Related Experiment Videos
Hypertension and the vasculature: arterioles and the myogenic response
Insights
Hypertension may stem from arterioles, not just small arteries. Arteriolar myogenic responses could be key to high blood pressure, challenging previous assumptions about vascular resistance.
Area of Science:
- Cardiovascular Physiology
- Vascular Biology
Background:
- Established hypertension is often characterized by normal cardiac output and increased peripheral resistance.
- This view assumes uniform vascular bed responsiveness, which may not hold true due to tissue specialization and vascular wall variations.
Discussion:
- Resistance to blood flow is highest in arterioles, while small arteries undergo structural changes leading to narrowing.
- Recent findings show blood pressure can drop post-stimulus despite structural changes, and some studies question vascular amplification under stress.
Key Insights:
- The vascular tree functions as an integrated circuit with specialized beds.
- Increased resistance in one vascular bed during a constrictor challenge may not reflect the entire circulation; resistance might decrease elsewhere.
Outlook:
- Structural changes in small arteries are likely a consequence, not the cause, of hypertension.
- The pathogenesis of hypertension may involve downstream arterioles, particularly their myogenic response.
Objective:
This editorial was invited by the Journal of Hypertension as one of a series designed to examine our current knowledge of several aspects of the pathophysiology of hypertension. This article considers small arteries and arterioles.
Setting:
The conclusion that established hypertension is characterized by a normal cardiac output and a raised peripheral resistance represents the integration of findings from haemodynamic studies using a variety of models of the disease examined by several different techniques. In some ways it assumes that all vascular beds conform to the same pattern of responsiveness. However, given the obvious heterogeneity of functions performed by specialized tissues, the recognized variations in receptor populations and the differences in innervation found in the vascular wall throughout the circulation, this might not be the case. Resistance to blood flow occurs throughout the vascular tree, but the majority is found at the level of arterioles. Upstream small arteries demonstrate growth and remodelling changes which result in luminal narrowing, but the exact contribution of such vessels to resistance is still not known. Perhaps the most interesting recent finding in this context is that blood pressure can fall immediately after a pressor stimulus has been removed, despite the demonstration of such structural changes in small arteries. Furthermore, some whole-animal studies have been reported which fail to show the expected vascular amplification when the circulation is stressed in total.
Conclusion:
Viewing the vascular tree as an integrated circuit with specialized functions when nourishing specific tissues suggests that when the resistance in one vascular bed increases because of a constrictor challenge, this might not be representative of the circulation as a whole: indeed, resistance may fall elsewhere. It is probable that structural changes in small arteries represent the consequence of hypertension. The pathogenesis of hypertension may reside downstream in arterioles, where a myogenic response might play a fundamental role.