Skip to main content
Log in

Are different hemodynamic patterns of antihypertensive drugs clinically important?

European Journal of Clinical Pharmacology Aims and scope Submit manuscript

Summary

Since vascular resistance is elevated in hypertension, it is suggested that vasodilators lower the blood pressure by a physiologic mechanism and therefore must be more useful than cardiac output-lowering drugs. This is not entirely correct. Drugs that lower cardiac output are also relative vasodilators, but the vasodilation occurs at a lower level of cardiac output. It is also not necessarily true that all vasodilators are good antihypertensive agents. The clinical profile of a vasodilator depends on its effect on the venous return, cardiac output, regional blood flow, renin-angiotensin system, and sympathetic reflexes. From the viewpoint of hemodynamics, an ideal antihypertensive drug is a vasodilator that does not excessively increase cardiac output, causes no fluid retention, does not induce a great deal of venodilation, and does not elicit substantial neurohumoral counterregulation. Angiotensin-converting-enzyme inhibitors, some calcium antagonists, and some combined alpha/beta-blocking agents come close to satisfying the hemodynamic definition of an ideal antihypertensive drug.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Institutional subscriptions

Similar content being viewed by others

References

  1. Julius S (1988) The blood pressure seeking properties of the central nervous system. J Hypertension 6: 177–185

    Google Scholar 

  2. Julius S, Egan B (1986) Hemodynamics of hypertension. In: Zanchetti A, Tarazi RC (eds) Handbook of hypertension, vol 7. Pathophysiology of hypertension — cardiovascular aspects. Elsevier, Amsterdam, pp 153–178

    Google Scholar 

  3. Strandgaards OJ, Skinhoj E, Lassen NA (1973) Autoregulation of brain circulation in severe arterial hypertension. Br Med J 1: 507–510

    Google Scholar 

  4. Hansson L, Zweifler AJ, Julius S, Hunyor SN (1974) Hemodynamic effects of acute and prolonged β-adrenergic blockade in essential hypertension. Acta Med Scand 196: 27–34

    PubMed  Google Scholar 

  5. Bevan RD (1975) Effect of sympathetic denervation on smooth muscle cell proliferation in the growing rabbit ear artery. Ore Res 37: 14–19

    Google Scholar 

  6. Hart MN, Heistad DD, Brody MJ (1980) Effect of chronic hypertension and sympathetic denervation on the wall/lumen ratio of cerebral vessels. Hypertension 2: 419–428

    PubMed  Google Scholar 

  7. Sen S, Tarazi RC, Bumpus FM (1977) Cardiac hypertrophy and antihypertensive therapy. Cardiovasc Res 11: 427–433

    PubMed  Google Scholar 

  8. Simpson P (1983) Norepinephrine-stimulated hypertrophy of cultured rat myocardial cells in an alpha1-adrenergic response. J Clin Invest 72: 732–738

    PubMed  Google Scholar 

  9. Ibsen H, Egan B, Julius S (1983) Baroreflex sensitivity during converting enzyme inhibition with Enalapril (MK-421) in normal man. J Hypertens 1 [Suppl 2]: 222–224

    Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Rights and permissions

Reprints and permissions

About this article

Cite this article

Julius, S. Are different hemodynamic patterns of antihypertensive drugs clinically important?. Eur J Clin Pharmacol 38 (Suppl 2), S125–S128 (1990). https://doi.org/10.1007/BF01409481

Download citation

  • Issue Date:

  • DOI: https://doi.org/10.1007/BF01409481

Key words

Navigation