Abstract
The blood pressure and heart rate responses to a laboratory task are most frequently used to assess an individual’s cardiovascular reactivity. Information from such observation is useful for general categorization and for the delineation of subgroups of hyper- and hyporesponders. Measurement of systemic and regional hemodynamics further complements reactivity studies by providing important information about qualitative differences which are not necessarily reflected in the overall magnitude of the blood pressure response. Hollenberg, Williams, and Adams (1981) engaged patients with borderline hypertension and normotensive control subjects in resolving Ravens progressive matrices. The blood pressure responses to this challenge were similar in both groups, but patients with borderline hypertension had a significant decrease of renal blood flow. This observation, that renal vasculature tends to overrespond to the mental stress, provided important inference as to how behavioral factors might lead to hypertension. As Light, Koepke, Obrist, and Willis (1983) suggest, mental stress might cause excessive salt retention in patients with borderline hypertension. It is not difficult to visualize how sodium retention might lead to hypertension. Another example of the differential behavior of local vasculature was provided by Mark, Lawton, and Abboud (1975). They observed that chronic salt loading does not alter the mean blood pressure in borderline hypertensive and normotensive subjects, but the forearm vascular resistance in normotensive individuals decreased whereas in patients with borderline hypertension it increased.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
Similar content being viewed by others
References
Bravo, E. L., Tarazi, R. C., Fouad, F. M., Vidt, D. G., & Gifford, R. W. (1981). Clonidine-suppression test: A useful aid in the diagnosis of pheochromocytoma. New England Journal of Medicine, 305, 623–626.
Colfer, H. T., Cottier, C., Sanchez, R., & Julius, S. (1984). Evidence for the autoregulatory theory of blood pressure reduction by beta-adrenoreceptor blocking agents in hypertension. Hypertension, 6, 145–151.
Conway, J., & Lauwers, P. (1960). Hemodynamic and hypotensive effects of long-term therapy with chlorothiazide. Circulation, 21, 21–27.
Dustan, H. P., Tarazi, R. C., & Bravo, E. L. (1972). Dependence of arterial pressure on intravascular volume in treated hypertensive patients. New England Journal of Medicine, 286, 861–866.
Esler, M., Zweifler, A., Randall, O., Julius, S., Bennett, J., & Rydelek, P. (1976). Suppression of sympathetic nervous function in low-renin essential hypertension. Lancet, 2, 115–118.
Esler, M., Julius, S., Zweifler, A., Randall, O., Harburg, E., Gardiner, H., & DeQuattro, V. (1977). Mild high-renin essential hypertension: Neurogenic human hypertension?. New England Journal of Medicine, 296, 405-411.
Esler, M., Zweifler, A., Randall, O., & DeQuattro, V. (1977). Pathophysiologic and pharmacokinetic determinants of the antihypertensive response to propranolol. Clinical Pharmacology and Therapeutics, 22, 299–308.
Folkow, B. (1982). Physiological aspects of primary hypertension. Physiological Reviews, 62, 347–503.
Frohlich, E. D., Tarazi, R. C., Dustan, H. P., & Page, I. H. (1968). The paradox of beta-adrenergic blockade in hypertension. Circulation, 37, 417–423.
Hollenberg, N. K., Williams, G. H., & Adams, D. F. (1981). Essential hypertension: Abnormal renal vascular and endocrine responses to a mild psychological stimulus. Hypertension, 3, 11–17.
Hollifield, J. W., Sherman, K., VanderZwagg, R., & Shand, D. G. (1976). Proposed mechanisms of propranolol’s antihypertensive effects in essential hypertension. New England Journal of Medicine, 295, 68–73.
Ibsen, H., Leth, A., Hollnagel, H., Kappelgaard, A. M., Damkjaer Nielsen, M., Christensen, N. J., & Giese, J. (1979). Renin angiotensin system and sympathetic nerve activity in mild essential hypertension: The functional significance of angiotensin II in untreated and thiazide treated hypertensive patients. Acta Medica Scandinavia, 625 (Suppl.), 97.
Julius, S., & Conway, J. (1968). Hemodynamic studies in patients with borderline blood pressure elevation. Circulation, 38, 282–288.
Julius, S., Pascual, A. V., Sannerstedt, R., & Mitchell, C. (1971). Relationship between cardiac output and peripheral resistance in borderline hypertension. Circulation, 43, 382–390.
Julius, S., Pascual, A. V., Abbrecht, P., & London, R. (1972). Effect of beta-adrenergic blockade on plasma volume in human subjects. Proceedings of the Society for Experimental Biology and Medicine, 140, 982–985.
Julius, S., Randall, O. S., Esler, M. D., Kashima, T., Ellis, C. N., & Bennett, J. (1975). Altered cardiac responsiveness and regulation in the normal cardiac output type of borderline hypertension. Circulation Research, 36–57 (Suppl. I), I199–I207.
Laragh, J. H. (1976). Biochemistry of the renin axis; prostaglandins, indomethacin and renin; angiotensin blockade; beta-blockers as antirenin drugs. American Journal of Medicine, 60, 733–736.
Light, K. C., Koepke, J. P., Obrist, P. A., & Willis, P. W. (1983). Psychological stress induces sodium and fluid retention in men at high risk for hypertension. Science, 220, 429–431.
Lund-Johansen, P. (1967). Hemodynamics in early essential hypertension. Acta Medica Scandinavica, 482 (Suppl.), 1–105.
Mark, A. L., Lawton, W. J., & Abboud, F. M. (1975). Effects of high and low sodium intake on arterial pressure and forearm vascular resistance in borderline hypertension. Circulation Research, 36–37 (Suppl. I), I194–I198.
Obrist, P. A., Langer, A. W., Light, K., & Koepke, J. P. (1983). Behavioral-cardiac interactions in hypertension. In D. S. Krantz, A. Baum, & J. E. Singer (Eds.), Handbook of psychology and cardiovascular disorders & behavior: Vol. 3. Health. Hillsdale, NJ: Erlbaum.
Sannerstedt, R., & Julius, S. (1972). Systemic haemodynamics in borderline arterial hypertension: Response to static exercise before and under the influence of propranolol. Cardiovascular Research, 6, 398–403.
Sannerstedt, R., Julius, S., & Conway, J. (1970). Hemodynamic response to tilt and beta-adrenergic blockade in young patients with borderline hypertension. Circulation, 42, 1057–1064.
Widimsky, J., Fejfarova, M. H., & Fejfar, Z. (1957). Changes of cardiac output in hypertensive disease. Cardiologia, 31, 381–389.
Williams, R. B. (1986). Patterns of reactivity and stress. In K. A. Matthews, S. M. Weiss, T. Detre, T. M. Dembroski, B. Falkner, S. B. Manuch, & R. B. Williams (Eds.), Handbook of stress, reactivity and cardiovascular disease (pp. 109–125). New York: Wiley-Interscience.
Author information
Authors and Affiliations
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 1989 Springer Science+Business Media New York
About this chapter
Cite this chapter
Julius, S. (1989). Hemodynamic Assessment and Pharmacologic Probes as Tools to Analyze Cardiovascular Reactivity. In: Schneiderman, N., Weiss, S.M., Kaufmann, P.G. (eds) Handbook of Research Methods in Cardiovascular Behavioral Medicine. The Springer Series in Behavioral Psychophysiology and Medicine. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-0906-0_26
Download citation
DOI: https://doi.org/10.1007/978-1-4899-0906-0_26
Publisher Name: Springer, Boston, MA
Print ISBN: 978-1-4899-0908-4
Online ISBN: 978-1-4899-0906-0
eBook Packages: Springer Book Archive