RESUMO
Brain infarction was induced in rats by injection of microspheres through the right internal carotid artery, and structural changes in the astrocytes were observed during the early period following the infarction. Necrotic foci, varying in size and shape, were found in the right hemisphere. After immunohistochemical staining for GFAP, GFAP-positive astrocytes in the perinecrotic area known as the ischemic penumbra had distinctly increased in number and size with elongation of cytoplasmic processes 3 days after infarction. Electron microscopic observation revealed that glycogen granules had markedly accumulated in the cytoplasm of astrocytes located in the ischemic penumbra 3 and 5 days after infarction. Seven days after infarction, however, the glycogen granules disappeared from the astrocytes. Intermediate filaments increasingly appeared in the protoplasmic astrocytes after 3 days and were abundant in the activated and hypertrophied astrocytes after 7 days. As a result of our present study, we conclude that: (1) the function of glucose uptake from blood vessels was not impaired in the astrocytes under hypoxic conditions; (2) the astrocytes actively ingested blood glucose through the endothelial cells and accumulated it as glycogen for activation of their functions, and the cell volume increased under hypoxic conditions; (3) the depression of energy metabolism and the decrease in the uptake of energy sources in the nerve cells promoted glycogen accumulation in the astrocytes under hypoxic conditions; (4) intermediate filaments (GFAP filaments) increased in number, coincident with the activation and enlargement of the astrocytes; and (5) protoplasmic astrocytes were transformed into fibrous astrocytes in the ischemic penumbra of the brain infarction.
Assuntos
Astrócitos/patologia , Infarto Encefálico/patologia , Isquemia Encefálica/patologia , Encéfalo/patologia , Gliose/patologia , Glicogênio/ultraestrutura , Animais , Astrócitos/metabolismo , Astrócitos/ultraestrutura , Encéfalo/fisiopatologia , Encéfalo/ultraestrutura , Infarto Encefálico/metabolismo , Infarto Encefálico/fisiopatologia , Isquemia Encefálica/metabolismo , Isquemia Encefálica/fisiopatologia , Proteína Glial Fibrilar Ácida/metabolismo , Gliose/metabolismo , Gliose/fisiopatologia , Glicogênio/metabolismo , Imuno-Histoquímica , Masculino , Microscopia Eletrônica , Neurônios/metabolismo , Neurônios/patologia , Ratos , Ratos WistarRESUMO
We isolated a rat homolog of thromboxane (TX) synthase cDNA (-1.8 kb) from the kidney with a fragment of human TX synthase cDNA amplified by polymerase chain reaction with placenta cDNA as a template. Northern blot analysis has shown that rat TX synthase gene is expressed abundantly in lung, liver, and uterus; moderately in kidney. TX synthase mRNA expression was up-regulated in hydronephrotic kidney made by ureter ligation. In conclusion, we have revealed the structure of rat kidney TX synthase. Up-regulation of renal TX synthase, which may cause stimulation of TX synthesis, is possibly implicated in the tissue injury in hydronephrotic kidney.
Assuntos
Clonagem Molecular , DNA Complementar/genética , Regulação da Expressão Gênica , Hidronefrose/enzimologia , Rim/enzimologia , Tromboxano-A Sintase/genética , Sequência de Aminoácidos , Animais , Sequência de Bases , Northern Blotting , Feminino , Humanos , Dados de Sequência Molecular , Placenta/química , Reação em Cadeia da Polimerase , RNA Mensageiro/análise , RNA Mensageiro/biossíntese , Ratos , Ratos Sprague-Dawley , Tromboxano-A Sintase/químicaRESUMO
Thromboxane A2 plays physiological and pathophysiological roles in many tissues. We isolated a cDNA for rat thromboxane synthase from the kidney and here show the location of rat thromboxane synthase gene (Tbxas) on rat chromosome 4q21-->q22 by fluorescence in situ hybridization to metaphase chromatin of rat lymphocytes.
