Concerted action of ANP and dopamine D1-receptor to regulate sodium homeostasis in nephrotic syndrome.

The edema formation in nephrotic syndrome (NS) is associated with a blunted response to atrial natriuretic peptide (ANP). The natriuretic effects of ANP have been related to renal dopamine D1-receptors (D1R). We examined the interaction between ANP and renal D1R in rats with puromycin aminonucleoside-induced NS (PAN-NS). Urinary sodium, cyclic guanosine monophosphate (cGMP) excretion, and D1R protein expression and localization in renal tubules were evaluated in PAN-NS and control rats before and during volume expansion (VE). The effects of zaprinast (phosphodiesterase type 5 inhibitor), alone or in combination with Sch-23390 (D1R antagonist), were examined in both groups. The increased natriuresis and urinary cGMP excretion evoked by acute VE were blunted in PAN-NS despite increased levels of circulating ANP. This was accompanied in PAN-NS by a marked decrease of D1R expression in the renal tubules. Infusion of zaprinast in PAN-NS resulted in increased urinary excretion of cGMP and sodium to similar levels of control rats and increased expression of D1R in the plasma membrane of renal tubular cells. Combined administration of Sch-23390 and zaprinast prevented natriuresis and increased cGMP excretion induced by zaprinast alone. We conclude that D1R may play a major role in the ANP resistance observed in PAN-NS.

Osteoprotegerin and diabetes-associated pathologies.

Osteoprotegerin (OPG) is a member of the tumour necrosis factor receptor superfamily of cytokines which, in spite of being initially described as a strong anti-resorptive factor, has lately been considered as a possible link between bone and vascular disease. In the last few years, several studies have evidenced its close relationship with the development of diabetes. In this review, we analyse the role of OPG in diabetic patients and its links with the most relevant associated diseases such as atherosclerosis, hypertension, endothelial dysfunction and diabetic nephropathy, as well as its connection with related pathologies as fibrosis, obesity and metabolic syndrome.

Involvement of small Ras GTPases and their effectors in chronic renal disease.

The mechanisms involved in the development of renal fibrosis are poorly understood. Small Ras GTPases control cell proliferation, differentiation, cellular growth and apoptosis, with cell-specific expression in the kidney. Cytokines, high glucose medium or advanced glycation end-products activate Ras in different renal cells. Increased Ras activation has been found in experimental tubulointerstitial fibrosis. Transforming growth factor-beta1 (TGF-beta1) and Ras signalling pathways are close related: TGF-beta1 overcomes Ras mitogenic effects, and Ras counteracts TGF-beta signalling. However, Ras activation is also an intracellular signal transduction point for several molecules (e.g. TGF-beta1) involved in kidney damage. Ras isoforms play different roles in regulating extracellular matrix synthesis in fibroblasts and mesangial cells. These data give evidence for a role for Ras in renal fibrosis, but no reviews are available on the role of p21 Ras in this process. Thus, our goal is to review the role of Ras activation and signalling in renal fibrosis.

Effect of ham protein substitution on oxidative stress in older adults.

Mediterranean diet has been related to a low risk of coronary hearth disease. In the present study, we have evaluated the effect of substituting 120 g of meat by 120 g of acorn-fed Iberian ham (one of the meat components of the Mediterranean diet) on body weight, blood pressure (MAP), plasma lipids and oxidant-antioxidant equilibrium in 13 males and 8 females with an average age of 71. Study was performed in three periods: basal diet evaluations (BD1), ham diet for 6 weeks (HD), and basal diet again for 6 weeks (BD2). MAP significantly diminished from 96 mmHg in BD1 to 89 mmHg after HD. After BD2, MAP remained in the same value. Plasma total antioxidant substances increased from 0.791 mmol/L in BD1, to 1.525 in HD, and to 1.213 in BD2. Glutathione reductase significantly increased from 49.5 U/L in BD1 to 57 in HD and decreased to 49.2 in BD2. Glutathione peroxidase rose from 33 U/gHb in BD1 to 72 in HD and decreased to 52 in BD2. Superoxide dismutase increased from 401 U/gHb in BD1 to 723 in HD and decreased to 433 in BD2. Plasma thiobarbituric acid reacting substances (TBARS) fall from 1.65 mmol/l in BD1 to 1.38 in HD and to 1.47 in BD2. TBARS in erythrocyte membranes also diminished but only in BD2. It can be concluded that including acorn-fed Iberian ham in the diet increased the antioxidant substances and decrease lipid peroxidation, with its subsequent beneficial effects on the atherogenic risk factors.

