Identifies left ventricular pressoreceptors that mediate vagus-dependent bradycardia, vasodilatation, and respiratory inhibition in response to increased left heart pressure.
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Should not alter clinical practice; leaves open translation of LV pressoreceptor reflexes to humans.
In anesthetized dogs increasing inflow into the left side of the heart (vascularly isolated from the lungs) causes bradycardia. This response is not mediated by the aortic depressor nerve but is dependent on an intact vagus. Obstruction of flow by inflating a balloon in the aortic valve causes bradycardia, vasodilatation of the perfused hind legs and respiratory inhibition which are dependent on an intact vagus. The participating pressoreceptors are believed to be in the walls of the left ventricle rather than the left atrium.
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Aviado et al. (1959) studied this question.
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