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C R Silva-Netto

Publications and source records attributed to C R Silva-Netto.

At least 19 recordsLinked 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

Renal sodium handling after noradrenergic stimulation of the lateral hypothalamic area in rats.

1. The participation of special nephron segments in the renal control of sodium handling after adrenergic stimulation was investigated by determining lithium clearance in groups of 5-12 male Wistar rats (230-300 g) microinjected with noradrenaline into the lateral hypothalamic area (LHA). 2. Microinjection of noradrenaline (12.5 to 100.0 nmol/microliters) into the LHA promoted a significant decrease in proximal sodium reabsorption (controls, 86.5 +/- 1.3; 12.5, 81.4 +/- 2.0; 25.0, 72.6 +/- 2.4; 50.0, 75.4 +/- 1.8 and 100.0, 77.2 +/- 1.7%) and a dose-related increase in distal sodium reabsorption (control, 13.4 +/- 1.6; 12.5, 18.4 +/- 1,25.0, 26.9 +/- 2.9; 50.0, 24.1 +/- 2.7; 100.0, 22.1 +/- 1.9%) with no significant changes in creatinine clearance. Fractional sodium reabsorption after different noradrenaline concentrations was significantly reduced in the proximal nephron sites up to the concentration of 25.0 nmol/microliter. Beyond this concentration, a smaller but progressive increase in fractional sodium reabsorption was observed in the post-proximal segment. 3. These findings suggest an effective participation of proximal and post-proximal nephrons in natriuresis after lateral hypothalamic noradrenergic stimulation.

Analysis of Variance↗
PubMed1991

Renal water handling evaluated by lithium clearance following adrenergic and cholinergic stimulation of the lateral hypothalamic area.

Male Wistar rats weighing 230-300 g were used to characterize the participation of adrenergic and cholinergic receptors of the lateral hypothalamic area (LHA) in the control of renal water excretion. Since stimulation of adrenergic or cholinergic receptors has no effect on glomerular filtration rate, the antidiuresis and significant delay in urinary flow observed after lateral hypothalamic stimulation with carbachol (CCh) (0.036 +/- 0.005 to 0.019 +/- 0.003 microliters min-1 100 g body weight-1) and noradrenaline (Nad) (0.024 +/- 0.005 to 0.025 +/- 0.004 microliters min-1 100 g body weight-1) are secondary to an increase in distal tubular fluid reabsorption (DFR). Data are reported as means +/- SEM for ten rats in each group. Tubular water handling measured by lithium clearance demonstrated that LHA simulation with CCh (2.8 nmol in 1 microliter) and Nad (30.0 nmol in 1 microliter) leads to a significant reduction in proximal water reabsorption (CCh, 93.3 +/- 2.6 to 85.4 +/- 1.4%; Nad, 92.7 +/- 0.9 to 88.6 +/- 1.3%), with a simultaneous and significant increase in fluid reabsorption along the post-proximal nephron segments when compared to control (CNa) (CCh, 6.7 +/- 0.7 to 14.5 +/- 1.1%; Nad, 8.2 +/- 0.8 to 11.4 +/- 1.6%). These effects are blocked by muscarinic (atropine, 5 nmol in 1 microliter) and alpha-1 adrenoceptors (prazosin, 4 nmol in 1 microliter) antagonists. The results indicate the effective participation of the post-proximal nephron in the antidiuresis occurring after cholinergic and adrenergic LHA stimulation.

Animals↗
PubMed1990

Effects of injection of selective adrenergic receptor antagonists into the lateral hypothalamic area on renal function.