Cyclosporin effect on rat aorta alpha(1)-adrenoceptors and their transduction mechanisms.

A possible explanation for cyclosporin-induced arterial hypertension may be its action on the adrenergic system. In spite of the controversial results reported in literature, it seems that cyclosporin changes the vascular response to noradrenaline. Therefore, after observation that two cyclosporin doses increase rat blood pressure and vascular reactivity in response to noradrenaline, the aim of this work was to study the cellular mechanisms beside the cyclosporin-induced changes in response to noradrenaline. Therefore, the cyclosporin influence on alpha(1)-adrenoceptors as well as on their transduction mechanism in smooth muscle cells was studied. Through Scatchard analysis of specific [(3)H]-prazosin binding, the alpha(1)-adrenoceptor number and related affinity were studied, before and after cyclosporin exposure. The cyclosporin influence on alpha1-adrenoceptor transduction mechanisms was also evaluated by the quantification of intracellular free calcium contents [Ca2+]i and inositol phosphate (InsP) turnover. All in vitro experiments were performed in rat aortic smooth muscle cells in culture. Results showed that both cyclosporin concentrations (10(-6) and 10(-7) M) changed alpha1-adrenoceptor number but only 10(-7) M cyclosporin increased its affinity for [(3)H]-prazosin. Compared with control cells, only 10(-7) M cyclosporin increased InsP levels. Stimulation by noradrenaline increased InsP in 10(-7) M cyclosporin-treated cells but decreased InsP in the presence of 10(-6) M cyclosporin. Both cyclosporin concentrations increased [Ca2+]i in basal conditions and after noradrenaline stimulation. The results suggest that after noradrenaline stimulation cyclosporin increases [Ca2+]i, probably through different mechanisms, depending on the cyclosporin concentration used. However, 10(-7) M cyclosporin increases alpha1-adrenoceptor affinity and their related transduction mechanisms. The higher cyclosporin concentration (10(-6) M) seems to induce downregulation of alpha1-adrenoceptors, probably by activation of protein kinase C.

Efectos renales de la inhibición crónica de la síntesis de óxido nítrico en ratas cirróticas con ascitis / Renal Effects Chronic Nitric Oxide Synthesis Inhibition In Cirrhotic Rats With Ascites

Estudios previos han demostrado que la inhibición aguda de la síntesis de óxidonítrico (NO) mejora la excreción de agua y sodio y la hipotensión arterial en ratascirróticas con. En este trabajo hemos analizado los efectos renales producidos por el tratamiento crónico (10 días) con aminoguanidina (AG, 100 mg/kg/día), un inhibidor preferente de la sin tasa inducible de NO (iNOS), o con Nw-Nitro-L-Arginina Methyl Ester (L-NAME, 0,5 mg/kg/día), un inhibidor no selectivo de la sintasa de NO, en un modelo experimental de cirrosis hepática y ascitis en ratas (inhalación de tetracloruro de carbono). Las ratas cirróticas no tratadas tenían menor presión arterial media (PAM), diuresis, natriuresis y tasa de filtración glomerular(TFG) y similar flujo sanguíneo renal (FSR) que sus controles. La administración crónica de AG no modificó ninguno de esos parámetros ni en las controles ni en las cirróticas. Sin embargo, el tratamiento crónico con L-NAME normalizó la PAM y aumentó significativamente la diuresis y natriuresis de los animales cirróticos, mientras que en los animales controles los efectos no fueron significativos. Estosdatos indican que la inhibición crónica de la síntesis de óxido nítrico con (..) (AU)

