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Redalyc.Feline Primary Hyperaldosteronism: an Emerging Ciência Rural ISSN: 0103-8478 [email protected] Universidade Federal de Santa Maria Brasil Diola Bento, Daniel; Soares Zahn, Fabíola; Duarte, Laura Carolina; de Araújo Machado, Luiz Henrique Feline primary hyperaldosteronism: an emerging endocrine disease Ciência Rural, vol. 46, núm. 4, abril, 2016, pp. 686-693 Universidade Federal de Santa Maria Santa Maria, Brasil Available in: http://www.redalyc.org/articulo.oa?id=33144324020 How to cite Complete issue Scientific Information System More information about this article Network of Scientific Journals from Latin America, the Caribbean, Spain and Portugal Journal's homepage in redalyc.org Non-profit academic project, developed under the open access initiative Ciência Rural, Santa Maria, v.46, n.4,Feline p.686-693, primary abr, hyperaldosteronism: 2016 an emerging endocrine http://dx.doi.org/10.1590/0103-8478cr20141327 disease. 686 ISSN 1678-4596 CLINIC AND SURGERY Feline primary hyperaldosteronism: an emerging endocrine disease Hiperaldosteronismo primário felino: uma enfermidade endócrina emergente Daniel Diola BentoI Fabíola Soares ZahnII Laura Carolina DuarteIII Luiz Henrique de Araújo MachadoIV – REVIEW – ABSTRACT aumento da excreção de potássio, que ocasionarão, respectivamente, hipertensão arterial sistêmica e hipocalemia grave. O diagnóstico The primary hyperaldosteronism, an endocrine é realizado com base na comprovação da hipersecreção hormonal disease increasingly identified in cats, is characterized by adrenal com supressão da liberação de renina, além de exames de imagem gland dysfunction that interferes with the renin-angiotensin- e avaliação histopatológica da adrenal. O tratamento pode ser aldosterone system, triggering the hypersecretion of aldosterone. curativo, com a adrenalectomia, em enfermidades unilaterais, Pathophysiological consequences of excessive aldosterone ou conservativo, por meio de antagonistas da aldosterona, secretion are related to increased sodium and water retention, suplementação de potássio e anti-hipertensivos. O prognóstico é and increased excretion of potassium, which induce hypertension bom e reservado com a terapia apropriada. and severe hypokalemia, respectively. The most common clinical findings in cats include: polydipsia, nocturia, polyuria, Palavras-chave: medicina felina, endocrinologia, enfermidade generalized weakness, neck ventroflexion, syncope, anorexia, adrenocortical, hipertensão. weight loss, pendulous abdomen and blindness. Diagnosis is based on the evidence of hormonal hypersecretion with suppression of renin release, imaging and histopathological evaluation of adrenal glands. Treatment may be curative with adrenalectomy, in cases INTRODUCTION of unilateral disease, or conservative, through administration of aldosterone antagonists, potassium supplementation and First described in humans in antihypertensives. Prognosis varies from fair to good with the appropriate therapy. This article reviews the main aspects of 1955, primary hyperaldosteronism, also called primary aldosteronism in cats, providing the clinician with Conn syndrome, is an adrenocortical disorder important information for the diagnosis of this disease. characterized by autonomous adrenal hypersecretion Key words: feline medicine, endocrinology, adrenocortical of aldosterone. Initially considered to be rare, disease, hypertension. hyperaldosteronism is found in approximately 6% of all hypertensive human patients and accounts for RESUMO 11% of those with hypertension non- responding O hiperaldosteronismo primário, doença endrócrina to therapy (FOGARI et al., 2007). The first case in cada vez mais identificada em felinos, caracteriza-se pela cats was reported in 1983 and currently, though little disfunção da glândula adrenal com interferência no sistema renina- known and diagnosed, it is considered an important angiotensina-aldosterona, desencadeando a hipersecreção de adrenocortical disease in the species (BISGNANO aldosterona. As consequências da secreção excessiva de aldosterona estão relacionadas com o aumento da retenção de sódio e água e & BRUYETTE, 2012). IHospital Veterinário Santa Inês, São Paulo, SP, Brasil. IIDepartamento de Reprodução Animal e Radiologia Veterinária, Faculdade de Medicina Veterinária e Zootecnia (FMVZ), Universidade Estadual Paulista (UNESP), Botucatu, SP, Brasil IIIEspecialidades Veterinárias VESP, Campinas, SP, Brasil IVDepartamento de Clínica Veterinária, Faculdade de Medicina Veterinária e Zootecnia (FMVZ), Universidade Estadual Paulista (UNESP), 18618-970, Botucatu, SP, Brasil. E-mail: [email protected]. Corresponding author. Received 09.06.14 Approved 09.22.15 Returned by the author 12.15.15 CR-2014-1327.R7 Ciência Rural, v.46, n.4, abr, 2016. 