Cardiovascular control from cardiac and pulmonary vascular receptors

Abstract

What is the topic of this review? The purpose of this review is to summarize present knowledge of the function of the afferent nerves arising from the heart and the coronary and pulmonary arteries. Although there is abundant evidence that atrial receptor stimulation influences heart rate and urine flow, with little or no effect elsewhere, and that ventricular receptors are strongly excited only by chemical stimuli, there is still the erroneous belief that they act as a homogeneous group causing cardiovascular depression. What advances does it highlight? Coronary receptors deserve to be recognized as a potentially important additional group of baroreceptors. Stimulation of pulmonary arterial baroreceptors at physiological pressures causes reflex vasoconstriction and could have a hitherto unacknowledged important role in cardiovascular control, for example in exercise. Although there has been a tendency to regard cardiac and pulmonary receptors as a single population of 'cardiopulmonary receptors', this cannot be justified as the various receptor types all induce their own particular pattern of responses. Stimulation of atrial receptors increases activity in sympathetic nerves to the sino-atrial node, causing tachycardia, but there is no effect on activity to the myocardium or to most blood vessels. Renal nerve activity, however, is decreased, and secretion of antidiuretic hormone is inhibited, causing diuresis. Ventricular receptors induce a powerful depressor response, but only in response to abnormal chemical stimulation and possibly to myocardial injury. Coronary arterial receptors function as baroreceptors, but have a lower threshold and a more prolonged effect than other baroreceptors. Pulmonary arterial baroreceptors induce vasoconstriction and respiratory stimulation at physiological pressures and may be of importance in mediating some of the responses to exercise, as well as in hypoxic conditions.

Paradoxical Muscle Sympathetic Reflex Activation in Human Heart Failure

“…22,23 The classic or anticipated cardiopulmonary reflex response (ie, reflex sympathoinhibition elicited by increased cardiac filling pressure, governed primarily by stimulation of unmyelinated vagal afferents located mainly in the left ventricle) is presumed to normally predominate. However, cardiac myelinated vagal afferents located primarily at venoatrial junctions elicit paradoxical reflex cardiac and peripheral sympathetic excitation when stimulated by similar mechanical stretch.…”

Clinical neurocardiology defining the value of neuroscience‐based cardiovascular therapeutics

“…These receptors respond to differing amounts of stretch caused by changes in arterial blood pressure and when stimulated by higher pressure they generally evoke reflex responses that serve to lower blood pressure including a reduction in heart rate and reduced sympathetic outflow, with directionally opposite responses seen when blood pressure falls. There are also stretch-sensitive receptors in the heart, great veins and lungs that respond to a number of stimuli related to the 'fullness' of the central circulation (Hainsworth, 2014).…”

The Thrill of Success: Central Arterial-Venous Anastomosis for Hypertension

“…Ultimately increased right-sided filling pressures would result in increased stimulation of mechanoreceptors in the right atrium, and caval draining veins would result in a peripheral sympathoinhibition (like renals sympathetic nervous system) with parallel activation of cardiac sympathetic activity (tachycardia), precipitated by the Bainbrige reflex [30]. At the same time, cardiac mechanoreceptors located in the left ventricle increase the vagal tone resulting in bradycardia (vagally mediated) and peripheral vasodilation [30]. Thus, the immediate hemodynamic effects of the anastomosis as well as the long-term neuro-humeral changes predict a significant and durable blood pressure decline.…”