Previous studies have shown that acute inhibition of nitric oxide (NO) synthesis improves sodium and water excretion and increases blood pressure in cirrhotic rats with ascites, thus suggesting that NO is an important factor contributing to the arterial hypotension and sodium retention of liver cirrhosis. In the present work we have analyzed the renal effects derived from the chronic oral treatment(10 days) with amino guanidine (AG, 100 mg/kg/day), a preferential inhibitor of inducible NO synthase (iNOS), or Nw-Nitro-L-Arginine Methyl Ester (L-NAME, 0.5mg/kg/day), a nonselective inhibitor of NOS, in an experimental model of livercirrhosis with ascites (carbon tetrachloride inhalation). Untreated cirrhotic rats showed lower mean arterial pressure (MAP), diuresis, natriuresis and glomerular filtration rate (GFR) and similar renal blood flow (RBF) compared with the (..) (AU)

Renal ischemia in the rat stimulates glomerular nitric oxide synthesis.

Renal ischemia in humans and in experimental animals is associated with a complex and possibly interrelated series of events. In this study, we have investigated the glomerular nitric oxide (NO) production after renal ischemia. Unilateral or bilateral renal ischemia was induced in Wistar rats by clamping one or both renal arteries. NO production was assessed by measuring glomerular production of nitrite, a stable end product of NO catabolism, and NO-dependent glomerular cGMP production and by assessing the glomerular NADPH diaphorase (ND) activity, an enzymatic activity that colocalizes with NO-synthesis activity. Furthermore, we determined the isoform of NO synthase (NOS) implicated in NO synthesis by Western blot and immunohistochemistry. Glomeruli from rats with bilateral ischemia showed elevated glomerular nitrite and cGMP production. Besides, glomeruli from this group of rats showed an increased ND activity, whereas glomeruli from the ischemic and nonischemic rats with unilateral ischemia did not show this increase in nitrite, cGMP, and ND activity. In addition, glomeruli from ischemic kidneys showed an increased expression of endothelial NOS without changes in the inducible isoform. Addition of L-NAME in the drinking water induced a higher increase in the severity of the functional and structural damage in rats with bilateral ischemia than in rats with unilateral ischemia and in sham-operated animals. We can conclude that after renal ischemia, there is an increased glomerular NO synthesis subsequent to an activation of endothelial NOS that plays a protective role in the renal damage induced by ischemia and reperfusion.

[Renal effects of the chronic inhibition of nitric oxide synthesis in cirrhotic rats with ascites]. / Efectos renales de la inhibición crónica de la síntesis de óxido nítrico en ratas cirróticas con ascitis.

Previous studies have shown that acute inhibition of nitric oxide (NO) synthesis improves sodium and water excretion and increases blood pressure in cirrhotic rats with ascites, thus suggesting that NO is an important factor contributing to the arterial hypotension and sodium retention of liver cirrhosis. In the present work we have analyzed the renal effects derived from the chronic oral treatment (10 days) with aminoguanidine (AG, 100 mg/kg/day), a preferential inhibitor of inducible NO synthase (iNOS), or Nw-Nitro-L-Arginine Methyl Ester (L-NAME, 0.5 mg/kg/day), a nonselective inhibitor of NOS, in an experimental model of liver cirrhosis with ascites (carbon tetrachloride inhalation). Untreated cirrhotic rats showed lower mean arterial pressure (MAP), diuresis, natriuresis and glomerular filtration rate (GFR) and similar renal blood flow (RBF) compared with the untreated control rats. Chronic administration of AG did not modify significantly any parameter in cirrhotic and control animals. Conversely, long-term L-NAME administration to cirrhotic rats normalized MAP and significantly increased water and sodium excretion, whereas in control animals these parameters were not significantly modified. These results show that chronic NO synthesis inhibition with L-NAME, but not with aminoguanidine, improves renal perfusion pressure and increases the lower sodium and water excretion of cirrhotic rats with ascites. Thus, an enhanced production of NO is an important factor contributing to the renal sodium and water retention characteristic of liver cirrhosis.

