Related Experiment Videos
Early structural changes in hypertension: pathophysiology and clinical consequences
1Department of Physiology, University of Göteborg, Sweden.
Insights
Hypertension causes long-term cardiovascular changes, including altered heart and vessel structure. Therapy should reverse these structural adaptations to normalize cardiovascular design and dimensions.
Area of Science:
- Cardiovascular Physiology
- Hypertension Pathophysiology
Background:
- Hypertension involves structural alterations in the heart and vasculature.
- Primary hypertension has polygenetic, environmental, and structural etiological factors.
- Early "structural upward resetting" affects cardiovascular hemodynamics.
Purpose of the Study:
- To outline principles of early "structural upward resetting" in hypertension.
- To discuss long-term hemodynamic effects of structural adaptations.
- To establish therapeutic goals for reversing structural changes.
Main Methods:
- Experimental illustration of physical and biological principles.
- Discussion of hemodynamic effects on resistance vessels, heart, and barostat mechanisms.
- Review of model studies in rats.
Main Results:
- Structural resetting of heart and vessels is a key long-term cardiovascular change in hypertension.
- Altered geometry of systemic precapillary resistance vessels has significant hemodynamic relevance.
- Adaptations affect systemic resistance, heart function, barostat mechanisms, and venous capacitance.
Conclusions:
- The primary therapeutic goal is to reverse structural cardiovascular changes toward normal design.
- Future treatments may focus on preventive measures.
- Therapy should reduce cardiac load and the influence of trophic factors.
Abstract:
The structural upward resetting of heart, vessels, and barostat functions represents what may be the most important long-term cardiovascular alteration in hypertension; the altered geometric design of the systemic precapillary resistance vessels is of profound hemodynamic relevance. This is especially true in primary (essential) hypertension, for which three major etiological elements can be distinguished: polygenetic predisposition, environmental factors, and the structural factor. The physical and biological principles behind the early "structural upward resetting" of heart and vessels in hypertension are outlined and experimentally illustrated. Further, the long-term hemodynamic effects of this per se "normal" structural adaptation are discussed, particularly concerning systemic precapillary resistance, but also concerning the heart, barostat mechanisms of reflex and renal nature, and the venous capacitance vessels. With this background in mind, the primary long-term goal of therapy must be to reverse these structural changes toward normal cardiovascular design and dimensions, whereas in the future preventive measures may be actualized. Thus, treatment should serve not only to reduce the increased load on heart and vessels but also, wherever possible, to reduce the influence of trophic, growth-promoting factors of local and remote nature, as exemplified by model studies in rats.