Severe Hypertension .net

Site updated at Thursday, 03 December 2015


What causes hypertension?

For more than 90 per cent of people with high blood pressure, the cause is unknown. This is called 'primary' or 'essential hypertension'. In the remaining 10 per cent or so, there is an underlying cause. This is called 'secondary hypertension'.

Some of the main causes for secondary hypertension are:
  1. chronic kidney diseases
  2. diseases in the arteries supplying the kidneys
  3. chronic alcohol abuse
  4. hormonal disturbances
  5. endocrine tumours

What factors increase the risk of hypertension?

Anyone can suffer from high blood pressure, but certain factors can seriously aggravate hypertension and increase the risk of complications:
  1. a tendency in the family to suffer hypertension
  2. obesity
  3. smoking
  4. diabetes Type 1 or Type 2
  5. kidney diseases
  6. high alcohol intake
  7. excessive salt intake
  8. lack of exercise
  9. certain medicines, such as steroids

Have a Question !

Why Focus upon Stress and Hypertension?

Acute Stress Responses

Although stress is clearly implicated in the etiology of essential hypertension, it is not easy to explain how a characteristic of a job, like degree of psychologic demand or job control, or exposure to an earthquake results in the physiologic tissue damage (like vascular hypertrophy) or altered regulatory system functioning (like baroreceptor insensitivity) observed in chronic hypertension. Just how can a characteristic of an environmental stimulus lead to these physiologic changes? Several of the theoretical perspectives that were highlighted in section 4 hypothesized that the intensity, pattern, and duration of the acute blood pressure response to stress are important to consider when addressing this question (Folkow, 1983; Julius and Esler, 1975; Laragh,1983). It is not surprising, then, that the comprehensive model of the stress-hypertension relation depicted in Figure 4.1 places the acute stress response in between stress and physiological change associated with essential hypertension.

As its position in the model indicates, exposure to environmental stressors leads to onset of essential hypertension via the acute stress response. Individuals who respond to stress with minimal acute stress responses, according to this model, exhibit no increased risk for development of a stress-induced hypertensive condition. This is not to say that these individuals could not possibly develop hypertension, but if they are diagnosed with high blood pressure, this model would predict that the onset of their hypertensive condition may be associated with risk factors other than stress (for example, obesity or a high-salt diet).

Borrowing heavily from the works of Selye (1956) and McEwen (1998), one can logically conclude that the relation between features of environmental stress and pathological conditions that lead to chronically elevated blood pressure is mediated by the patterning and magnitude of the acute stress response. Although both Selye and McEwen focused on the acute physiological stress response, this idea can be extended to include other components of the acute stress response (cognitive, affective, or behavioral).

For example, it is possible that persons who respond to environmental stress with intensely hostile emotions (affective reactions) or increased alcohol and caffeine use (behavioral reactions) may increase their risk for developing essential hypertension through these channels. However, because the majority of theoretical and empirical work that has examined mechanisms involved in explaining the stress-hypertension association has focused on acute physiological responses, this chapter is heavily weighted in this area.

image The investigation of acute stress responses associated with essential hypertension has employed both case control and prospective methods. Case control studies involve measurement of parameters associated with the acute stress response in samples carefully selected on the basis of hypertensive status. Responses of hypertensive patients (cases) are compared with those of non-hypertensive controls to stressful stimuli either presented in the laboratory or during daily life.

Although these types of studies can be conducted fairly quickly due to the high prevalence of essential hypertension and the relative ease of locating samples of hypertensive patients, the causal nature of their findings can always be challenged. After all, if significant differences in acute stress responses were observed between hypertensive and normotensive patients, one could always conclude that the observed response differences were a consequence of essential hypertension rather than an etiologic factor.

For example, if hypertensive patients were shown to exhibit heightened blood pressure responses to stress in comparison to normotensive controls, it would still be unknown whether the exaggerated reactivity leads to onset of hypertension or whether the physiologic changes associated with essential hypertension lead to the expression of exaggerated blood pressure responses to stress.

In order to clarify the direction of relations observed in case control studies, the more time-consuming prospective designs are essential. In contrast to case control methodology, prospective designs involve measuring acute stress responses hypothesized to be associated with the onset of hypertension during an initial time point and then conducting follow-up visits with the same patients years later to assess change in blood pressure status. With this methodology, acute stress responses can be measured before onset of hypertension, and should significant relations between them and subsequent blood pressure status be observed, the findings make a much more convincing causal statement. The majority of studies reported in this chapter have employed case control methods, which suggests that definitive causal conclusions regarding these variables are limited. However, with some parameters (for example, cardiovascular response to stress), prospective evidence has emerged.

Revision date: Dr. Felix Yankovsky, M.D.
Last revised: March 4, 2011

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