Role of calcium in gentamicin-induced mesangial cell activation.

Gentamicin-induced decreases in glomerular filtration rate have been associated to a marked decline in the glomerular capillary ultrafiltration coefficient which could be due to an active contraction of mesangial cells. In the present work we assessed a possible role of cytosolic Ca2+ as a mediator that leads to contraction and proliferation induced by gentamicin on mesangial cells. Gentamicin (10(-5)M) induced an increase in cytosolic free Ca2+, that was fully inhibited by the calcium channel blocker, verapamil, and by the endoplasmic reticulum calcium release blocker, TMB8. Gentamicin induced a planar surface area reduction in cultured mesangial cells, that was blunted by verapamil and TMB-8. Gentamicin also stimulated [3H]thymidine incorporation into DNA and increased viable cell number, effects that were reduced by both, verapamil and TMB-8. Gentamicin stimulated the expression of the AP1 protein; this expression was partially blunted by verapamil and TMB-8. Moreover, verapamil inhibited gentamicin-induced PAF synthesis from mesangial cells. In summary, gentamicin directly raised intracellular Ca2+ activating both calcium influx from external medium and calcium release from internal stores. This increase is responsible of cellular activation (contraction and proliferation) and PAF synthesis induced by gentamicin on mesangial cells.

Increased apoptosis susceptibility in mesangial cells from spontaneously hypertensive rats.

We have examined the susceptibility to apoptosis in mesangial cells from spontaneously hypertensive rats (SHR) or from normotensive rats (WKY) and the possible involvement of nitric oxide in this process. Mesangial cells monolayers from either SHR or normal rats were incubated for 12 h in medium with or without fetal calf serum (FCS) and with or without thapsigargin (Tg, 10(-6) M). A series of cultures from rats of both groups was treated with N(G)-nitro-l-arginine methyl ester (l-NAME, 10(-4) M). We assessed apoptosis by propidium iodide staining, by TUNEL nitrite production (Griess reaction), by inducible nitric oxide synthase (iNOS) and Bcl-2 and Bax by Western blot. Incubated with a FCS-free medium, cells from SHR showed a significantly higher apoptotic rate (10.7 +/- 2.0) than with 10% FCS (10% FCS, 4.7 +/- 0.3), while WKY cells did not show this increment (10% FCS, 4.7 +/- 0.3; 0% FCS, 5.9 +/- 0. 3). Apoptosis in cells from WKY increased when incubated with thapsigargin in FCS-free medium (0% FCS+ Tg, 17.7 +/- 2.9%) and increased even more in SHR cells (0% FCS+ Tg, 19.7 +/- 2.9%). Treatment with l-NAME decreased thapsigargin-induced apoptosis in both SHR (8.2 +/- 2.4%) and WKY cells (9.3 +/- 2.4%). An increase in nitrite production and iNOS expression was detected in groups in which the apoptosis rate was elevated. A high rate of apoptosis was also associated with a decrease in the Bcl-2/Bax ratio. Our results indicate that in SHR cells, short-term serum deprivation and the increase in intracellular free calcium concentration with thapsigargin are able to enhance the apoptosis rate in primary cultures and that the expression of iNOS, and hence NO production, is involved in this effect.

Unexpected findings of a female team in Xochimilco, Mexico.