Assuntos
Mapeamento Cromossômico , Tromboxano-A Sintase/genética , Animais , Sequência de Bases , DNA Complementar , Humanos , Hibridização in Situ Fluorescente , Dados de Sequência Molecular , RatosRESUMO
We have reported two isoformes of rat prostaglandin EP3 receptor with their different carboxyl-terminal tails (rEP3A and rEP3B receptors), which are derived by alternative RNA splicing, and both receptors have been shown to be localized to renal distal tubules. In the present study, we characterized the signal transduction system of rat kidney EP3 receptors either in a renal cell line mimicking renal distal tubule cells, TKC2, or in COS-7 cells by functional expression of these receptors. We also examined the chromosomal localization of the EP3 receptor gene by fluorescence in situ hybridization (FISH). In TKC2 cells, vasopressin (AVP, 10(-7) M), prostaglandin (PG) E2 (10(-7) M), or forskolin (10(-8) M) markedly stimulated cyclic AMP formation. Overexpression of the rEP3A receptor significantly attenuated the AVP-, PGE2- or forskolin-induced cyclic AMP formation, whereas there was no change with rEP3B receptor expression. On the other hand, in COS-7 cells transfected with rEP3A receptor cDNA, PGE2 (10(-7) M) did not affect cytosolic free calcium concentration ([Ca2+]i), whereas transfection of rEP3B receptor cDNA evoked PGE2-induced increases in [Ca2+]i. Moreover, we have revealed that the rEP3 receptor gene is localized to rat chromosome 2q44-45. In conclusion, rEP3A or rEP3B receptor is suggested as a mediator of the natriuretic/diuretic action of PGE2 in renal distal tubules via a decrease in cyclic AMP formation or an increase in [Ca2+]i, respectively. Information of the gene assignment of rat EP3 receptor to rat chromosome 2q44-45 is useful for further analysis of the role of EP3 receptor in genetically hypertensive rat models.
Assuntos
Alprostadil/análogos & derivados , Rim/metabolismo , Receptores de Prostaglandina E/genética , Alprostadil/metabolismo , Animais , Cálcio/metabolismo , Linhagem Celular , Mapeamento Cromossômico , AMP Cíclico/metabolismo , Hibridização In Situ , Rim/ultraestrutura , Camundongos , Camundongos Transgênicos , Ratos , Receptores de Prostaglandina E/metabolismo , Sistemas do Segundo Mensageiro/fisiologiaRESUMO
Thromboxane plays physiological and pathophysiological roles in many tissues. Recently, we cloned a cDNA for rat kidney thromboxane receptor (Tbxa2r) and showed that Tbxa2r is expressed in the renal glomerulus, vasculature, and transitional cell epithelium of renal pelvis. Here, we map the gene for this receptor (Tbxa2r) to rat chromosome 7q11 by fluorescence in situ hybridization.
Assuntos
Ratos/genética , Receptores de Tromboxanos/genética , Animais , Células Cultivadas , Mapeamento Cromossômico , DNA Complementar/genética , Hibridização in Situ Fluorescente , Linfócitos/ultraestruturaRESUMO
1. The effects of prolonged chlorothiazide treatment of left ventricular failure on cardiac hypertrophy, circulating vasoactive hormones and exchangeable body sodium were examined in rats with chronic myocardial infarction induced by left coronary artery ligation. Chlorothiazide therapy commenced either immediately or 2 weeks after infarction. For 4 weeks, the rats were given either chlorothiazide (50 mg day-1 kg-1) in their drinking water or drinking water alone. 2. Cardiac weight increased in untreated rats with infarction in comparison with sham-operated controls, indicating the presence of chronic left ventricular dysfunction, although exchangeable body sodium, plasma renin activity, plasma vasopressin and plasma osmolality remained unchanged. 3. Chlorothiazide raised haematocrit and plasma renin activity equally in rats with and without infarction, although exchangeable body sodium, plasma vasopressin and plasma osmolality were not changed by the treatment. Plasma atrial natriuretic peptide was 2-fold higher in rats with infarction and this response was not affected by chlorothiazide treatment. Chlorothiazide therapy did not prevent or reverse cardiac hypertrophy. 4. Chronic diuretic therapy in this experimental model of heart failure did not reduce extracellular sodium, plasma vasopressin or the extent of ventricular hypertrophy, possibly because the condition was associated with activation of the renin-angiotensin system.
