consistent with the hypothesis that lisinopryl acts as a CE blocking agent in the brain. The thrist challenge induced by hypotension using isoprenaline acts primarily by generating ANGII systemically and centrally. The other thirst challenges such as cellular dehydration are independent of the ANGII in the brain. This conclusion was made possible by utilizing a new CE blocking agent at a smaller dose than normally used for other ANG I-CE inhibitors.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1992

Role of opioid peptides and subfornical organ in the renal function of intact and hypophysectomized rats.

An inhibitory effect on water, sodium and potassium excretion occurs after both systemic and central injections of morphine, beta-endorphin and other opioid peptides. Some investigators claimed that antidiuretic hormone release could be a mechanism explaining opioid-induced oliguria. Injection into the subfornical organ of a synthetic Met-enkephalin analog (FK 33824) reduced urine outflow as well as renal Na+ and K+ excretion. Identical effects were observed in hypophysectomized or in median eminence-lesioned rats. In addition, no changes were seen in blood pressure after FK 33824 injection into the subfornical organ. These results suggest that opioid stimulation of this structure induces an inhibitory effect on renal water, Na+ and K+ excretion, and that antidiuretic hormone release is probably not important to these phenomena.

Animals↗

PubMed1992

Opiate activation suppresses the drinking, pressor and natriuretic responses induced by cholinergic stimulation of the medial septal area.

The present study investigates the participation and interaction between cholinergic and opiate receptors of the medial septal area (MSA) in the regulation of Na+, K+ and water excretion, drinking and blood pressure regulation. Male Holtzman rats were implanted with stainless steel cannulae opening into the MSA. Na+, K+ and water excretion, water intake and blood pressure were measured after injection of carbachol (cholinergic agonist), FK-33824 (an opiate agonist) + carbachol or naloxone (an opiate antagonist) + carbachol into MSA. Carbachol (0.5 or 2.0 nmol) induced an increase in Na+ and K+ excretion, water intake and blood pressure and reduced the urinary volume. FK-33824 reduced the urinary volume and Na+ and K+ excretion. Previous injection of FK-33824 (100 ng) into the MSA blocked the increases in Na+ and K+ excretion, water intake and blood pressure induced by carbachol. Naloxone (10 micrograms) produced no changes in the effect of 2.0 nmol carbachol, but potentiated the natriuretic effect induced by 0.5 nmol dose of carbachol. These data show an inhibitory effect of opiate receptors on the changes in cardiovascular, fluid and electrolyte balance induced by cholinergic stimulation of the MSA in rats.

Analysis of Variance↗

PubMed1992

Thyroidectomy blocks stress-induced prolactin rise in rats: role of the central serotonergic system.

Thyroidectomized (TX) adult Wistar male rats and their sham-operated controls were submitted to immobilization stress during forty minutes. Thyroidectomy partially blocks stress-induced prolactin (PRL) secretion. Previous administration of MK 212, a serotonin agonist, reverts this picture. The effect of MK 212 is specifically due to its interaction with 5HT2 receptors, since the injection of LY 53857, a selective blocker of these receptors, 30 min before MK 212, prevents the effect of this serotonin agonist. LY 53857, injected alone, yields a partial blockade of PRL secretion during stress in sham-operated rats. TX rats receiving LY 53857 or saline have comparable low values of plasma PRL during stress. It is suggested that thyroidectomy disrupts the functional integrity of the central serotonergic pathways involved in the stress-induced PRL rise.

Animals↗

PubMed1992

Brain serotoninergic stimulation reduces the water intake induced by systemic and central beta-adrenergic administration.

1. This study was undertaken to determine if the stimulation of central serotoninergic receptors affects the thirst-inducing action of systemically or intracerebroventricularly (icv) injected isoproterenol. 2. Male Wistar rats weighing 220-300 g were used in groups of 10-14 animals each. Normally hydrated rats implanted with a delay cannula into the third ventricle were injected icv with the 5HT1C/5HT2 agonist MK212 (50 nmol/2 microliters) prior to administration of isoproterenol sc (330 micrograms/kg body weight) or icv (10 and 25 and 50 micrograms/2 microliters). 3. Icv injections of MK212 reduced the water intake induced by isoproterenol injected systemically (56%) and by the two lowest doses of isoproterenol injected icv (76 and 86%, respectively). 4. The results suggest that the central serotoninergic system modulates the central beta-adrenergic system involved in water intake. 5. Taken together with previous results showing that the activation of 5HT1C/5HT2 receptors promotes a reduction of the dipsogenic response evoked by water deprivation or by icv injection of angiotensin II or carbachol, the present data suggest that the central serotoninergic system plays a ubiquitous role in the modulation of water intake behavior.

