Orthostatic Hypertension: When Pressor Reflexes Overcompensate

Joshua Fessel; David Robertson


Nat Clin Pract Nephrol. 2006;2(8):424-431. 

In This Article

Summary and Introduction


Orthostatic hypertension—a rise in blood pressure upon assuming upright posture—is an underappreciated and understudied clinical phenomenon. There is currently no widely agreed-upon definition of clinical orthostatic hypertension, the current definitions being operational within the context of particular studies. The underlying pathophysiology is thought to involve activation of the sympathetic nervous system, but the actual etiology is poorly understood. Orthostatic hypertension is observed in association with a variety of other clinical conditions, including essential hypertension, dysautonomias, and type 2 diabetes mellitus. Orthostatic hypertension has been associated with increased occurrence of silent cerebrovascular ischemia and possibly with neuropathy in type 2 diabetes. So, appreciation of the true incidence of orthostatic hypertension, elucidation of the underlying pathophysiology, and an understanding of potentially effective treatment approaches and their associated risks and benefits might all have major clinical significance. Orthostatic hypertension is an aspect of hypertension that is in need of further focused investigation.


It has long been recognized that minor minute-to-minute fluctuations in blood pressure occur in healthy individuals, and that many factors influence these fluctuations. Perhaps the easiest to observe is the influence of posture. Assumption of upright posture from a recumbent position results in a small but measurable decrease in systolic blood pressure (SBP) due primarily to a redistribution of blood volume into the lower abdomen, buttocks and legs under the influence of gravity. In most people, this decrease in blood pressure is very slight and evanescent, as a whole host of response mechanisms are immediately engaged to maintain blood pressure. Chief among these responses is the baroreflex constellation,[1] in which stretch receptors in the carotid artery in the neck, and major vessels and structures in the thorax, quickly sense decreases in arterial pressure and central thoracic volume and trigger a coordinated increase in activity of the sympathetic nervous system, decrease in activity of the parasympathetic nervous system, and modulation of cascades of hormones. These pathways converge to stabilize blood pressure in a normal individual through a wide range of postures. Problems arise when any of these pathways responds inappropriately. The result can have clinical significance in the presence or absence of overt symptoms.

The influence of body position on blood pressure in normal individuals derives from perturbations elicited by gravity with the assumption of an upright posture. The resulting decrease in effective plasma volume is accompanied by a slight decrease in SBP, a slight increase in diastolic blood pressure (DBP), an increased heart rate, and an increase in circulating levels of norepinephrine, epinephrine, active plasma renin, aldosterone, and vasopressin. In addition, rates of sodium reabsorption and potassium excretion are increased at the level of the kidney, without net change in plasma osmolarity.[2] These responses are primarily a reflection of coordinated activation of the sympathetic nervous system and a decrease in activity of the parasympathetic nervous system, both mediated by the baroreflex pathway.

When blood pressure is measured in a clinical setting, the reading can be influenced by the focus and expectation of the individual making the determination. If the examiner is blind to the true blood pressure (for example when a random-zero sphygmomanometer is employed) greater excursions in pressure are often reported. Both orthostatic hypotension and orthostatic hypertension are more commonly encountered when pressures are measured by a blinded observer.[3] Therefore, as blind recording of blood pressure is rarely employed in a clinical setting, there might be widespread underreporting of both these types of orthostatic changes in blood pressure.

Perhaps the most familiar clinical syndrome involving the baroreflex response pathway is orthostatic hypotension. This topic has been reviewed extensively elsewhere[4,5] and will only be briefly discussed here. Orthostatic hypotension occurs when the change in blood pressure upon assumption of upright posture is ineffectively compensated. The objective physical finding is a drop in blood pressure of 20/10 mmHg. Orthostatic hypotension is clinically important when the decrease in blood pressure is accompanied by symptoms of cerebral hypoperfusion, including dizziness or lightheadedness, visual changes, discomfort in the head and neck, fatigue, and frank syncope. The most dramatic examples of orthostatic hypotension are observed in syndromes involving failure of the effector arm of the baroreflex, namely, the autonomic nervous system. These syndromes include pure autonomic failure[6] and multiple system atrophy (Shy-Drager syndrome).[7] It is also noteworthy that a variety of pharmacologic agents, particularly antidepressants and antihypertensives, can cause iatrogenic orthostatic hypotension and must be ruled out initially when considering a differential diagnosis for orthostatic hypotension.[8,9]

Two other conditions are worth mentioning here, as they will be discussed later. Baroreflex failure, which involves loss of afferent input into brainstem blood-pressure control centers, and which is often confused with pheochromocytoma, can involve a component of orthostatic hypotension.[10,11] Unlike pure autonomic failure or multiple system atrophy, however, episodic tachycardia and labile hypertension are prominent features in baroreflex failure.[11,12,13] The postural tachycardia syndrome (POTS) also presents clinically with symptoms of cerebral hypoperfusion.[14,15] Interestingly, however, this disorder more often involves either no change in blood pressure or orthostatic hypertension of mild severity.


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