Assuntos
Clorotiazida/farmacologia , Diuréticos/farmacologia , Infarto do Miocárdio/tratamento farmacológico , Sulfonamidas , Disfunção Ventricular Esquerda/tratamento farmacológico , Animais , Arginina Vasopressina/metabolismo , Fator Natriurético Atrial/metabolismo , Cardiomegalia/patologia , Doença Crônica , Feminino , Infarto do Miocárdio/metabolismo , Infarto do Miocárdio/patologia , Miocárdio/patologia , Tamanho do Órgão , Ratos , Ratos Wistar , Fatores de Tempo , Disfunção Ventricular Esquerda/metabolismo , Disfunção Ventricular Esquerda/patologiaRESUMO
We have reported the isolation of a rat cDNA for MDCK-type chloride channel (RKCL) which is expressed in many tissues including the kidney. In the present study, intrarenal expression distribution of RKCL mRNA and the effect of dehydration on its expression were examined. In situ hybridization showed that RKCL mRNA is more abundantly expressed in the renal medulla and papilla than in the cortex. Reverse transcription and polymerase chain reaction using microdissected nephron segments showed that RKCL mRNA is expressed in several nephron segments, notably the ascending thin limb of Henle's loop and inner medullary collecting duct. Under dehydration, renal RKCL mRNA expression level was not significantly changed for 5 days. In conclusion, RKCL mRNA is expressed in most nephron segments, playing a role in the renal tubular chloride ion homeostasis.
Assuntos
Canais de Cloreto/biossíntese , Rim/metabolismo , RNA Mensageiro/biossíntese , Animais , Northern Blotting , Citosol/metabolismo , Homeostase/fisiologia , Hibridização In Situ , Técnicas In Vitro , Medula Renal/metabolismo , Reação em Cadeia da Polimerase , Ratos , Ratos Sprague-DawleyRESUMO
Thromboxane (TX) plays important roles in control of renal hemodynamics and water and electrolyte metabolism, and is involved in the pathophysiology of many renal diseases. The aim of the present study is to isolate a rat kidney cDNA encoding functional TX receptor, and to reveal its intrarenal expression localization. A clone (rTXR2) was isolated from a rat kidney cDNA library by a homology screening approach. rTXR2 was shown to encode the amino acid sequence containing seven transmembrane spanning domains representing rat (r) TX receptor. The membrane from COS-7 cells transiently transfected with rTXR2 cDNA was shown to be specifically bound by a thromboxane receptor antagonist, SQ29548. Either in Xenopus oocyte expression or in transfected COS-7 cells, rTX receptor was shown to be linked with Ca2+ messenger system. TX receptor-mediated increase in cytosolic Ca2+ was also observed in cultured glomerular mesangial cells. In situ hybridization showed that rTX receptor mRNA was detected in renal glomeruli, smooth muscle cells in renal arterioles, and transitional cell epithelium of renal pelvis. Reverse transcription linked to PCR applied to microdissected nephron segments indicated the presence of rTX receptor mRNA exclusively in the glomerulus. In conclusion, we have cloned a functional rat kidney TX receptor, which is expressed specifically in renal glomerulus, arterial smooth muscle cells, and transitional cell epithelium of renal pelvis. The present study will provide important insights into the etiology and pathophysiology of renal diseases with relation to TX metabolism.
