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Review
. 2016 May;12(3):339-49.
doi: 10.2217/fca.16.5. Epub 2016 Apr 19.

Hypertension: a problem of organ blood flow supply-demand mismatch

Maarten P Koeners  1 , Kirsty E Lewis  1 , Anthony P Ford  2 , Julian Fr Paton  1
Affiliations
Review

Hypertension: a problem of organ blood flow supply-demand mismatch

Maarten P Koeners et al. Future Cardiol. 2016 May.

Abstract

This review introduces a new hypothesis that sympathetically mediated hypertensive diseases are caused, in the most part, by the activation of visceral afferent systems that are connected to neural circuits generating sympathetic activity. We consider how organ hypoperfusion and blood flow supply-demand mismatch might lead to both sensory hyper-reflexia and aberrant afferent tonicity. We discuss how this may drive sympatho-excitatory-positive feedback and extend across multiple organs initiating, or at least amplifying, sympathetic hyperactivity. The latter, in turn, compounds the challenge to sufficient organ blood flow through heightened vasoconstriction that both maintains and exacerbates hypertension.

Keywords: hypertension; hypoperfusion; organ blood flow; sympathetic hyperactivity; visceral afferent hyper-reflexia.

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Conflict of interest statement

Financial & competing interests disclosure This work was supported by the British Heart Foundation (no. FS/14/2/30630 and RG/12/6/29670), the Royal Society (RG140387) and the European Union, Seventh Framework Programme, Marie Curie Actions (CARPEDIEM no. 612280). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. No writing assistance was utilized in the production of this manuscript.

Figures

<b>Figure 1.</b>
Figure 1.. Visceral afferent activation hypothesis of hypertension.
When afferents become sensitized due to, for example, high sympathetic activity, circulating angiotensin II, atheroma or congenital predisposition (although exact mediator[s] remain to be identified) they reflexly increase sympathetic vasomotor tone reducing making an organ vulnerable to hypoxic-hypoperfusion and reducing its blood flow reserve/capacity. We propose that this triggers release of metabolites that activate excessive afferent nerve activity, which exacerbate the reflex-evoked sympathetic vasoconstriction. Widespread sympathetic activation may recruit additional afferent systems resulting in additional drivers for maintaining pathologically high levels of sympathetic activity and total peripheral resistance. Thus, the system degenerates into a positive feedback loop in hypoxic-hypoperfusion and reduced blood flow reserve/capacity acts as an amplifier and conceivable initiator of sympatho-excitatory afferent drive. Consequently, vasoconstriction, arteriole remodeling increased total peripheral resistance, and end organ damage will amplify the organ blood flow supply–demand mismatch compounding the problem of hypoperfusion and the development and maintenance of hypertension. We do not rule out that excessive sympathetic activity itself sensitizes the afferent nerves mediating the reflex-evoked sympatho-excitation. Artwork was provided by Michel Cekalovic [12].
See this image and copyright information in PMC

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