Adrenergic beta-Agonists↗

PubMed1991

Lesions of the hypothalamus and pituitary inhibit volume-expansion-induced release of atrial natriuretic peptide.

Expansion of the blood volume causes a release of atrial natriuretic peptide (ANP) that is believed to be important in induction of the subsequent natriuresis and diuresis which, in turn, acts to reduce the increase in blood volume. Since stimulation of the anteroventral portion of the third cerebral ventricle (AV3V) induced a rapid elevation of plasma ANP, whereas lesions of the AV3V were followed by a marked decline in plasma concentration of the peptide, we hypothesized that release of ANP from the brain ANP neuronal system might be important to the control of plasma ANP. The perikarya of the ANP-containing neurons are densely distributed in the AV3V and their axons project to the median eminence and neural lobe. To test the hypothesis that these neurons are involved in volume-expansion-induced ANP release, by using electrolysis we destroyed the AV3V, the site of the perikarya, in male rats. Other lesions were made in the median eminence and posterior pituitary, sites of termination of the axons of these neurons, and also hypophysectomy was performed in other animals. In conscious freely moving animals, volume expansion and stimulation of postulated sodium receptors in the hypothalamus were induced by injection of hypertonic NaCl solution [0.5 or 0.3 M NaCl; 2 ml/100 g (body weight)]. Volume expansion alone was induced with the same volume of an isotonic solution (NaCl or glucose). In the sham-operated rats, volume expansion with hypertonic or isotonic solutions caused equivalent rapid increases in plasma ANP that peaked at 5 min and returned nearly to control values by 15 min. Lesions caused a decrease in the initial levels of plasma ANP on comparison with values from the sham-operated rats, and each type of lesion induced a highly significant suppression of the response to volume expansion on testing 1-5 days after lesions were made. Because a common denominator of the lesions was elimination of the brain ANP neuronal system, these results suggest that the brain ANP plays an important role in the mediation of the release of ANP that occurs after volume expansion. Since the content of ANP in this system is much less than that in the atria, there must be a remarkable increase in synthesis and release of brain ANP associated with this stimulus. It is also possible that blockade of volume-expansion-induced release of other neurohypophyseal hormones, such as endothelin, may block release of ANP from atrial myocytes. It is probable that volume expansion detected by stretch of atrial and carotid-aortic baroreceptors causes afferent input to the brain ANP system, thereby causing increased release of the peptide from the median eminence and neural lobe. Our results emphasize the importance of brain ANP to the control of ANP release to the blood.

Animals↗

PubMed1991

Natriuresis, not seizures, induced by cholinergic stimulation of the locus coeruleus is affected by forebrain lesions and water deprivation.

Two groups of rats with electrolytic lesions of the medial and upper septal area (MUL) or, alternatively, of the anteroventral portion of the third ventricle (AV3V) and a third group of sham-operated rats were water loaded and received three carbachol injections into the locus coeruleus according to the following schedule: 1) prelesion, 2) on the second postlesion day and 3) on the seventh postlesion day. Both MUL and AV3V lesions inhibited the carbachol-induced natriuresis on the second postlesion day. Recovery was almost complete after MUL but not after AV3V lesion on the seventh day. Water deprivation also reduced the carbachol-induced natriuresis but passive hydration of AV3V animals did not avoid the impairment induced by the lesion. Transient seizure phenomena such as clonic convulsions, salivation and analgesia subsequent to carbachol injection were not altered by the lesions.

Animals↗

PubMed1991

Role of central beta-adrenoceptors on stress-induced prolactin release in rats.

Adult Wistar male rats underwent immobilization stress (IS) during forty minutes. PRL secretion presented a remarkable increase after 5 minutes, and it was higher than pre-stress values during the entire duration of the experiment. The blockade of beta-1 adrenoceptors by icv injections of practolol did not modify IS-induced PRL release. IPS 339, a selective antagonist of beta-2 adrenoceptors, also injected icv, reduced PRL secretion during stress in a dose dependent fashion. The blockade of PRL secretion due to IPS 339 was reverted by a previous icv administration of salbutamol, a classical beta-2 agonist. The data presented here suggest that central beta-2 adrenoceptors activation is an important step in the control of stress-induced PRL secretion.

Adrenergic beta-Antagonists↗

PubMed1991

Effects of central epinephrine synthesis inhibition on stress-induced prolactin secretion in male rats.