This is a reflection about the methodological circumstances that led the author to certain unexpected information during the course of a qualitative approach to the perception of health problems of a group of poor families in the south of Mexico City. Special attention is paid to the influence of the research team composition (four women with different professional backgrounds, ages, marital statuses, and styles of personal interaction) and the psychoanalytic technique that influenced the study. The inclusion of people of different ages, professions, and personality traits proved extremely valuable both as a means of widening the possibilities for empathetic relations between the research group and the population studied and for increasing the shades of meaning that the team was able to capture.

Nitric oxide is involved in apoptosis induced by thapsigargin in rat mesangial cells.

The purpose of this study was to examine the mechanisms of thapsigargin-induced apoptosis in rat glomerular mesangial cells and the possible involvement of nitric oxide (NO) in this process. In mesangial cell monolayers incubated for 12 h in a medium without growth factors and with 10(-6) M thapsigargin, a known specific inhibitor of endoplasmic reticulum Ca(2+)-ATPase, a high percentage of cells showed typical nuclear features of apoptosis, assessed either by staining with propidium iodide (23 vs. 9% in control conditions) or by terminal desoxynucleotidyl transferase-mediated dUTP biotin nick end labelling (TUNEL; 17 vs. 5% in control conditions). When cells were maintained in a medium containing 10% fetal calf serum (FCS) or in a free-calcium medium, the thapsigargin-induced apoptosis rate was very low. In rat mesangial cells treatment with thapsigargin decreased the expression of BCL-2 protein and bcl-2 mRNA, whereas it did not alter the levels of BAX protein or bax mRNA. When mesangial cells were incubated with thapsigargin in the absence of FCS, we detected a significant increase in nitrite production (3.78 +/- 0.96 vs. 1.76 +/- 0.44 micromol/well). Furthermore, the treatment with the NO synthesis inhibitor L-NAME (10(-4) M) induced a significant decrease in the number of apoptotic cells (9%), whereas incubation with the NO donor SIN-1 (10(-5) M) induced a marked increase in the rate of apoptosis (29%). Western and Northern blot analysis of macrophage-type inducible NO synthase (iNOS) demonstrated that thapsigargin treatment induces the expression of the iNOS protein and iNOS mRNA. Treatment with L-NAME prevented the thapsigargin-induced BCL-2 decrease, whereas incubation with SIN-1 potentiated the effect of thapsigargin on BCL-2. Double labelling by immunohistochemistry for iNOS and TUNEL revealed that the same cells that suffered apoptosis were positive for iNOS. In summary, our results indicate that thapsigargin is able to enhance the apoptosis rate of rat mesangial cells by a mechanism that is mediated by an increase in cytosolic free calcium. Increased iNOS expression, and hence increased NO production, seems to be involved in this effect.

Effect of cyclosporin A on rat smooth-muscle cell proliferation.

Cyclosporin A (CsA) is a potent immunosuppressive agent that has significantly improved graft survival in organ- and bone-marrow-transplant recipients. However, in the context of graft transplantation, CsA has been suggested to potentiate vascular disease by stimulating smooth-muscle cell (SMC) proliferation. As previous studies on the effect of CsA on smooth-muscle proliferation have afforded conflicting results, we conducted an in vitro study of the effect of two concentrations of CsA--10(-6) M (corresponding to the maximal concentration in patients) and 10(-7) M (corresponding to trough concentrations)--on cultured rat SMC proliferation, as assessed by [3H]thymidine incorporation into DNA and measuring cell number by a colorimetric method based on the quantitative staining of cell nuclei. In the presence of 0.5% fetal calf serum (FCS), 10(-6) M CsA induced an increase in [3H]thymidine incorporation into DNA (from 614.44 +/- 67.76 to 1,472.6 +/- 177.63 cpm/well; p < 0.05) with no increase in the number of cells. A cytotoxic effect for this dose was ruled out owing to the absence of significant levels of lactate dehydrogenase (LDH) activity in the supernatant. CsA, 10(-7) M, induced an increase in both [3H]thymidine incorporation into DNA (from 614.44 +/- 67.76 to 1,220.91 +/- 145.59 cpm/well) and cell number (82.49 +/- 6.16 to 165.79 +/- 10.48 cells x 10[3]; p < 0.05). In the presence of 10% FCS, the highest CsA concentration increased [3H]thymidine incorporation to 2,115.91 +/- 224.06 cpm/well, with no significant changes in cell number. However, the lowest CsA concentration increased both [3H]thymidine incorporation (to 3.752.58 +/- 525.06 cpm/well) and cell number (to 181.27 +/- 14.2 cells x 10[3]). These findings suggest that the proliferative effect of CsA on SMCs is variable and that it depends on the concentration of the drug, in support of the discordant results reported previously.

