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. 1989 Sep;7(4):S1-4.

Myogenic mechanisms in the control of systemic resistance. Introduction and historical background

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  • PMID: 2681587

Myogenic mechanisms in the control of systemic resistance. Introduction and historical background

B Folkow. J Hypertens Suppl. 1989 Sep.

Abstract

This paper surveys the early studies and ideas that led to the development of the Bayliss theory in 1902 of a pressure-dependent myogenic tone in the systemic resistance vessels; this important concept was not experimentally verified until about 50 years later. Studies of the complex interactions between this 'active' intrinsic vascular tone, 'passive' wall distensibility and tissue-produced vasodilator factors gradually led to a better understanding of local circulatory control. Precapillary smooth muscles seem to function almost like 'stretch (and/or tension?) receptors with built-in contractility', where transmural pressure serves as a limited positive feedback and tissue vasodilator factors as a potentially powerful negative feedback. Together, these positive and negative feedback factors automatically adjust blood supply to local tissue needs and also protect the capillary exchange section from undue pressure increases thanks to the ensuing 'functional autoregulation'. Observations in these early studies also led to experimental analyses of what was later called 'structural autoregulation', as a long-term analogue to 'functional autoregulation'. 'Structural autoregulation' is the rapid morphological adaptation of the precapillary resistance vessels in hypertension whereby, by a structurally based inner radius reduction and hypertrophic wall (media) thickening, systemic resistance becomes reset upwards for functional operation at a higher pressure level. Like 'functional autoregulation', 'structural autoregulation' is essentially a local vascular response to pressure changes. Finally, myogenic activity, functional and structural autoregulation may have important cellular mechanisms in common, while 'extrinsic' influences, from nexa-connected endothelial cells and neurohormonal mechanisms for example, are likely to act as important modulators of intrinsic smooth muscle activities.

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