Systemic hypertension in animals has largely been thought to be secondary to another disease (e.g., renal disease and endocrinopathies),
as opposed to idiopathic (primary or essential). This has recently been called into question. For example, in a report of
69 hypertensive cats, seen at North Carolina State University (NCSU) for ocular disease, revealed that at least 17%, and possibly
as many as 50%, of cats had no identifiable cause for their systemic hypertension. Elliott and associates at the Royal Veterinary
College in London have documented that approximately 20% of hypertensive cats, diagnosed in primary-care practices, were idiopathic.
Another retrospective study, which used very strict criteria for the diagnosis of primary (essential, idiopathic) hypertension,
revealed a prevalence of 11%.
Described and potential etiologies of secondary hypertension include acute and chronic renal disease, hyperthyroidism, hypothyroidism,
hyperadrenocorticism, hyperaldosteronism, pheochromocytoma, diabetes mellitus, and obesity. Chronic kidney disease has the
greatest association with hypertension and may often be causal. A recent report suggested approximately 29% of elderly cats
with CKD were hypertensive, with the range reported in 4 studies being 19-65%. In dogs with CKD, approximately one-third
will be normotensive, one-third will have borderline hypertension, and one-third will be hypertensive.
Systemic hypertension may contribute to progressive nephron loss by causing irreversible glomerular damage via increased intraglomerular
pressures and glomerulosclerosis. By altering pre-glomerular resistance, healthy kidneys can maintain relatively static glomerular
capillary pressures despite variations in systemic blood pressure via autoregulation. Inappropriate dilation of the afferent
glomerular arteriole occurs in dogs and cats with CKD and diminishes the ability of the afferent arteriole to protect the
glomerulus from variations in systemic blood pressure. Although the exact mechanism of the CKD-associated hypertension is
not known, a combination of glomerular capillary and arteriolar scarring, decreased production of renal vasodilatory prostaglandins,
increased responsiveness to normal pressor mechanisms, and activation of the renin-angiotensin-aldosterone system (RAAS) may
be involved. The increased renin secretion leads to increased production of angiotensin II and aldosterone. In addition
to its direct pressor effects, angiotensin II also has a stimulatory effect on the sympathetic nervous system, increasing
vascular tone, and, in CKD vasoconstriction of the efferent arteriole which further contributes to the intraglomerular hypertension.
Finally, angiotensin and aldosterone may also stimulate renal tissue remodeling via increased matrix production and fibrosis.
The consequences of systemic hypertension are usually dependent on the magnitude and duration of the blood pressure elevations.
Acute ocular and central nervous system abnormalities can occur associated with hemorrhage or edema formation. Renal damage
associated with hypertension tends to be more chronic and characterized by glomerular lesions (e.g., glomerulosclerosis) and
proteinuria. Finally, functional/adaptive changes like ventricular hypertrophy can occur due to increased after-load in patients
with hypertension. Diagnosis and treatment of hypertension in dogs and cats with CKD renal may prevent development of retinal
lesions or may limit or slow progression of renal and cardiac lesions.