1. The present study was designed to examine the role of central epinephrine pathways in the control of stress-induced prolactin secretion in male adult Wistar rats. 2. Intracerebroventricular administration of two epinephrine synthesis inhibitors, SKF 64139 (5 and 10 micrograms/rat) and LY 134046 (10 and 20 micrograms/rat), 6 h before the onset of immobilization stress blocked prolactin secretion in a dose-dependent manner. Prolactin values before stress were about 4.0 ng/ml and increased to almost 50 ng/ml in the control group. SKF 64139 injection in the higher dose (10 micrograms/rat) induced a complete blockade of the stress-induced prolactin release, whereas partial blockade was observed after the higher dose (20 micrograms/rat) of LY 134046. 3. Salbutamol pretreatment (10 micrograms/rat) completely restored stress-induced prolactin secretion in animals receiving a central injection of both epinephrine synthesis inhibitors under the same conditions as described above. 4. It is suggested that epinephrine pathways in the brain play an important role in the control of prolactin release occurring during immobilization stress.

Albuterol↗

PubMed1991

Participation of the median raphe nucleus and central serotoninergic pathways in the control of water electrolyte excretion.

1. The role of the median raphe nucleus (MRN) and of increased central serotonin (5HT) synthesis/release in the mediation of Na+ excretion (UNaV) and K+ excretion (UKV) and of urine output (UV) was evaluated for 120 min. 2. Male Wistar rats weighing 220-280 g were used in each group of 12-13 animals. The rats implanted with a cannula in the MRN were injected with saline (0.5 microliters) or with 5.0 and 15.0 ng/0.5 microliters kainic acid (KA), an excitatory amino acid (EAA). Another group of rats was injected ip with 200 mg/kg saline or tryptophan, the initial precursor of 5HT synthesis. 3. Injection of both kainic acid and tryptophan led to increased Na+ excretion, but the magnitude and time course were different for each treatment. 4. Both KA doses were effective in increasing UNaV (0.61 +/- 0.08, mean +/- SEM, and 0.95 +/- 0.19 microEq/min, respectively, vs 0.27 +/- 0.04 microEq/min for saline at 60 min). The effect on UKV was statistically significant with the 15.0 ng dose (0.44 +/- 0.05 microEq/min vs 0.25 +/- 0.03 microEq/min for saline) at 20 min. 5. Tryptophan administration caused an initial gradual increase in UNaV which became steady and significant after 60 min (1.02 +/- 0.15 microEq/min vs 0.36 +/- 0.06 microEq/min for saline), as well as an increase in UKV (0.58 +/- 0.06 microEq/min vs 0.26 +/- 0.04 microEq/min for saline) at 60 min and throughout the remainder of the observation period. 6. KA-induced MRN stimulation and systemic tryptophan overload significantly increased UV at 60, 80 and 100 min (30 to 97% above control values).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

Effect of central administration of serotoninergic agonists on electrolyte excretion control.

1. The participation of different central serotoninergic (5HT) receptors in the mediation of Na+ excretion (UNaV), K+ excretion (UKV) and urine output (UV) was evaluated. 2. Male Wistar rats weighing 220-280 g were used in each group of 9-18 animals. The rats were injected intracerebroventricularly (icv) with the 5HT agonists MK212 (1.5, 15.0 and 30.0 micrograms), 8-OH-DPAT (5.0 and 15.0 micrograms), 5HT (2.5, 12.5 and 25.0 micrograms) and DOI (10.0 and 25.0 micrograms). 3. At the lowest MK212 dose, UNaV was significantly reduced (0.18 +/- 0.04 microEq/min vs 0.35 +/- 0.04 microEq/min for saline) at 20 min. At the highest dose, MK212 provoked a significant increase in UNaV (0.60 +/- 0.06 microEq/min vs 0.34 +/- 0.03 microEq/min for saline) at 40 min. UKV values were significantly modified only at the 1.5-micrograms dose (0.18 +/- 0.04 microEq/min vs 0.35 +/- 0.04 microEq/min for saline) at 20 min. 4. Icv injection of 8-OH-DPAT provoked a significant reduction in UNaV (0.16 +/- 0.05 microEq/min vs 0.35 +/- 0.03 microEq/min for saline) and UKV (0.15 +/- 0.05 microEq/min vs 0.34 +/- 0.02 microEq/min for saline) at 40 min both doses. 5. Icv injection of 5HT at the highest dose provoked a significant increase in UNaV (0.92 +/- 0.10 microEq/min vs 0.33 +/- 0.04 microEq/min for saline) and in UKV (0.55 +/- 0.08 microEq/min vs 0.24 +/- 0.07 microEq/min for saline) at 40 min. 6. Icv administration of DOI caused a natriuretic response (0.69 +/- 0.12 microEq/min vs 0.31 +/- 0.04 microEq/min for saline) at 40 min, with no significant effect on UKV.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

Proposal of an experimental model for the study of polycystic ovaries.