Involvement of phospholipase A2 in gentamicin-induced rat mesangial cell activation.

The role of the phospholipase A2 (PLA2) activation in the gentamicin (Gent)-induced rat mesangial cell activation has been studied. Gent (10(-5) M) induced a time-dependent mesangial planar cell surface area reduction that was significantly inhibited by the PLA2 inhibitors aristolochic acid (AA) and quinacrine, by the platelet-activating factor (PAF) blocker BN-52021 (BN), and by verapamil. These substances also inhibited Gent-induced [3H]thymidine incorporation into DNA (AA, 504 +/- 20; quinacrine, 555 +/- 66; BN, 1,126 +/- 120; and verapamil, 896 +/- 109; vs. 1,818 +/- 35 cpm/well in cells treated with Gent alone) and the Gent-induced increase in cell number (AA, 20,116 +/- 2,696; quinacrine, 24,687 +/- 1,481; BN, 26,122 +/- 1,016; and verapamil, 27,566 +/- 1,214; vs. 47,486 +/- 1,124 cells/well in cells treated with Gent alone). Gent induced a twofold increase in [3H]acetate incorporation into PAF (27 +/- 3 vs. 12 +/- 2 cpm/microgram protein in control conditions) that was completely blocked by AA, BN, or verapamil. Gent increased thromboxane B2 and prostaglandin E2 (PGE2) production, with both increases inhibited by either AA or verapamil. BN only inhibited the Gent-induced mesangial PGE2 production. In addition, Gent increased PLA2 activity (measured as [3H]arachiodonic acid release, 29,849 +/- 2,151 vs. 20,104 +/- 2,308 cpm/well in basal conditions), an effect that was blocked by AA (11,804 +/- 684 cpm/well). These data suggest a major role for PLA2 activation in Gent-induced mesangial cell contraction, proliferation and prostanoid secretion.

Gentamicin treatment increases mesangial cell nitric oxide production.

Gentamicin-induced decreases in glomerular filtration rate have been associated with a marked decline in the glomerular capillary ultrafiltration coefficient which could be mediated by mesangial cell contraction. We have assessed a possible role of endogenous nitric oxide (NO) as a modulator of the proliferative and contractile effects of gentamicin on mesangial cells. NO synthesis and release, measured as nitrite production, were increased in the presence of gentamicin; this increase was blocked by coincubation with L-NAME. Mesangial cells treated with gentamicin, but not cells under control conditions, expressed mac-iNOS mRNA and presented positive immunoreactivity for mac-iNOS. Gentamicin induced a reduction of the planar surface area of cultured rat mesangial cells; cell treatment with gentamicin plus L-arginine significantly decreased the contractile effect of gentamicin. Gentamicin increased both [3H]thymidine incorporation into DNA and viable cell number; when L-arginine was added together with gentamicin, this abolished the effect of gentamicin on mesangial cell proliferation. The present studies demonstrate that gentamicin induces the expression of mac-iNOS and produces contraction and proliferation in mesangial cells. These actions seem to be modulated by mesangial NO synthesis and release.

Adenosine activates mesangial cell proliferation.