Studies were undertaken to characterize the participation of specific alpha-1,alpha-2 and beta adrenoceptors of the lateral hypothalamic area (LHA) in the urinary excretion of sodium and potassium. Alpha-1 and alpha-2 LHA receptors were shown to participate in the regulation of renal sodium and potassium excretion. The effects of noradrenaline microinjection (30 nmol in 1 microliter) into the LHA on urinary sodium excretion (UNaV) are blocked by previous injection of the alpha-1 antagonist prazosin (4 nmol in 1 microliter) from 3.22 +/- 0.25 to 0.59 +/- 0.04 microEq min-1 100 g body weight-1. Pre-injection of yohimbine, an alpha-2 antagonist (4 nmol in 1 microliter), synergistically potentiated the action of noradrenaline on UNaV (3.22 +/- 0.25 to 4.02 +/- 0.27 microEq min-1 100 g body weight-1) and on urinary potassium excretion (UKV) (0.70 +/- 0.08 to 1.15 +/- 0.12 microEq min-1 100 g body weight-1). The beta-adrenergic blockers metoprolol (100 nmol in 1 microliter) and propranolol (100 nmol in 1 microliter) had no synergistic or antagonistic action on the sodium excretion fraction, suggesting that neither of these receptors is present in LHA. Our results indicate that natriuresis occurs even in the absence of changes in glomerular filtration rate and demonstrate an inhibitory natriuretic effect of an alpha-1 blocker (prazosin) injected into the LHA before adrenaline, while an alpha-2 antagonist (yohimbine) yielded a potentiating effect.

Adrenergic alpha-Antagonists↗
PubMed1990

Inhibition of gastric acid secretion by cholinergic stimulation of the lateral hypothalamic area.

Cholinergic stimulation of the lateral hypothalamic area with carbachol (1 microgram in 1 microliter) markedly inhibited gastric acid secretion in the anesthetized rat. Inhibition was blocked by prior micro-injection of atropine (4 micrograms/microliters) into the same brain area and was accompanied by an increased sodium content in the stomach. Muscarinic receptor mediated cholinergic inhibitory influence of the hypothalamus on gastric acid secretion is suggested by these results.

Animals↗
PubMed1990

Inhibition of renal electrolyte excretion by gabaergic pathways of the lateral hypothalamic area.

Injection of gamma amino butyric acid (GABA) into the lateral hypothalamic area of unrestrained conscious rats caused a decrease in renal electrolyte excretion with an increase in urinary flow. When picrotoxin, a specific inhibitor of gabaergic pathways, was administered, a significant increase in renal water and electrolyte excretion occurred. The effect of simultaneous injection of picrotoxin and GABA into the same site indicated that picrotoxin was less potent in reversing the effect induced by GABA than GABA was in reversing the effect of picrotoxin. We conclude that GABA acts directly on the neuronal mechanisms involved in the control of water and electrolyte excretion, perhaps by exerting a tonic inhibitory action on renal electrolyte excretion.

Animals↗
PubMed1990

Participation of opiate pathways in the lateral hypothalamic area in the control of renal electrolyte and water excretion.

Injection of Met-enkephalin (0.05, 0.25 and 0.50 micrograms in 1 microliter) solutions into the lateral hypothalamic area (LHA) of unrestrained and unanesthetized rats caused a significant decrease of sodium (0.39 +/- 0.13 to 0.07 +/- 0.01, P less than 0.05) and potassium (0.61 +/- 0.17 to 0.21 +/- 0.04, P less than 0.05) excretion. When the blocking agent naloxone (0.20 micrograms in 1 microliter) was injected alone, a significant increase of sodium (0.34 +/- 0.04 to 0.96 +/- 0.28, P less than 0.05) and potassium (0.76 +/- 0.13 to 1.72 +/- 0.30, P less than 0.05) excretion was observed. However, a dose-response relationship was not observed. However, when in another experiment naloxone was injected before Met-enkephalin into the same area, reversal of the effect of naloxone occurred, with decreased sodium and potassium excretion. We conclude that the enkephalinergic pathway of the LHA when stimulated with Met-enkephalin plays an inhibitory role in the control of sodium and potassium excretion.

Animals↗
PubMed1988

Influence of age on the production of rat spermatozoa, on their concentration in the cauda epididymidis, and on FSH, LH and testosterone plasma levels.

