INTRODUCTION

The definition of normal blood pressure in dogs and cats has been quite elusive and remains the subject of significant research, debate, and confusion.¹ It has been demonstrated that normal values for dogs appeared to be somewhat breed specific, but for cats they are not.²

The definition of hypertension has been lowered. At this time it is thought that blood pressure values higher than 150/95 mm Hg on three separate visits in a patient that demonstrates no clinical signs are compatible with hypertension, as is a single reading higher than 150/95 mm Hg in a patient with evidence of clinical disease in organs susceptible to end-organ damage.^1,3

ETIOLOGY

Patients are classified as having primary (essential) or secondary hypertension. In the seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure for Humans (JNC7), a third category termed prehypertension was established.⁴

Prehypertension describes blood pressures ranging from 120 to 139 mm Hg systolic or 80 to 89 mm Hg diastolic, or both. This new designation is intended to identify those individuals in whom early intervention (changing to a healthy lifestyle and diet) could reduce blood pressure or decrease the rate of increase in blood pressure to hypertensive levels.⁴

Primary hypertension is the result of an imbalance in the relationship between cardiac output and systemic vascular resistance. The exact cause is not known. There is little known about the prevalence of primary hypertension in animals. There have been reports of both dogs and cats with primary hypertension when secondary causes could not be determined.^5-7

Secondary hypertension is defined as elevated blood pressure that results from systemic disease or medication. Secondary hypertension accounts for almost all identified cases of elevated blood pressure in veterinary patients. The following disorders are associated with a significant risk of developing hypertension: renal disease, diabetes mellitus, hyperadrenocorticism, thyroid disease, and hepatic disease. Additionally, more uncommon causes include pheochromocytoma, hyperaldosteronism, polycythemia, and chronic anemia. Drugs such as erythropoietin and glucocorticoids have also been associated with elevations in blood pressure.^8-16

PROPOSED MECHANISM OF BLOOD PRESSURE ELEVATION

A number of diseases and a variety of hypotheses have been associated with elevations in blood pressure. In patients with hyperadrenocorticism, glucocorticoids induce hepatic production of angiotensinogen, resulting in an exaggerated response of the renin-angiotensin system.⁸ The hypertension that develops in animals with hyperthyroidism is secondary to the increased cardiac output secondary to the effect of thyroid hormone on cardiac muscle.¹²

The mechanism by which renal disease results in hypertension is not completely understood. It has been hypothesized that increased blood volume secondary to either a maladaptive increase in renin secretion or inability of the kidneys to process fluids and electrolytes properly may lead to increased venous return of blood to the heart.¹¹ Increased levels of endogenous vasoconstrictors such as endothelin, thromboxane, and adrenergic stimuli combined with decreased levels of endogenous vasodilators such as prostacyclin and nitric oxide may also be contributing factors.

The mechanism by which hepatic disease results in hypertension is undetermined. In animals with diabetes mellitus, there are possibly four different mechanisms. In humans with type 1 diabetes, hypertension is thought to develop secondary to the effects of diabetes on renal function. With type 2 diabetes, three different mechanisms have been proposed.¹⁴ One is that hyperinsulinemia secondary to insulin resistance causes sodium and water retention and increased sympathetic activity. This leads to increased peripheral resistance via changes in blood volume and vasoconstriction, respectively. The second proposed mechanism is that hypertrophy of vascular smooth muscle occurs secondary to the mitogenic effects of insulin. The last mechanism is that elevations in insulin levels may lead to increased intracellular calcium. The increased calcium results in hyperresponsive vascular smooth muscle contraction and increased peripheral vascular resistance.

Chromocytomas release epinephrine and norepinephrine, resulting in vasoconstriction and increased cardiac output (see Chapter 74, Pheochromocytoma).¹⁵ Administration of erythropoietin has been associated with the development of hypertension. Anemia leads to chronically dilated capillary beds. With resolution of the anemia, overcompensation of capillary constriction occurs, with a resultant increase in peripheral vascular resistance.¹⁶

ANTIHYPERTENSIVE DRUGS

Angiotensin-Converting Enzyme Inhibitors

Mechanism of Action

Angiotensin-converting enzyme (ACE) inhibitors are often the initial to treatment of choice to control hypertension. ACE inhibitors competitively inhibit the conversion of angiotensin I to angiotensin II. Angiotensin II is one of the most powerful endogenous vasoconstrictors; its inhibition results in systemic vasodilation (Table 178-1).

Table 178-1 Summary of Antihypertensive Drugs

Drug	Effect	Indications
Angiotensin-converting enzyme inhibitors Benazepril, enalapril	Arterial and venous vasodilation Decrease preload Decrease afterload	Hypertension Heart failure Proteinuria
Calcium channel antagonists Amlodipine	Arterial vasodilation	Hypertension Hypertensive crisis
β-Adrenergic antagonists Propranolol, atenolol	Decrease cardiac output Decrease sympathetic outflow Decrease blood pressure Cardiodepressant Nonselective (β1 and β2) Cardioselective (β1)	Hypertension Hypertrophic cardiomyopathy Arrhythmias Pheochromocytoma
α-Adrenergic antagonists Prazosin	Balanced vasodilation	Hypertension Pheochromocytoma
Arteriolar vasodilator Hydralazine	Nonspecific arterial vasodilation Reduced peripheral vascular resistance Reduced blood pressure	Hypertension Hypertensive crisis
Arteriolar vasodilator Sodium nitroprusside	Nitric oxide donor Vasodilation	Hypertensive crisis
Angiotensin II receptor blocker Losartan, irbesartan	Arterial and venous vasodilation	Hypertension
Aldosterone blockers Spironolactone, eplerenone	Vasodilation	Hypertension Proteinuria
Dopamine-1 agonist Fenoldopam	Vasodilation Decrease blood pressure Natriuresis Increase in renal blood flow	Hypertension Hypertensive crisis Acute renal failure

The primary effects of ACE inhibitors result in a decrease in angiotensin I and II, as well as an increase in bradykinin. Drugs in this class induce arterial and venous vasodilation. Because angiotensin II directly stimulates the kidneys to retain sodium, its inhibition results in a reduced plasma volume. In addition, ACE inhibitors inhibit aldosterone release, leading to a decrease in sodium and water retention and decreased blood volume. There is a reduction in both preload and afterload. The other beneficial effect of ACE inhibitors is that they reduce intraglomerular pressure and inhibit growth factors that lead to glomerular hypertrophy and sclerosis.^1,17-22

Only gold members can continue reading. Log In or Register to continue

Share this:

• Click to share on Twitter (Opens in new window)
• Click to share on Facebook (Opens in new window)

Related

Related posts:

1. Deteriorating Mental Status
2. Hyperthermia and Fever
3. Ventilator-Associated Lung Injury
4. Allergic Airway Disease in Dogs and Cats and Feline Bronchopulmonary Disease

Stay updated, free articles. Join our Telegram channel

Join