687 Bento et al. Aldosterone plays important roles both of sodium and chloride in the distal convoluted tubules. in the modulation of vascular tone and in the Through this mechanism, it regulates systemic blood central nervous system function. Mineralocorticoid pressure and homeostasis of extracellular fluid in receptors have been identified in non-epithelial response to hemodynamic and electrolyte changes tissues such as heart fibroblasts, endothelial cells, (SCHULMAN, 2010). vascular smooth muscle cells and brain. Experiments Its secretion is primarily regulated by indicate that increased aldosterone concentrations the renin-angiotensin-aldosterone system and the are associated with increased sympathetic excitatory extracellular concentrations of potassium. In addition responses and elevated blood pressure. Aldosterone to these mechanisms, there is evidence that aldosterone is considered pro-inflammatory and pro-fibrotic secretion is also influenced by the adrenocorticotropic in blood vessels periphery and plays a key role hormone (ACTH), natriuretic peptides and certain in vascular remodelling and vasoconstriction, neurotransmitters. In spite of the significant difference in thus leading to endothelial dysfunction. Persistent plasma concentrations of aldosterone observed before hypertension in primary aldosteronism is therefore and after administration of synthetic ACTH (DECLUE a consequence of the synergic effects of sodium et al., 2011), none of these compounds was proven to and fluid retention, increased sympathetic tone, directly or indirectly regulate the secretion of aldosterone endothelial dysfunction and increased total (DJAJADININGRAT-LAANEN et al., 2011). peripheral resistance (JEPSON, 2011). Potassium has a direct effect on the zona glomerulosa of the adrenal glands for the secretion Endocrine physiology of aldosterone of aldosterone. Hyperkalemia stimulates aldosterone Target organs and tissues secretion by depolarization of the zona glomerulosa Aldosterone is a steroid hormone with cells and hypokalemia inhibits such depolarization. strong mineralocorticoid activity. It was previously Sodium (Na+) and potassium (K+) ions are thought to be produced only in the adrenal glands; extremely important and are directly involved in recent studies have shown its production by other establishing the resting membrane potential. Low tissues including heart, brain and blood vessels, in serum potassium concentrations prevent the cell which it presents both autocrine and paracrine action from exercising its action potential thus leading to (CONNELL et al., 2008). muscle weakness. The nerve cell remains in idle state The circulating aldosterone, whose classical and can not perform the ion exchange necessary for targets are kidney epithelium, colon and salivary impulse conduction and muscle tone. glands, overpasses the plasma membrane of such Through the signaling of kidney tissues and binds to the cytoplasmic mineralocorticoid baroreceptors located in the afferent arterioles, receptor. Although this receptor presents equal affinity juxtaglomerular apparatus cells increase or reduce for cortisol and aldosterone, the mineralocorticoid the renin secretion in response to decreased or receptors in these tissues enzymatically convert cortisol increased circulating blood volume or renal blood to cortisone, which has little affinity to the receptor, flow, respectively. The baroreceptors have the function ensuring the availability of mineralocorticoid receptors of regulating blood pressure; when blood pressure is for the circulating aldosterone (DJAJADININGRAT- decreased, kidney baroreceptors are activated and LAANEN et al., 2011). sympathetic activity is increased, resulting in increased Additionally, aldosterone affects other heart rate and peripheral vasoconstriction. epithelial and non-epithelial tissues that contribute to Sympathetic stimulation acts directly the homeostasis of blood pressure, including cardiac on the macula densa, a group of modified cells in tissue. Aldosterone increases blood pressure both by the distal tubules near the end of the loop of Henle the expanding the extracellular fluid, and by increasing and closely associated with juxtaglomerular cells. peripheral vascular resistance (CONNELL et al., 2008). The concentration of sodium in the tubular lumen is As demonstrated in humans, long-term excessive monitored by the macula densa cells, and its reduction mineralocorticoids can trigger microangiopathy, can trigger communication between the macula densa fibrosis and proliferation of endothelium and smooth and juxtaglomerular cells, resulting in renin release. muscle in tissues such as the heart and kidneys. This released renin is responsible for cleavage of angiotensinogen, produced by hepatic metabolism, in Regulation of aldosterone secretion angiotensin
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