INTRODUCTION Hypertension has been documented in 90 per cent of humans with naturally occur- ring Cushing’s disease (Grünfeld 1990, Guyton and Hall 2000). Likewise, sys- temic hypertension occurs in over 50 per cent of dogs with untreated hyperadreno- corticism (HAC) (Kallet and Cowgill 1992). Moreover, in humans and dogs affected by HAC, hypertension is fairly resistant to HAC treatment in some cases, despite resolution of hypercortisolaemia (Feldman and Nelson 1996, Ortega and others 1996, Nichols 1997). Mechanisms underlying hypertension in HAC remain incompletely understood. Hypotheses include excessive secretion of renin, activation of the renin-angiotensin system and reduction of vasodilator prostaglandins (Melby 1989, Yasuda and others 1994, Feldman and Nelson 1996, Nichols 1997). Glucocorticoids also seem to play an important role, such as in the induction of mineralocorticoid-like changes in renal sodium excretion and enhancement of vascular reactivity to vasoactive sub- stances (Schimmer and Parker 1996). Ortega and others (1995) showed that plasma aldosterone levels (pre- and post- adrenocorticotropic hormone [ACTH] administration) were higher in dogs with untreated pituitary-dependent hyper- adrenocorticism (PDH), compared with normal dogs. Therefore, mineralocorticoids are suspected to contribute to hypertension in HAC by increasing sodium and water retention (Guyton and Hall 2000). Chronic glucocorticoid and mineralocorti- coid excess can lead to deleterious cardio- vascular effects perpetuating hypertension in some humans being treated for HAC (Schimmer and Parker 1996). Conversely, o,p’-DDD treatment is supposed to have few effects on the zona glomerulosa (Feld- man and Nelson 1996), resulting in persis- tently high levels of aldosterone, which perpetuate hypertension. The aim of this study was to evaluate whether hormonal changes initiate hyperten- sion in PDH dogs before o,p’-DDD treat- ment through aldosterone effects. Moreover, the authors sought to determine whether aldosterone is a perpetuating factor in hypertension after treatment or if prolonged high levels of adrenal hormones before treatment could induce vascular effects responsible for persistent hypertension. MATERIALS AND METHODS Animals Thirteen dogs with PDH were diagnosed on the basis of clinical examination, an ACTH stimulation test, low dose dexamethasone suppression test, urinary cortisol:creatinine ratio and adrenal ultrasonography. Age, breed and gender of the 13 dogs are given I. GOY-THOLLOT , D. PÉCHEREAU†, S. KÉROACK, J-C. DEZEMPTE AND J-M. BONNET* Journal of Small Animal Practice (2002) 43, 489–492 The aim of this study was to evaluate the role of aldosterone as an initiating and/or perpetuating factor in hypertension associated with pituitary-dependent hyperadrenocorticism (PDH) in dogs. Thirteen dogs with PDH and 11 healthy control dogs were used. In all dogs, arterial blood pressure and plasma sodium, potassium, basal aldosterone, post-ACTH aldosterone, basal cortisol and post- ACTH cortisol concentrations were measured. The tests were repeated 10 days and three months after the beginning of o,p’-DDD treatment in PDH dogs. In untreated PDH dogs, plasma aldosterone was significantly decreased, whereas cortisol, sodium and arterial blood pressure were significantly increased compared to healthy dogs. Hypertension remained in most treated PDH dogs despite normalisation of cortisol and persistently low aldosterone levels. These results did not demonstrate that aldosterone is involved in the development and perpetuation of hypertension in PDH. However, glucocorticoids seemed to play a major role as an initiating and perpetuating factor in PDH in dogs. Investigation of the role of aldosterone in hypertension associated with spontaneous pituitary-dependent hyperadrenocorticism in dogs JOURNAL OF SMALL ANIMAL PRACTICE • VOL 43 • NOVEMBER 2002 489 Département des Animaux de Compagnie, and *Département des Sciences Fondamentales, Ecole Nationale Vétérinaire de Lyon, 1 avenue Bourgelat, 69 280 Marcy l’Etoile, France †Clinique Vétérinaire, 55 avenue Jean Mermoz, 64 000 Pau, France