Assuntos
Rim/química , Receptores de Tromboxanos/fisiologia , Sequência de Aminoácidos , Animais , Sequência de Bases , Compostos Bicíclicos Heterocíclicos com Pontes , Cálcio/fisiologia , Linhagem Celular Transformada , Células Cultivadas , Chlorocebus aethiops , Clonagem Molecular , Sequência Consenso , DNA Complementar/genética , Epitélio/metabolismo , Ácidos Graxos Insaturados , Expressão Gênica , Mesângio Glomerular/metabolismo , Humanos , Hidrazinas/metabolismo , Pelve Renal/metabolismo , Camundongos , Dados de Sequência Molecular , Proteínas Musculares/biossíntese , Músculo Liso Vascular/metabolismo , Oócitos , RNA Mensageiro/biossíntese , Ratos , Receptores de Tromboxanos/análise , Receptores de Tromboxanos/genética , Receptores de Tromboxanos/metabolismo , Proteínas Recombinantes de Fusão/biossíntese , Alinhamento de Sequência , Homologia de Sequência de Aminoácidos , Transdução de Sinais , Especificidade da Espécie , Xenopus laevisAssuntos
Ácido 8,11,14-Eicosatrienoico/análogos & derivados , Ácido 8,11,14-Eicosatrienoico/metabolismo , Flavanonas , Músculo Liso Vascular/citologia , Animais , Divisão Celular/efeitos dos fármacos , Epoprostenol/metabolismo , Compostos de Epóxi/metabolismo , Flavonoides/farmacologia , Indometacina/farmacologia , Cetoconazol/farmacologia , Veias Mesentéricas/citologia , Veias Mesentéricas/efeitos dos fármacos , Veias Mesentéricas/metabolismo , Músculo Liso Vascular/efeitos dos fármacos , Músculo Liso Vascular/metabolismo , Piridinas/farmacologia , Ratos , Ratos Endogâmicos SHR , Ratos Sprague-Dawley , Timidina/metabolismoRESUMO
We have cloned two isoforms of rat kidney prostaglandin E2 receptor EP3 subtype (rEP3A and rEP3B), which differ only in their cytosolic carboxyl-terminal tails (30 and 29 amino acids, respectively). The aim is to clarify the functional difference between two rEP3 receptor isoforms by examining formation of adenosine 3',5'-monophosphate (cAMP) and change in cytosolic free calcium ([Ca2+]i) in cultured cells transiently transfected with cloned rEP3A or rEP3B receptor cDNA. In immortalized renal distal tubule cells (TKC2), vasopressin (VP) stimulated cAMP formation, and the cAMP formation was significantly attenuated by a non-peptide VP receptor antagonist, OPC-31260. The VP-induced increase in cAMP formation was also attenuated by over-expression of rEP3A receptor but not that of rEP3B receptor. On the other hand, in COS-7 cells transfected with rEP3B receptor cDNA, PGE2 induced an increase in [Ca2+]i, but no increase in [Ca2+]i was observed in the cells transfected with rEP3A cDNA. In conclusion, rEP3A receptor is suggested to antagonize VP (V2) receptor by inhibiting cAMP formation, whereas rEP3B receptor is linked with Ca2+ messenger system.