Testis samples were taken from young (3 months), middle-aged (12 months) and aged (24 months) male rats, processed, stained and examined via a light microscope. There were no prominent abnormal germinal epithelium and interstitial tissue. However, the aging process promoted a significant decrease in the mean amount of spermatids 19 per cross tubular section, and in the amount of Sertoli cells per cross tubular section in 24-month-old rats. The concentration of spermatozoa in the cauda epididymidis showed a gradual decrease from 3 to 12 and 24 months. After hCG injection all groups of animals exhibited an increase in plasma testosterone level, although the response was smaller in 12- and 24-month animals compared to the young mature (3 months) ones.

Aging↗
PubMed1986

Cholinergic stimulation of the hypothalamus and natriuresis in rats: role of the renal nerves.

The role of the renal nerves in the natriuresis seen after cholinergic stimulation of the hypothalamus was studied in anesthetized rats treated with injection into the lateral hypothalamus (LH) of 1 microgram of carbamylcholine chloride (carbachol) in 1 microliter of 0.15 M NaCl or NaCl alone. Injection of carbachol exhibited diuresis and natriuresis both in acutely denervated kidneys (P less than 0.01) and in contralateral innervated kidneys (P less than 0.01) without changes in glomerular filtration rate (GFR) or renal plasma flow (RPF) (n = 10). Salt and water excretion was unchanged in 10 rats after injection of NaCl. Micropuncture studies in denervated kidneys showed that, after carbachol injection, tubular fluid-to-plasma inulin concentration ratio [(F/P)In] in the late proximal tubule fell from 1.86 +/- 0.08 to 1.64 +/- 0.07 (P less than 0.01) without changes in single-nephron GFR. In nine other carbachol-treated rats in which renal perfusion pressure was maintained low and constant, diuresis and natriuresis, although attenuated, were again observed both in denervated (P less than 0.01) and in contralateral innervated kidneys (P less than 0.05). In another group of 11 animals, efferent renal nerve activity (ERNA) was recorded before and after LH injection of carbachol and isotonic saline. ERNA was significantly depressed for 30 min, only after carbachol injection. Our results suggest that the renal nerves, although involved, are not essential for the natriuretic response after cholinergic stimulation of LH. By exclusion, other factors, presumably hormones, must contribute to the response.

Animals↗
PubMed1985

Role of renal nerves in maintaining sodium balance in unrestrained conscious rats.

This study was designed to investigate the effects of bilateral renal denervation on sodium and water balance, the renin-angiotensin system, and systemic blood pressure in unrestrained conscious rats maintained on a normal- or low-sodium diet. Renal denervation was proven by chemical and functional tests. Both bilaterally denervated rats (n = 18) and sham-denervated rats (n = 15) maintained positive sodium balance while on a normal sodium intake. Both groups were in negative sodium balance for 1 day after dietary sodium restriction was instituted but were in positive sodium balance for the following 9 days. Systolic blood pressure was higher in sham-denervated (115 +/- 3 mmHg) than in denervated rats (102 +/- 3 mmHg) while on a normal diet (P less than 0.05) and remained so during sodium restriction. Plasma renin concentration (PRC) and plasma aldosterone concentration (PAC) were significantly diminished in the denervated rats during normal sodium intake (P less than 0.05). After dietary sodium restriction, PRC increased in both groups but remained significantly lower in the denervated rats (P less than 0.05). Following dietary sodium restriction, PAC also increased significantly to levels that were similar in both groups of rats. These results demonstrate that awake unrestrained growing rats can maintain positive sodium balance on a low sodium intake even in the absence of the renal nerves. However, efferent renal nerve activity influenced plasma renin activity in these animals.

Aldosterone↗
PubMed1985

Study of sodium and potassium excretion after renal denervation and cholinergic stimulation of the lateral hypothalamic area of the rat.

