Hypertension: a problem of organ blood flow supply-demand mismatch.
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.
School of Physiology, Pharmacology & Neuroscience, Biomedical Sciences, University of Bristol, Bristol, UK.
Maarten P
MP
Koeners
School of Physiology, Pharmacology & Neuroscience, Biomedical Sciences, University of Bristol, Bristol, UK.
Kirsty E
KE
Lewis
Afferent Pharmaceuticals, 2929 Campus Drive, San Mateo, CA, USA.
Anthony P
AP
Ford
School of Physiology, Pharmacology & Neuroscience, Biomedical Sciences, University of Bristol, Bristol, UK.
Julian Fr
JF
Paton
D000344:Afferent Pathways / Q000502:physiology; D002344:Carotid Body / Q000098:blood supply; D004525:Efferent Pathways / Q000502:physiology; D025461:Feedback, Physiological; D006439:Hemodynamics; D006706:Homeostasis; D006801:Humans; D006973:Hypertension / Q000209:etiology* / Q000503:physiopathology; D007668:Kidney / Q000098:blood supply / Q000294:innervation; D018482:Muscle, Skeletal / Q000098:blood supply / Q000294:innervation; D012039:Regional Blood Flow / Q000502:physiology*; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D014655:Vascular Resistance
hypertension; hypoperfusion; organ blood flow; sympathetic hyperactivity; visceral afferent hyper-reflexia