Assuntos
Dinoprostona/farmacologia , Rim/metabolismo , Receptores de Prostaglandina E/fisiologia , Animais , Antígenos Transformantes de Poliomavirus/biossíntese , Cálcio/metabolismo , Linhagem Celular , Linhagem Celular Transformada , Chlorocebus aethiops , Clonagem Molecular , AMP Cíclico/metabolismo , Citosol/metabolismo , Dinoprostona/metabolismo , Túbulos Renais Distais/metabolismo , Camundongos , Camundongos Transgênicos , Ratos , Receptores de Prostaglandina E/biossíntese , Proteínas Recombinantes/biossíntese , Proteínas Recombinantes/metabolismo , Transdução de Sinais , Vírus 40 dos Símios/genética , Transfecção , Vasopressinas/farmacologiaRESUMO
Vasopressin (VP) stimulates adenosine 3',5'-monophosphate (cAMP) formation in an immortalized renal tubule cell line, TKC2, which is derived from transgenic mouse harboring temperature-sensitive SV40 T-antigen gene. VP (10(-8) M)-induced cAMP formation was significantly attenuated by either non-peptide vasopressin receptor V1 or V2 subtype antagonist, OPC-21268 (10(-8) and 10(-6) M) or OPC-31260 (10(-8) and 10(-6) M), respectively, and it was completely abolished by combination of both agents (10(-6) M). VP (10(-8) M) also induced an increase in cytosolic free Ca2+ and prostaglandin (PG) E2 synthesis, both of which were significantly inhibited by OPC-21268 (10(-8) M), but not by OPC-31260 (10(-6) M). Either OPC-21268 (10(-8) M), depletion of extracellular Ca2+ or inhibition of cyclooxygenase attenuated both VP-induced PGE2 synthesis and cAMP formation. In conclusion, both V1 and V2 receptors can stimulate cAMP formation. V1 receptor, however, stimulates cAMP formation via Ca(2+)-dependent PGE2 synthesis, whereas V2 receptor may stimulate it directly.
Assuntos
AMP Cíclico/biossíntese , Túbulos Renais/metabolismo , Receptores de Vasopressinas/fisiologia , Vasopressinas/farmacologia , Animais , Antagonistas dos Receptores de Hormônios Antidiuréticos , Antígenos Transformantes de Poliomavirus/genética , Benzazepinas/farmacologia , Cálcio/metabolismo , Linhagem Celular Transformada , Dinoprostona/biossíntese , Indometacina/farmacologia , Túbulos Renais/efeitos dos fármacos , Camundongos , Camundongos Transgênicos , Piperidinas/farmacologia , Quinolonas/farmacologiaRESUMO
The present study was carried out as an approach from intracellular Ca2+ to clarify the preventive effects of a traditional Chinese medicine, Sho-saiko-to (Kampo prescription, TJ-9), against various metabolic disorders during endotoxemia. In this experiment, we estimated the cytosolic-free Ca2+ concentration ([Ca2+]i) in liver single cells using a photonic microscope system. The [Ca2+]i in a single liver cell of endotoxin (6 mg/kg, i.p.)-injected mice was greater at 18 h post-intoxication than that in the control, whereas the administration of endotoxinin to TJ-9 (500 mg/kg/d, p.o.)-pretreated mice resulted in a markedly lower level of [Ca2+]i than that in endotoxin-treated mice. In the mice pretreated with TJ-9, the CA(2+)-ATPase activity in liver plasma membrane 18 h after endotoxin injection was markedly increased as compared to that in the endotoxin-treated mice. By contrast, the Ca(2+)-ATPase activity in liver mitochondria was lower in endotoxemic mice pretreated with TJ-9 than in mice given endotoxin alone. State 3 respiration and the respiratory control index (RCI), which are the parameters of mitochondrial function, were 41% and 35% lower, respectively, in the liver of mice given endotoxin than those levels in the control. However, the levels of state 3 and RCI in endotoxin-TJ-9-treated mice were markedly increased as compared to those of the endotoxin-treated mice. These findings suggest the protective effect of TJ-9 in the damage of liver mitochondrial function in endotoxin-poisoned mice.(ABSTRACT TRUNCATED AT 250 WORDS)