Studies were undertaken to characterize the renal responses to acute unilateral renal denervation and chronic bilateral denervated kidneys after cholinergic stimulation of the anterior part of the lateral hypothalamus. Denervation was produced in anesthetized and conscious nondiuretic rats by application of phenol to the renal artery. Studies were also performed in sham denervated rats. Whole kidney function in anesthetized animals showed a significant increase of fractional sodium excretion (0.7 +/- 0.1 to 1.7 +/- 0.4%, P less than 0.01) both in the denervated and in the innervated kidney (0.09 +/- 0.02 to 1.1 +/- 0.2%, P less than 0.005) after carbachol injection into the LHA, whereas the percentage of filtered potassium excreted increased only in the innervated kidney (11.4 +/- 1.3 to 16.3 +/- 1.1%, P less than 0.01). Similarly, in conscious rats, fractional sodium excretion increased after cholinergic stimulation in animals having denervated kidneys (2.1 +/- 0.1 vs 3.6 +/- 0.2%, P less than 0.005). Fractional potassium excretion also increased both in rats with sham-denervated and denervated kidney. There was an acute elevation in mean arterial blood pressure and glomerular filtration rate (GFR) during the first 20-min after carbachol injection. Sodium excretion was statistically significant during the three 20-min collections of the experimental period. This suggests that the natriuresis is not associated with increased arterial pressure, GFR or renal plasma flow. Our results indicate that natriuresis occurs even in the absence of the renal nerves.

Animals↗
PubMed1984

Interaction between cholinergic and osmolar stimulation of the lateral hypothalamic area (LHA) on sodium and potassium excretion.

Hypotonic and isotonic solutions into the LHA of unrestrained rats caused no alteration in renal water and electrolyte excretion. Similar results were obtained after injecting hypo, iso and hypertonic glucose solutions. On the other hand, a hypertonic NaCl solution produced an increase in natriuresis and kaliuresis immediately after being injected into the LHA. The carbachol elicited an increase in natriuresis and kaliuresis as well as a decrease in urine output in the first urine samples collected after the injection being injected into the LHA. This response was not modified when the same dose of carbachol was injected associated with NaCl or glucose solutions. The observation of a lack of summation between the effects of carbachol and hypertonic NaCl, as well as the maintenance of the natriuretic and kaliuretic effects in response of the injection of the hypertonic solution even in the presence of blocked cholinergic pathways (atropine), suggests a dissociation between the mechanisms activated by the hypertonic solution and the cholinergic stimulation of the LHA.

Animals↗
PubMed1984

Changes in sodium and potassium excretion and urinary volume in rats submitted to hypervitaminosis A.

Hypervitaminosis A induces the following changes in rat kidney: decrease in sodium and potassium excretion and an increase of urinary volume. In order to determine the possible reversibility of these alterations, the authors allowed the hypervitaminotic animal to recover for 30 and 60 days. After a 30-day recovery period for urinary volume, a 20-day recovery period for sodium excretion, and a 10-day recovery period for potassium excretion, the alterations were reverted to normal.

Animals↗
PubMed1983

Identification of pathways involved in the natriuretic, kaliuretic and diuretic responses induced by cholinergic stimulation of the medial septal area (MSA).

Natriuresis, kaliuresis and diuresis have been studied in rats following water loading and cholinergic stimulation in the MSA before and after bilateral electrolitic lesion of the habenula, or medullary stria, or supraoptic nucleus or paraventricular nucleus, or fornix. Carbachol injection in MSA elicited an increase of natriuresis and kaliuresis. These responses were blocked by bilateral electrolytic lesion of the habenula, medullary stria, or supraoptic nucleus but not of the paraventricular nucleus or the fornix. Urinary output plotted as a function of time showed antidiuresis in periods of 20 and 40 minutes after carbachol injection into the MSA. The lesion of the supraoptic nucleus inhibited this antidiuresis and natriuresis. The lesion of the habenula or medullary stria blocked natriuresis but not antidiuresis suggesting an independence between the mechanisms of antidiuretic hormone release and natriuresis regulation. The integrity of the habenula, medullary stria and supraoptic nucleus seems to be important in the mediation of the natriuretic response induced by carbachol injection into the MSA.

