ABSTRACT
Hyperadrenocorticism is one of the most common endocrine disorders in dogs. Regarding to the kidneys, chronic hypercortisolemia can cause damage to the glomerulus, and evolve into chronic kidney disease. This study evaluated nine normotensive dogs with pituitary dependent hyperadrenocorticism, before and after therapy with trilostane, during the follow-up period of six months, in order to investigate the development of pathological proteinuria by quantitative (urinary protein-to-creatinine ratio) and qualitative (urinary protein electrophoresis) methods, and also to monitor its intensity over the course of the disease and therapy. The main renal lesion detected in dogs with hyperadrenocorticism was in the tubular segment, evidenced by the prevalence of urinary protein bands of lower molecular weight, indicating the lack absorption of these proteins in the proximal segment of the nephron. Low molecular weight proteins persisted throughout the follow-up. Regarding the future of routine veterinary medical clinic in the care of patients with hyperadrenocorticism, the assessments of proteinuria determinations by the urinary protein-to-creatinin ratio and urinary protein electrophoresis, according to the results obtained in this study, can add more information about the renal damage in these animals, and contribute to the prognosis.(AU)
Hiperadrenocorticismo (HAC) é uma das doenças endócrinas mais comuns em cães. A hipercortisolemia crônica pode causar danos glomerulares, pelo aumento da taxa de filtração glomerular, podendo levar ao desenvolvimento de doença renal crônica. Este estudo avaliou nove cães normotensos com hiperadrenocorticismo hipófise-dependente, antes e após a terapia com trilostano, durante o período de acompanhamento de seis meses, a fim de investigar o desenvolvimento de proteinúria patológica por métodos quantitativo (relação proteína e creatinina urinária) e qualitativos (eletroforese de proteínas urinárias) e também para monitorar a sua intensidade ao longo do curso da doença e terapia. A principal lesão renal detectada em cães com HAC foi no segmento tubular, evidenciada pela prevalência de bandas de proteínas urinárias de peso molecular mais baixo, indicando a falta de absorção destas proteínas no segmento proximal do néfron. A proteinúria de baixo peso molecular persistiu durante todo o acompanhamento. Em relação ao futuro da rotina clínica médica veterinária no tratamento de cães com hiperadrenocorticismo, as avaliações de proteinúria pela relação proteína e creatinina urinária e eletroforese de proteínas urinárias, de acordo com os resultados obtidos neste estudo, podem adicionar mais informações sobre a lesão renal nestes animais e contribuir para o prognóstico.(AU)
Subject(s)
Animals , Dogs , Proteinuria/veterinary , Hydrocortisone/antagonists & inhibitors , Adrenocortical Hyperfunction/veterinary , Electrophoresis/veterinaryABSTRACT
Effect of prolonged administration of substance P on the plasma cortisol level in the albino rats has been investigated. An inhibitory impact on intact individuals and a stimulatory effect in pharmacologically annulled rats has been observed. It is concluded that in normal conditions substance P presumably acts as a preventive agent for any excess secretion of cortisol while during stress or disturbed HPA or RAS conditions, it stimulates the secretion of cortisol. An intraglandular modulatory role of substance P has been suggested.
Subject(s)
Adrenal Glands/drug effects , Animals , Hydrocortisone/antagonists & inhibitors , Hypothalamo-Hypophyseal System/pathology , Injections, Subcutaneous , Neurotransmitter Agents/pharmacology , Rats , Stress, Physiological/pathology , Substance P/administration & dosageABSTRACT
Hydrocortisone (HC) injection in rabbits induced eosinopoenia (reduction in absolute eosinophil count) which could be successfully abolished by beta--adrenoceptor antagonists, a propranolol, sotalol, practolol and H 35/25 but not by alpha--adrenoceptor antagonist, phenoxybenzamine. Reserpine per se produced eosinopoenia followed by eosinophilia. However, reserpine pretreatment failed to abolish HC-induced eosinopoenia. It is suggested that the eosinopoenia is mediated through beta--adrenoceptors, which could not be differentiated into beta 1/beta 2--adrenoceptor subtypes as has been possible for other beta-adrenoceptor mediated responses.