Assuntos
Cálcio/metabolismo , Medicamentos de Ervas Chinesas/farmacologia , Endotoxinas/sangue , Fígado/metabolismo , Animais , ATPases Transportadoras de Cálcio/metabolismo , Membrana Celular/enzimologia , Endotoxinas/toxicidade , Injeções Intraperitoneais , Fígado/citologia , Fígado/enzimologia , Masculino , Camundongos , Microscopia de Fluorescência , Mitocôndrias Hepáticas/efeitos dos fármacos , Mitocôndrias Hepáticas/metabolismoRESUMO
The preventive effects of a traditional Chinese medicine Sho-saiko-to (Kampo prescription, TJ-9) were determined from oxygen toxicity and membrane damage in liver during endotoxemia. The liver lipid peroxide level and xanthine oxidase activity 18 h after administration of endotoxin (6 mg/kg, i.p.) to TJ-9 (500 mg/kg/d, p.o.)-pretreated mice were markedly lower than that in endotoxin-treated mice, whereas the administration of TJ-9 significantly increased superoxide dismutase and glutathione peroxide activities in liver of endotoxin-injected mice. In the mice pretreated with a TJ-9, the levels of alpha-tocopherol and nonprotein SH in liver tissue 18 h after endotoxin injection were markedly increased as compared to those in endotoxin-treated mice. Leakages of acid phosphatase and lactate dehydrogenase isozyme in serum were markedly lower in endotoxin-TJ-9-treated mice than those in mice given endotoxin. The administration of TJ-9 clearly prevented the membrane protein damage arising from endotoxin challenge. Kampo prescription Sho-saiko-to thus appears to protect the liver plasma membrane from injury by free radicals which occur in a tissue ischemic state during endotoxemia.
Assuntos
Anti-Inflamatórios não Esteroides/uso terapêutico , Doença Hepática Induzida por Substâncias e Drogas/prevenção & controle , Medicamentos de Ervas Chinesas/uso terapêutico , Oxigênio/antagonistas & inibidores , Choque Séptico/prevenção & controle , Fosfatase Ácida/sangue , Animais , Membrana Celular/efeitos dos fármacos , Membrana Celular/enzimologia , Membrana Celular/metabolismo , Doença Hepática Induzida por Substâncias e Drogas/patologia , Eletroforese em Gel de Poliacrilamida , Sequestradores de Radicais Livres , Técnicas In Vitro , Isoenzimas , L-Lactato Desidrogenase/sangue , Peróxidos Lipídicos/metabolismo , Fígado/efeitos dos fármacos , Fígado/enzimologia , Masculino , Camundongos , Camundongos Endogâmicos , Oxigênio/toxicidade , Choque Séptico/patologia , Compostos de Sulfidrila/metabolismo , Vitamina E/metabolismoRESUMO
The present study describes the activity of Ca(2+)-ATPase in liver plasma membrane and cytosolic-free Ca2+ concentration ([Ca2+]i) in an individual vital cell in mouse liver 18 h after endotoxin administration. Ca(2+)-ATPase activity in liver plasma membrane in the poisoned mice was markedly decreased to 28% of that in the control. The membrane protein damage in liver was found mostly in the molecular weight (M.W.) regions near 60,000-150,000 in endotoxemic mice, and was markedly injured near 140,000 (M. W. of Ca(2+)-ATPase in liver plasma membrane). The level of [Ca2+]i in liver cells in endotoxin-poisoned mice was greater at 18 h postintoxication than that of the control. These findings suggest the possibility that the depression of Ca(2+)-ATPase activity in liver plasma membrane in mice may contribute to membrane damage caused by the endotoxin, and that the increase of [Ca2+]i in liver cytoplasm may partially explain various endotoxin-induced metabolic disorders.