Animals↗
PubMed1983

Factors causing natriuresis after hypothalamic injection of a cholinergic drug in rats.

We investigated possible mechanisms for the natriuresis seen after injection of the cholinergic drug carbamylcholine chloride (carbachol) into the lateral hypothalamus of conscious rats. In unrestrained rats injection of 1 microgram of carbachol in 1 microliter of 0.15 M NaCl solution through a permanently implanted cannula produced a significant natriuresis and kaliuresis. Injection of vehicle produced no changes. The same animals were then subjected to bilateral renal denervation (n = 13) or sham denervation (n = 13) and injected with the same solutions 1 wk later. Carbachol injection produced a natriuresis (P less than 0.0001) and a kaliuresis (P less than 0.01) in all animals studied. Both responses were of a magnitude similar to the responses seen before denervation. We studied other rats while awake but restrained, which permitted the performance of clearance studies and blood pressure measurements. Injection of carbachol produced diuresis, natriuresis, and kaliuresis in all rats, with no change in p-aminohippurate clearance and only transient change in inulin clearance. An increase in blood pressure occurred in some but not all rats. The response in rats with bilaterally denervated kidneys (n = 7) was similar to that of rats with innervated kidneys (n = 5). The natriuresis seen after cholinergic stimulation of the hypothalamus in conscious rats is not primarily mediated by inhibition of renal nerve activity and can be dissociated from changes in blood pressure, glomerular filtration rate, and renal plasma flow.

Animals↗
PubMed1981

The control of sodium chloride intake: functional relationship between hypothalamic inhibitory areas and amygdaloid complex stimulating areas.

Sodium chloride intake was studied in rats submitted to different neurosurgical procedures. Intake decreased in animals submitted to bilateral destruction of the basolateral amygdaloid complex, and increased after the same animals were submitted to destruction of the anterior lateral hypothalamus, a procedure which is known to cause increased intake in intact rats. In the reverse experiment, where the anterior lateral hypothalamus was destroyed before the basolateral amygdaloid complex, the effect of increased sodium chloride intake induced by destruction of the hypothalamus overcame the decreased expected upon destruction of the amygdaloid complex. These results permit us to conclude that the hypothalamic areas which inhibit sodium chloride intake predominate over the stimulating areas of the amygdaloid complex in the control of sodium chloride intake.

Amygdala↗
PubMed1980

Hypothalamic stimulation and electrolyte excretion: a micropuncture study.

The anterior part of the lateral hypothalamus was stimulated by injection of carbachol through a stereotaxically implanted cannula in the rat. Re-collection micropuncture experiments showed that this procedure, which leads to diuresis and natriuresis with only transient changes in glomerular filtration rate and renal plasma flow, reduced the TF/P inulin ratio along proximal and distal tubules without significant alteration of single nephron glomerular filtration rate in most experimental groups. Fractional proximal sodium reabsorption was significantly reduced from 0.54 +/- 0.02 to 0.34 +/- 0.05. Treatment with DOCA, vasopressin, and oxytocin caused natriuresis, but additional hypothalamic stimulation (HS) led to further reduction in TF/P inulin ratio and proximal fractional sodium reabsorption from 0.42 +/- 0.03 to 0.33 +/- 0.03. Fluid transport across proximal and distal epithelium was also studied by the split-droplet method. It was markedly reduced in both segments after HS. During hormone treatment only distal segments showed reduction of fluid transport by HS. These experiments indicate that HS caused inhibition of fluid transport in the proximal and distal tubule. This effect was only partly due to the liberation of neurohypophysial hormones, since during their administration an additional effect of HS was still observed.

Animals↗