The Role of the Brain in Prehypertension

  • Stevo JuliusEmail author
Part of the Updates in Hypertension and Cardiovascular Protection book series (UHCP)


Prolonged blood pressure (BP) elevation causes changes in the structure and function of cardiovascular organs. Therefore, our research group focused on young patients with prehypertension.

One third of young adults with prehypertension have a hyperkinetic circulation characterized by increased BP and heart rate. In such patients sympathetic stimulation is increased, whereas the parasympathetic inhibition is decreased. This strongly suggests that the abnormality originates from the brain (medulla oblongata) where the sympathetic and parasympathetic tones are regulated in a reciprocal fashion. Patients with hyperkinetic prehypertension are not hyper-responders to stressors, and there is no evidence of increased BP variability in response to various stressors. Rather, in prehypertension the brain operates in a normal fashion around a preset higher basal BP level. In achieving the higher BP goal, the brain shows a remarkable plasticity; if the stressor is associated with increased cardiac output and that increase is blocked (by beta-blockers), an equal BP increase will be achieved by a higher vascular resistance. Similarly, if the original stressor induced increased vascular resistance and this was blocked (with alpha-blockers), the same degree of BP elevation will be achieved by increased cardiac output.

It was suggested that the hyperkinetic BP elevation may be a stressful response to the invasive hemodynamic measurement (cardiac and arterial catheterization). However, in the Tecumseh study, we used a noninvasive method of measurement, and, akin to invasive procedure, 37% of young adults with prehypertension had a hyperkinetic circulation. These patients had elevated BP at 5, 8, 21, and 23 of age, and their parents also had higher BP.

Overall these findings prove that the brain plays an important role in the pathophysiology of one third of patients with prehypertension.


Hemodynamics Prehypertension Hyperkinetic circulation Central nervous system Brain Sympathetic tone Parasympathetic tone Tachycardia 


  1. 1.
    Freis ED. Hemodynamics of hypertension. Physiol Rev. 1960;40:27–54.CrossRefPubMedGoogle Scholar
  2. 2.
    Eich RH, Peters RJ, Cuddy RP, et al. The hemodynamics of labile hypertension. Am Heart J. 1962;63:188–95.CrossRefPubMedGoogle Scholar
  3. 3.
    Widimski J, Fejfarova MH, Fejfar Z. Changes of cardiac output in hypertensive disease. Cardiologia. 1957;31:381–9.CrossRefGoogle Scholar
  4. 4.
    Finkielman S, Worcel M, Agrest A. Hemodynamic patterns in essential hypertension. Circulation. 1965;31:356–68.CrossRefPubMedGoogle Scholar
  5. 5.
    Julius S. Neurogenic component in borderline hypertension. Chapter 14. In: Julius S, Esler MD, editors. The nervous system in arterial hypertension. Springfield: Charles C Thomas Publisher; 1976.Google Scholar
  6. 6.
    Julius S, Conway J. Hemodynamic studies in patients with borderline blood pressure elevation. Circulation. 1968;38:282–8.CrossRefPubMedPubMedCentralGoogle Scholar
  7. 7.
    Julius S, Pascual A, London S. Role of parasympathetic Inhibition in the hyperkinetic type of borderline hypertension. Circulation. 1971;44:413–8.CrossRefGoogle Scholar
  8. 8.
    Julius S, Pascual AV, Sannerstedt R, Mitchel C. Relationship between cardiac output and peripheral resistance in borderline hypertension. Circulation. 1971;43:382–90.CrossRefPubMedGoogle Scholar
  9. 9.
    Osterziel K, Julius S, Brant DO. Blood pressure elevation during hindquarter compression in dogs is neurogenic. J Hypertens. 1984;2:411–7.CrossRefPubMedGoogle Scholar
  10. 10.
    Julius S, Sanchez R, Brant D. Pressure increase to external hind quarter compression in dogs: a facultative regulatory response. J Hypertens. 1986;4:54–6.Google Scholar
  11. 11.
    Julius S. The blood pressure seeking property of the central nervous system. J Hypertens. 1988;6:177–85. Editorial review.CrossRefPubMedGoogle Scholar
  12. 12.
    Levy RL, White PD, et al. Transient tachycardia; prognostic significance alone and in association with transient hypertension. Med Press Egypt. 1946;38:207–12.PubMedGoogle Scholar
  13. 13.
    Palatini P, Julius S. Association of tachycardia with morbidity and mortality: pathophysiological considerations. J Hum Hypertens. 1997;11:S19–27.PubMedGoogle Scholar
  14. 14.
    Ferguson RJ, Faulkner JA, Julius S, Conway J. Comparison of cardiac output determined by CO2 rebreathing and dye dilution methods. J Appl Physiol. 1968;25:450–4.CrossRefGoogle Scholar
  15. 15.
    Kiowski W, Randall OS, Steffens TG, Julius S. Reliability of echocardiography in assessing cardiac output. A comparative study with a dye dilution technique. Klin Wochenschr. 1981;59:1115–20.CrossRefPubMedGoogle Scholar
  16. 16.
    Julius S, Jamerson K, Mejia A, Krause L, Schork N, Jones K. The association of borderline hypertension with target organ changes and higher coronary risk Tecumseh blood pressure study. JAMA. 1990;264:354–8.CrossRefPubMedPubMedCentralGoogle Scholar
  17. 17.
    Julius S, Jamerson K. Sympathetics, insulin resistance and coronary risk in hypertension: the ‘chicken-and-egg’ question. J Hypertens. 1994;12:495–502. Editorial review.CrossRefPubMedPubMedCentralGoogle Scholar

Copyright information

© Springer International Publishing AG, part of Springer Nature 2019

Authors and Affiliations

  1. 1.Michigan Medicine, Frankel Cardiovascular CenterUniversity of MichiganAnn ArborUSA

Personalised recommendations