This study investigates the proliferative effect of adenosine (ADO) in cultured mesangial cells, and the possible mediation of A1 and/or A2 receptors in this proliferative effect of ADO. ADO (10(-5) M) induced a significant increase in the [3H]thymidine incorporation into DNA with respect to quiescent cells. This increase was similar to that obtained with the ADO A1 receptor agonist, R-PIA (10(-5) M), and with the ADO A2 receptor agonist, NECA (10(-5) M). Theophylline (10(-4) M), and ADO receptors inhibitor, completely inhibits the ADO-induced proliferation. The combinations NECA + A2 receptor antagonist, PD 116,948 (AT1, 10(-6) M) and PIA + A2 receptor antagonists, PD 115,199 (AT2, 10(-2) M) did not induce any significant difference with respect to cells maintained in control conditions. These findings demonstrate the proliferative effect of ADO in cultured mesangial cells, and that this effect is not specific to either of A1 or A2 receptors activation.

Effect of hypothalamic-hypophysary inhibitory factor on mesangial cell activation.

We examined the effect of a sodium pump inhibitor isolated from bovine hypothalamus and pituitary tissues on contraction, proliferation, and calcium mobilization in primary cultures of rat mesangial cells. Hypothalamic-hypophysary inhibitory factor (HHIF) inhibited rubidium uptake in a concentration-dependent manner (0.2 U/mL: 56.8 +/- 6.3% inhibition). It also induced a concentration- and time-dependent decrease in planar cell surface area. Maximal contraction (25 +/- 5% reduction in cell size) was reached at 60 minutes with a concentration of 0.2 U/mL. This effect was inhibited by both verapamil and TMB-8 (10(-5) mol/L). HHIF was also observed to increase DNA synthesis (0.2 U/mL: 4361 +/- 168 versus 2129 +/- 162 cpm per well under control conditions) and cell proliferation (0.2 U/mL: 52,290 +/- 1931 versus 10,512 +/- 121 cells per well under control conditions). Both effects were also inhibited by verapamil and TMB-8. Moreover, HHIF induced the expression of immediate early genes c-fos and c-jun mRNA. HHIF-induced effects were accompanied by an increase in cytosolic free calcium (203 +/- 58 versus 101 +/- 2 nmol/L under control conditions), which was inhibited by verapamil and TMB-8. In summary, HHIF induces mesangial cell contraction and proliferation; these effects seem to be mediated by an increase in cytosolic free calcium levels.

[Reflections on a psycho-anthropological approach to population studies]. / Reflexiones a partir de un abordaje psicoantropologico para los estudios de poblacion.

PIP: This work explores the potential complementarity of the sociodemographic, psychoanthropological, and sociopsychoanalytical perspectives for achieving understanding of the individual and familial roots of demographic behavior. Examination of the sociodemographic focus was stimulated and enriched by a 1986 seminar that considered theoretical and methodological problems in the integration of demographic dynamics into social research. Specific questions raised concerned the advantages and shortcomings of attitude and opinion surveys, the specifics of microsocial investigation, and the importance of the family as a mediator between larger social influences and individual behavior. Reflections on the relevance of the psychoanthropological tradition to the problems of microsocial research were influenced by a work published in the mid 1960s by the anthropologist and psychoanalyst Devereux. The affective distancing and unconscious defensive reactions of the investigator must, according to Devereux, be taken into account but also offer rich possibilities for analysis. Devereux also stressed that the study of human behavior occurs in the context of a reciprocal relation between the observer and the observed, with the observed playing a far from passive role. The presence of the observer occasions certain reactions but also is a source of complementary and relevant data for the study of behavior. A third possibility suggested by Devereux is that of approaching the unconscious of the study subjects through examination of the anxiety and other unconscious reactions of the researcher. Interpretative questionnaires, finally, are a tool of the sociopsychoanalytical tradition of potential use in demographic study. Interpretative questionnaires are applied to individuals in order to study personal psychic aspects, but their goal is the study of the socioeconomic and cultural environment that molds the personal characteristics of the respondents.^ieng