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This Article Full Text Full Text (PDF) All Versions of this Article: 92/1/3    most recent expphysiol.2006.035378v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Coote, J. H. Search for Related Content PubMed PubMed Citation Articles by Coote, J. H. Related Collections Lectures

¹ Division of Neuroscience, The Medical School, University of Birmingham, Birmingham B15 2TT, UK

Abstract

In this Paton Lecture I have tried to trace the key experiments that have developed ideas on how the brain regulates the cardiovascular system. It is a personal view and inevitably, owing to constraints on space and time, I have not been able to cover areas such as the nucleus tractus solitarius and cardiac vagal neurones, although I acknowledge that some may consider the story is incomplete without them. Starting with the crucial discovery of vasomotor nerves and ‘vasomotor tone’, the patterns of activity in sympathetic nerves which led to the important idea of central oscillating networks of neurones are described. I discuss how this knowledge has informed current controversies on the origin of vasomotor activity in presympathetic neurones in the ventral medulla, which identify intrinsic pacemaker activity or synaptic input from multiple oscillators as prime mechanisms. I present an emerging view that the role of other regions of the brain, in particular supramedullary sites, has been underplayed. These regions are pivotal for the non-uniform distribution of cardiac output that is unique to each reflex and behavioural state. I discuss the most recent evidence for ‘central command’ neurones that offers a plausible explanation for how these patterns of sympathetic activity are achieved. Finally, I stress the importance of these current ideas to the understanding of pathological changes in sympathetic activity in cardiovascular diseases such as hypertension or congestive heart failure.

(Received 18 August 2006; accepted after revision 3 October 2006; first published online 9 October 2005)
Corresponding author J. H. Coote: Division of Neuroscience, The Medical School, University of Birmingham, Birmingham B15 2TT, UK. Email: j.h.coote{at}bham.ac.uk

This lecture was given at the joint international meeting of The Physiological Society and FEPS at the University of Bristol, UK on 21st July 2005.

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