Comparison of the Reflex Effects of Arterial Baroreceptors and Cardiac Receptors on the Heart Rate of Conscious Rabbits

Abstract

The reflex effects on heart rate (HR) of presumptive cardiac receptors have been differentiated from those of the arterial baroreceptors in conscious rabbits by inflating cuffs on the ascending aorta, descending aorta, inferior vena cava and pulmonary artery. When the outflow from the right ventricle was progressively impeded the accompanying increase in HR was entirely explicable by unloading of the arterial baroreceptors. As the outflow from the left ventricle was progressively impeded there was an initial increase in HR due to unloading of the arterial baroreceptors, followed by a progressive decline. This decline was attributed to a reflex arising from vagally-innervated receptors in the left side of the heart. The threshold of this cardiac receptor-HR reflex occurred at a higher level of mean aortic pressure than that at which the effects of the arterial baroreceptors on HR were maximal. Cholinergic (vagal) efferent nerves were responsible for two-thirds of the decline in HR caused by the reflex. The properties of the cardiac receptor-HR reflex were altered by drugs that affect myocardial contractility. Isoprenaline raised the mean aortic pressure at which the threshold occurred, but lowered the corresponding level of left ventricular end-diastolic pressure. Propranolol virtually abolished the reflex, even though left ventricular end-diastolic pressure reached a high level. It is concluded that in the conscious rabbit the arterial baroreceptor reflexes normally prevent the threshold of the cardiac receptor-HR reflex from being attained.

Acute Deletion of Arterial Baroreceptor Input in the Conscious Rabbit

“…This is because there is functional redundancy among the baroreceptor population, at any rate with respect to the retlex control of blood pressure, which is reflected in the demonstration that interaction among the inputs from the different sets of baroreceptors is usually inhibitory (Spyer, 1981;Abboud and Thames, 1984). In this connection it is noteworthy that the resting levels of blood pressure and heart rate in our rabbits (Table 1), in which only the baroreceptors in one carotid sinus were intact, were very similar to those found in normal rabbits of the same strain with all baroreceptors intact (Blombery and Korner, 1979;Dorward et ai, 1982;Ludbrook, 1984). It is also noteworthy that after 7 days the blood pressure and heart rate were elevated by 24 mmHg and 42 beats min ' respectively (Table 1), values that are very similar to those reported 6 to 7 days after surgical denervation of all baroreceptors (Blombery and Korner, 1979;Ludbrook, 1984).…”

“…The abrupt rise of blood pressure that followed carotid sinus denervation might be expected to excite other cardiovascular receptors, especially those in the left side of the heart (Thoren, 1979). Indeed, the rise of blood pressure exceeds the threshold in conscious rabbits for a heart rate depressor reflex that originates from vagally innervated left-sided cardiac receptors (Ludbrook, 1984), but this is a reflex that acts powerfully within seconds. It has been suggested that a rise of blood pressure increases the renal excretion of water and sodium, and so reduces blood volume (Guyton et ai, 1974).…”

Baroreflex resetting but no vascular tolerance in response to transdermal glyceryl trinitrate in conscious rabbits

“…Excessive increases in MAP caused reflex bradycardic responses that lay obviously below the level of the lower plateau of the fitted baroreceptorheart rate reflex curve (barocurve). These points were removed as outliers, indicative of cardiac reflex activation and not a component of the baroreceptor reflex (Ludbrook, 1984).…”

Chemosensitive cardiopulmonary afferents and the haemodynamic response to simulated haemorrhage in conscious rabbits

“…Baroreceptor-heart rate reflex This was elicited by inflating the aortic and caval cuffs so that MAP rose or fell at 1-2 mmHg s 1 (Ludbrook, 1984).…”

“…At first, peripheral resistance increases along with the fall of cardiac output, so that mean arterial pressure is maintained at a near-normal level (Ludbrook & Graham, 1984;Schadt et al, 1984;Ludbrook & Rutter, 1988;Ludbrook et 1 Author for correspondence. al., 1988).…”