From Dog

Hypertension is defined as a sustained blood pressure above the normal cut-off value of 160 mmHg.

In dogs, blood pressure is ultimately a function of cardiac output and systemic peripheral resistance, both of which are directly and ­indirectly affected by the com­plex interaction among the autonomic nervous system, the renin-angiotensin system, and endothelial signaling mechanisms[1]. For example, activation of the renin-angiotensin system of the kidneys has a direct effect on the vasculature, causing increased systemic peripheral resistance and indirectly increasing cardiac output by affecting stroke volume. Therefore, regulation of blood pressure and development of hypertension are complicated multifactorial processes that involve the heart, autonomic nervous system, endothelial signaling intercellular mechanisms, vasculature, and kidneys.

Dogs with hypertension are classified as having wither primary (essential) or secondary hypertension[2]

  • Primary hypertension is the result of an imbalance in the relationship between cardiac output and systemic vascular resistance, although the exact cause is not known.
  • Secondary hypertension is elevated blood pres­sure that occurs because of systemic disease or medication.

Although primary hypertension accounts for more than 90% of all cases of hypertension in humans, ­secondary hypertension accounts for almost all identified cases of elevated blood pressure in veterinary patients[3]. This distinction is important because it allows definition of patients at risk of developing elevated blood pressure on the basis of the diagnosis of a ­predisposing illness.

Patients with the following conditions or treatments have a significant risk of developing hypertension and warrant blood pressure evaluation:

- Hyperadrenocorticism[4]
- Chronic renal disease[5]
- Hyperthyroidism[6]
- Diabetes mellitus[7]
- Hyperaldosteronism

The exact definition of normal blood pressure in cats and dogs has been the subject of significant research, debate, and confusion because previous studies used systolic blood pressures ranging from 141 to 185 mm Hg to define hypertension.6,13"15 There has been even less consensus about normal values for diastolic blood pressure. Nevertheless, it is now believed that blood pressure values higher than 150/95 mm Hg on three separate visits in a patient that demonstrates no clinical signs directly attributable to the pressure elevation is ­com­patible with hypertension, as is a single reading higher than 150/95 mm Hg in a symptomatic patient[9].

In cases of mild to moderate elevations in systolic blood pressure, physical examination findings and laboratory data are often consistent with the underlying disease.3 For example, hyperadrenocorticism in dogs often leads to polyuria and polydipsia, alopecia, muscle wasting, pendulous abdomen, and hepatomegaly. Elevations in liver enzyme values (i.e., alkaline phosphatase, alanine aminotransferase), hypercholesterolemia, stress leukogram, and isosthenuria are common laboratory findings. However, often no clinical signs are directly attributable to the elevated blood pressure.

Clinical signs of hypertension include hypertensive retinopathy[10], cardiac murmurs, arrhythmia[11] and hypertensive encephalopathy (head tilt, ataxia, depression, disorientation and seizures.

The initial response of the kidneys to elevated systemic blood pressure is increased renal excretion of sodium and water. This condition, referred to as ­pressure natriuresis, initially acts to reduce blood volume and thereby helps control systemic hypertension. Eventually, elevations in renal arterial blood pressure lead to renal tubular degeneration and interstitial fibrosis, whereas glomerular hypertension results in glomerulosclerosis, glomerular atrophy, and proliferative glo­merulitis. Together, these changes are associated with glomerular hyperfiltration and progression of glomerular and tubular damage. The end result is worsening of the hypertension and eventual renal failure.

Treatment commonly employs use of ACE inhibitors drugs include benazepril and amlodipine[12].

Other drugs which have been commonly employed include spironolactone[13], hydralazine[14], esmolol and atenolol.


  1. Cain AE, Khalil RA (2002) Pathophysiology of essential hypertension: Role of the pump, the vessel and the kidney. Semin Nephrol 22(1):3-16
  2. Williams GH (1994) Hypertensive vascular disease, in Isselbacher KJ, Martin JB, Fauci A, Braunwald E (eds): Harrison's Principles of Internal Medicine, ed 13. New York, McGraw-Hill, pp:1116-1123
  3. Brown SA, Henik RA (1998) Diagnosis and treatment of systemic hypertension. Vet Clin North Am Small Anim Pract 28(6):1481-1494, 1998
  4. Brody AR, Michell AR (1996) Epidemiological study of blood pressure in domestic dogs. J Small Anim Pract 37(3):116"125, 1996
  5. Stiles J, Polzin DJ, Bistner SL (1994) The prevalence of retinopathy in cats with systemic hypertension and chronic renal failure or hyperthyroidism. JAAHA 30(6):564-572
  6. Panciera DL (2000) Cardiovascular complications of thyroid disease, in Bonagura JD (ed): Kirk's Current Veterinary Therapy XIII, Small Animal Practice, ed 13. Philadelphia, WB Saunders, 2000, pp 716"719
  7. Struble AL, Feldman EC, Nelson RW, Kass PH (1998) Systemic hypertension and proteinuria in dogs with diabetes mellitus. JAVMA 213(6):822-825
  8. Mellian C, Peterson ME (2000) The incidentally discovered adrenal mass, in Bonagura JD (ed): Kirk's Current Veterinary Therapy XIII, Small Animal Practice, ed 13. Philadelphia, WB Saunders, pp:368-372
  9. Kraft W, Egner B (2003) Causes and effects of hypertension, in Egner B, Carr A, Brown S (eds): Facts of Blood Pressure in Dogs and Cats. Babenhausen, Beate Egner Vet Verlag, pp:61-86
  10. Smith PJ (2000) Hypertensive retinopathy, in Bonagura JD (ed): Kirk's Current Veterinary Therapy XIII, Small Animal Practice, ed 13. Philadelphia, WB Saunders, pp:1082-1085
  11. Chetboul V, Lefebvre HP, Pinhas C, et al (2003) Spontaneous feline hypertension: Clinical and echocardiographic abnormalities, and survival rate. J Vet Intern Med 17(1):89-95
  12. Mathur SM, Syme H, Brown CA, et al (2002) Effects of the calcium channel antagonist amlodipine in cats with surgically induced hypertensive renal insufficiency. Am J Vet Res 63(6):833-839
  13. Epstein M (2001) Aldosterone as a mediator of progressive renal disease: Pathology and clinical implications. Am J Kidney Dis 37:677-688
  14. Pariser MS & Berdoulay P (2011) Amlodipine-induced gingival hyperplasia in a Great Dane. J Am Anim Hosp Assoc 47(5):375-376