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Videomorphometric Analysis of Hypoxic Pulmonary Vasoconstriction of Intra-pulmonary Arteries Using Murine Precision Cut Lung Slices
Published on: January 14, 2014
Respiratory modulated sympathetic activity: a putative mechanism for developing vascular resistance?
Linford J B Briant1,2, Erin L O'Callaghan1, Alan R Champneys2
1School of Physiology & Pharmacology, Medical Sciences Building, University Walk, University of Bristol, Bristol, BS81TD, UK.
Respiratory modulation of sympathetic nerve activity (SNA) enhances vasoconstriction in normal rats but not in hypertensive rats. This pattern dependency, linked to noradrenaline reuptake, may contribute to hypertension development.
Area of Science:
- Cardiovascular Physiology
- Neuroscience
- Hypertension Research
Background:
- Sympathetic nerve activity (SNA) shows respiratory modulation, influencing vascular tone.
- The precise impact of this modulation on vasoconstriction is not fully understood, particularly in hypertension.
Purpose of the Study:
- To investigate if respiratory modulation of SNA increases vasoconstriction more than tonic stimulation.
- To examine this effect in both normotensive and spontaneously hypertensive (SH) rats.
- To elucidate the underlying mechanisms, including noradrenaline reuptake.
Main Methods:
- Mathematical modeling of sympathetic innervation of arterioles.
- In vivo stimulation of the sympathetic chain in Wistar and SH rats.
- Measurement of vascular resistance (VR) changes in response to different SNA patterns.
Main Results:
- Respiratory modulated SNA significantly increased vasoconstriction compared to tonic stimulation in Wistar rats.
- This pattern-dependent increase in VR was quicker with modulated SNA.
- In SH rats, the difference in VR between modulated and tonic SNA was not significant.
- Mathematical modeling suggested dysfunctional noradrenaline reuptake in SH rats may explain the lack of pattern dependency.
Conclusions:
- Respiratory modulation of SNA is an effective mechanism for prompt vasoconstriction in normotensive rats.
- This pattern dependency is mediated by a noradrenergic mechanism.
- Dysfunctional noradrenaline reuptake in hypertensive rats may lead to system saturation, impairing the vasoconstrictive response.
- Respiratory modulated SNA may play a role in the development of hypertension.
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