Assuntos
ATPases Transportadoras de Cálcio/metabolismo , Cálcio/metabolismo , Endotoxinas/farmacologia , Fígado/metabolismo , Salmonella typhimurium , Animais , Membrana Celular/efeitos dos fármacos , Membrana Celular/enzimologia , Citosol/efeitos dos fármacos , Citosol/metabolismo , Eletroforese em Gel de Poliacrilamida , Fígado/efeitos dos fármacos , Fígado/enzimologia , Masculino , Camundongos , Camundongos Endogâmicos , Peso MolecularRESUMO
We investigated the age-related changes of renal cytochrome P450-dependent arachidonic acid metabolism in 3-, 5-, 7-, 9-, 11-, 13- and 20-week-old male Dahl salt-sensitive (DS) and -resistant (DR) rats on a low sodium diet (0.3% NaCl). NADPH-dependent arachidonic acid metabolism was separated and measured by a radio-HPLC system. The formation of 19-hydroxyeicosatetraenoic acid (HETE), 20 HETE, 1,20-dioic acid, epoxyeicosatrienoic acids (EETs), and dihydroxyeicosatrienoic acid (DHET) was age dependent in both DS and DR rats. omega-Hydroxylase (20-HETE and 1,20-dioic acid formation) and (omega-1)-hydroxylase (19-HETE formation) were increased from 3 to 5 weeks age, then decreased with aging in DR rats. Whilst omega/(omega-1)-hydroxylase activities were increased from 3- to 9-week-old rats, they decreased with aging in DS rats. omega/(omega-1)-Hydroxylase activities were higher in 3-5-week-old DR than DS rats. Epoxygenase activities (EETs and DHET formations) were highest in 3-week-old DS and DR rats, and showed no significant differences between two strains of rats at any ages tested. Renal cytochrome P450-dependent arachidonic acid metabolites have a wide and contrasting spectrum of biological and renal effects, and their relative rates of production may influence not only renal hemodynamics but also pro- and antihypertensive mechanisms of hypertension in Dahl rats.
Assuntos
Envelhecimento/metabolismo , Ácido Araquidônico/metabolismo , Sistema Enzimático do Citocromo P-450/metabolismo , Rim/metabolismo , Animais , Citocromo P-450 CYP2J2 , Citocromo P-450 CYP4A , Resistência a Medicamentos , Hipertensão/etiologia , Hipertensão/metabolismo , Rim/efeitos dos fármacos , Masculino , Oxigenases de Função Mista/metabolismo , Oxigenases/metabolismo , Ratos , Cloreto de Sódio/farmacologiaRESUMO
Cytochrome P450 represents the third metabolic pathway of arachidonic acid giving rise to several biologically active compounds, such as 19-HETE, 20-HETE and EETs and their corresponding DHETs. The kidney is the rich source of these metabolites which have some important biologic actions within the kidney. These metabolites have a wide and contrasting spectrum of biological and renal effects, from vasodilation to vasoconstriction and from inhibition to stimulation of Na-K-ATPase, their relative production rates may influence not only renal hemodynamics but also pro- and anti-hypertensive mechanisms of hypertension. There is increasing evidence that the abnormality of these metabolites in animal models of hypertension. However, sufficient evidence of the physiological and pathophysiological roles of hypertension in man is still lacking.
Assuntos
Ácido Araquidônico/metabolismo , Sistema Enzimático do Citocromo P-450/metabolismo , Hipertensão/enzimologia , Rim/enzimologia , Animais , HumanosRESUMO
The approximate surface development, skin length, and surface area of the left side of the trunk of 51 female students were compared with regard to static and stretched postures. The data for each subject were obtained from geometrical models generated by moiré topography with a computer. When the chest was stretched, the anterior surface, the shoulder line, and the arm-base line were transformed from concave to convex, and a gap oriented toward the nipple widened out. The skin elongated vertically and transversely, except at the side of the waistline, where the skin contracted. The area at the top of the trunk decreased about 25%, while the other parts of the trunk increased 8-15%. The total anterior area was 1.20 m2 for the static posture and 1.29 m2 for the stretched posture. When the posterior surface was stretched, the shoulder line changed from convex to concave, the side line from quasi-straight to concave, and gaps oriented toward the chest line disappeared. The skin elongated most at the infrascapular region (20-35%), while the neck base line contracted (-11%). The center of the back and the lower arm base areas enlarged the most (25%) and the lumbar area enlarged the least (12%). The total posterior area was 1.26 m2 in the static posture and 1.37 m2 in the back-stretched posture. In conclusion, the back skin elongated and enlarged more when stretched than the frontal skin.