In view of the correlation of the circadian system with the estrous cycle in the rat, some investigators have proposed the induction of polycystic ovaries by exposing rats to continuous light. However, there is divergence with respect to time of exposure and light intensity. In the present paper we propose a simple and efficient experimental model for the study of polycystic ovarian physiopathology in rats. Twenty female Wistar rats weighing 200-220 g were initially submitted to a 14-h light/10-h dark cycle. Of the animals with regular estrous cycles, 9 were exposed to continuous light (600 lux) for 74 days (group 1) and 6 remained under the initial lighting conditions. A daily vaginal smear was used as indirect evidence for the changes in the estrous cycle. Plasma gonadotropin measurement and histological ovarian analysis showed that 90% of the animals in group 1 developed cystic follicles with the absence of the corpus luteum, despite the lack of reduction in ovarian weight commonly observed under 24-h lighting. This observation may be explained by the reduced time of stress to which the animals were submitted, since polycystic ovarian development occurred within less than 75 days of continuous exposure to 600-lux light, a time relatively shorter than commonly reported in the literature.

Animals↗

PubMed1990

Natriuresis induced by cholinergic stimulation of the locus coeruleus in the rat.

Carbachol injected into the locus coeruleus (LC) induced a dose-dependent natriuresis in the rat. This natriuresis was maintained above control levels during the 120 min of urine sampling. Seizures and arterial blood pressure increase were also observed but they disappeared within 20 min after carbachol injection. Natriuresis was not obtained with either injections of carbachol outside the LC or with hypertonic solutions injected into the LC. Injection of atropine into the LC blocked the natriuresis induced by carbachol. In summary, our data show that carbachol induces natriuresis by an action on muscarinic receptors located in the LC region.

Animals↗

PubMed1990

Role of substance P in the medial preoptic area in the regulation of gonadotropin and prolactin secretion in normal or orchidectomized rats.

The present studies were designed to evaluate the role of substance P (SP) in the control of the release of luteinizing hormone (LH), follicle stimulating hormone (FSH) and prolactin (PRL). SP was microinjected into the medial preoptic area (MPOA) of conscious, freely moving intact or orchidectomized (ORCX; 21 days post-ORCX) adult male rats. Microinjection of SP into the MPOA induced a significant decrease in plasma LH and FSH concentrations, effects which were accompanied by an elevation in plasma PRL concentration. To examine the participation of endogenously secreted SP in the activity of the MPOA neurons controlling release of these cited pituitary hormones, another study was performed in which either a potent and specific antagonist to SP (D-Pro2, D-Trip7,9-SP; SP-ANT) or an antibody against SP (SP-AB), was injected into the MPOA. SP-ANT and SP-AB both elevated plasma LH, FSH and decreased plasma PRL concentration. These data suggest that endogenous SP within the MPOA exerts an important inhibitory tonus over LH and FSH release and an excitatory tonus over PRL release. In conclusion, SP seems to participate as a neurotransmitter or neuromodulater in the control of LH, FSH and PRL secretion, at least in part, by acting at the level of MPOA, a region in which the neuronal cell bodies that produce LH-releasing hormone and the associated gonadotropin-releasing hormone-associated peptide are located.

Animals↗

PubMed1990

Interaction between cholinergic and opiate receptors of the lateral hypothalamus in the control of renal excretion in rats.

The present study was carried out to investigate the participation and interaction between cholinergic and opiate receptors of the lateral hypothalamus (LH) in the regulation of Na+, K+ and water excretion. Male Holtzman rats were implanted with chronic cerebral cannulas into the LH. Urine was collected over a period of 2 h after injection of carbachol, FK-p33824 + carbachol or naloxone + carbachol into the LH. Carbachol (8 nmol) reduced urinary volume and increased Na+ excretion. Previous injection of FK-33824 (100 ng) into the LH increased the antidiuretic effect of carbachol, but blocked the increase in Na+ excretion and decreased K+ excretion. Naloxone (10 micrograms) produced no changes in the effect of carbachol on renal excretion. These data show an inhibitory effect of opiate receptors on the changes in urinary Na+ and K+ excretion that are induced by cholinergic stimulation of the LH in rats, and a potentiating effect on antidiuresis.

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

Drinking behavior in thyroidectomized rats: effects of central cholinergic stimulation and of water deprivation.

Normally hydrated thyroidectomized (TX) rats stimulated intracerebroventricularly with carbachol and dehydrated TX rats drank significantly smaller volumes of water than their respective controls. This suggests lower central sensitivity to thirst and to drinking behavior induced by both cholinergic activation and extracellular fluid depletion. Dehydrated TX rats excreted a significantly larger urinary volume than the controls, suggesting the existence of changes in the renal mechanisms of water retention. Such changes could be related to a reduction in vasopressin binding sites.

Animals↗