Page 320 - Feline Cardiology

Chapter 21: Systemic Hypertension 329

respectively, in contrast to human or canine counter­
parts (Brown et al. 2007). Such other disorders as
pheochromocytoma and primary hyperaldosteronism
have a high prevalence of systemic hypertension, but
these disorders are very uncommon in cats (Brown et al.
2007).
*
ETIOLOGY, PATHOPHYSIOLOGY, AND
GROSS PATHOLOGY

The concept of normal regulation of blood pressure is
A central to systemic hypertension, since it is regulation
failure that underlies the clinical disorder of systemic
hypertension. Blood pressure regulation refers to the
array of autonomic, endocrine, and other mechanisms
that maintain a cat’s arterial blood pressure within an
optimal range. Excess function of pathways that raise
blood pressure, failure of adequate function in pathways
that reduce blood pressure, or both, can lead to systemic
* hypertension.
Long­term control maintenance of normotension
requires the interaction of several systems (Figure 21.9)
(Brown 2005). Principal among these is the renin­
angiotensin­aldosterone system (RAAS). The powerful
B vasoconstricting effects of angiotensin II, classically the
product of angiotensin converting enzyme (ACE)­ Systemic Hypertension
mediated transformation of circulating, inactive angio­
tensin I (in turn created from the action of renally
derived renin in hepatically synthesized angiotensino­
gen), are central in the normal prevention of hypoten­
sion. Angiotensin II elicits the release of aldosterone
from the adrenal cortex, augmenting sodium resorption
in the distal renal tubule and thus increasing circulating
blood volume. Aldosterone’s binding to mineralocorti­
coid receptors in the peripheral vasculature causes vaso­
constriction (Franco et al. 2007). Dysregulation of these
and other elements of the RAAS is an important con­
tributor to systemic hypertension (Franco et al. 2007).
C
In some cats with chronic kidney disease­associated sys­
Figure 21.8. Gross pathologic specimens from cats with sub- temic hypertension, the plasma aldosterone level, or the
acute encephalopathy due to systemic hypertension. Brain in sag- ratio of aldosterone to plasma renin activity, is elevated
ittal plane; 2 cats. (A) and (B) Brain edema with expansion of the compared to healthy controls, suggesting that excessive
cerebellum cranially over the corpora quadrigemina (asterisk) and plasma aldosterone concentrations could contribute to
caudally toward the foramen magnum (arrowhead). The cerebral hypertension in chronic kidney disease (Jensen et al.
gyri are widened and flattened. (C) Normal brain for comparison. 1997; Pedersen et al. 2003). The autonomic nervous
Reproduced with permission from Brown et al., 2005.
system plays an important role in maintaining or raising
BP. Adrenergic stimulation of the heart raises myocar­
temic hypertension in 9/40 (22.5%) previously dial contractility and heart rate, both of which increase
normotensive cats (Syme and Elliott 2003), suggesting BP, and adrenergic stimulation of vascular smooth
an unmasking of concurrent chronic kidney disease or muscle causes vasoconstriction, which also increases BP.
other hypertensive factors. These effects are at least partly responsible for systemic
The prevalence of systemic hypertension in obese hypertension associated with hyperthyroidism because
cats and in feline diabetes mellitus is low or near­zero, thyroid hormone sensitizes the myocardium to the