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*All
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 Definition
Vascular reactivity refers to changes in the blood vessels in response to a stimulus. Proximal stimuli for vascular reactivity can be neural firing, neurochemical, or physical stimuli (e.g. passive distension). Given psychological influences on the neural, endocrine, and immune systems, a distal cause of vascular reactivity can be psychological stress. 
Measurement The most prominent and important measure of vascular reactivity in mind-body medicine is blood pressure reactivity. Vascular narrowing due to stress will increase the total peripheral resistance encountered by the heart and increase blood pressure. Blood pressure may also increase due to increased contractility of the heart, however. Thus blood pressure change is not typically a pure measure of vascular reactivity. Measures more directly related to the vasculature are photo, impedance, and strain gauge plethysmography (Jennings, Tahmoush, & Redmond, 1980). These provide indices of the peripheral pressure and flow pulses noninvasively in humans. |
| . | These indices
are complexly determined, i.e. difficult to relate directly to blood pressure
or blood
flow, and derivative measures are often used. Use of more than one device permits measurement of pulse wave velocity. This speed of transit of a vascular pulse between two arterial sites measures the elasticity of the vessel, which will change with reactivity to stress. Temporary occlusion of venous return from the forearm permits assessment of arterial inflow to the forearm, thus noninvasively measuring forearm blood flow. Doppler ultrasound also provides noninvasive measures of blood flow, albeit with relatively expensive technology. This technology can assess blood flow as well as pulse wave velocity. Examination of components of the flow waveform added by reflection of the flow wave has also been employed. Degree of reflection is modulated by the stiffness of the arterial tree and thus can be related to aging and disease (Davies & Struthers, 2003). Electromagnetic flow meters and catheter tip pressure sensors are central to work with animal models, but not typically useful in mind-body research.
Physiological Mechanisms Vascular reactivity is an interesting, but complex physiological topic. The text by Guyton and Hall (2000) should be consulted for information beyond the brief note presented here. The most well know neural mechanism of vascular reactivity is the activation of the sympathetic nervous system. Activation can be general or regionally specific and will act primarily on alpha-adrenergic receptors in the vascular smooth muscle. Activation will induce vasoconstriction (increase in diameter); inhibition vasodilation. The attendant stiffing of the vessel with sympathetic activation will also increase pulse wave velocity in these vessels. Literally, a host of neurochemicals have potent effects on the vasculature, e.g. adenosine, nitric oxide, carbon dioxide, vasopressin. These are typically discussed in explanations for why blood vessels respond to global and local metabolic debts such as created by exercise. Nitric oxide is particularly interesting because it is a gas that diffuses to exert regional control (not mediated by the nervous system).
Areas of Application in Mind-Body Science Successes of the cardiovascular reactivity hypothesis (Krantz & Manuck, 1984) have been with vascular reactivity, most particularly, blood pressure reactivity. Individual differences in such reactivity have been prospectively related to hypertension as well as coronary heart disease indices (e.g., Jennings et al., 2004; Menkes et al., 1989). Further understanding this reactivity is an important topic. Interesting work has been done showing that stress interacts with the presence or absence of damage to the inner lining (intima) of coronary arteries. Potentially damaging vasoconstrictive change during stress is damped in the presence of an intact lining (presumably because nitric oxide is present to exert a countering vasodilative influence, see Yeung et al.,1991).
References  Davies
JI, Struthers AD: Pulse wave analysis and pulse wave velocity: a critical
review
 of
their strengths and weaknesses. J Hypertension 21: 463-72, 2003.
Guyton
AC, Hall JE: Textbook of Medical Physiology (10th ed). New York: Elsevier,
2000.
Jennings
JR, Tahmoush AJ, Redmond DP: Non-invasive measurement of peripheral vascular
activity.
In: I Martin, PH Venables (eds). Techniques in Psychophysiology. Chichester:
Wiley,
1980, pp. 69-137.
Jennings
JR, Kamarck TW, Everson-Rose SA, Kaplan GA, Manuck SB, Salonen JT:
Exaggerated
blood pressure responses during mental stress are prospectively related
to
enhanced
carotid atherosclerosis in middle-aged Finnish men. Circulation 110:
2198-203,
2004.
Krantz
DS, Manuck SB: Acute psychophysiologic reactivity and risk of cardiovascular
disease:
a review and methodologic critique. Psychol Bull 96: 435-64, 1984.
Menkes
MS, Matthews KA, Krantz DS, Lundberg U, Mead LA, Qaqish B, Liang KY,
Thomas
CB, Pearson TA: Cardiovascular reactivity to the cold pressor test as a
predictor of
hypertension.
Hypertension 14: 524-530, 1989.
Yeung
AC, Vekshtein VI, Krantz DS, Vita JA, Ryan TJ Jr, Ganz P, Selwyn
AP: The effect
of
atherosclerosis on the vasomotor response of coronary arteries to mental
stress.
New
Engl J Med 325: 1551-1556, 1991.
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| Revised 10/23/2006 la/tc |
