After the discovery ofthe pulmonary circulation by Ibn-an-Nafis in the thirteenth century and by Servetus in the sixteenth century and the discovery of the systemic circulation of the blood by Harvey in 1628, arterial pressure was first measured by Stephen Hales in 1733 and then by Poiseuille in 1828 and Ludwig in 1847, wno recorded arterial blood pressure by means ofa glass tube or a mercury manometer connected with an artery. As a result of numerous observations, the physiologists concluded that the arterial pressure was subject to regulation and tried to clarify the mechanisms. In 1836 Astley Cooper observed that compression of both common carotid arteries, which induced a fall of arterial pressure in the head and brain, provoked acceleration of the heart rate and a rise in the systemic arterial pressure (1). This observation was confirmed by Magendie in 1838 (2). Experiments done between 1877 and 1926 by several workers (3-10) showed that a rise of blood pressure in the carotid-cephalic circulation induces bradycardia and a fall of the systemic arterial pressure, while a drop in the carotid-cephalic pressure provokes acceleration ofthe heart rate and a rise ofsystemic arterial pressure. All these experimental observations were considered to be a demonstration ofa direct sensitivity of the cardiovascular centers to blood pressure variations. The direct central regulation and homeostasis of arterial pressure by means of the action of blood pressure variations on the cardiovascular centers was thus generally accepted. But as early as 1900 Pagano (11) and Siciliano (12), of the laboratory of Spallitta in Palermo, published an interesting series of experiments. Siciliano showed that while clamping of both common carotid arteries induced tachycardia and a rise in the systemic arterial pressure, clamping of

Reflexogenic Areas of the Cardiovascular System

THE SEARCH for natriuretic hormones or factors by studies of negative pressure breathing, atrial distension experiments, head-out water immersion, expansion of blood volume, Na+/K+-ATPase inhibitors and parabiosis experiments in Dahl rats has led to the finding that the atria are a peptide-secreting endocrine gland. This new natriuretic hormone has now been purified, sequenced and synthetized, and its cDNA and gene have been cloned. The native and synthetic hormones exert identical wide ranging effects (possibly through particulate guanylate cyclase stimulation and adenylate cyclase inhibition) on the kidney, blood vessels, adrenal cortex, and pituitary. Physiopathologic implications of the hormone in experimental hypertension, congestive heart failure, and expansion of blood volume are beginning to emerge.

The Heart and the Atrial Natriuretic Factor

Role of cardiac vagal C-fibers in cardiovascular control.

Impulse activity in vagal afferent fibres and changes in heart rate were simultaneously recorded during rapid hemorrhage or blood pooling in cats in order to elucidate whether the sudden reflex bradycardia, sometimes evoked with the mentioned interventions, was correlated to an increased activity in any type of heart receptors. The results show that the slowing of the heart, resulting from an emptying of the central blood reservoirs was correlated to, and preceded by, an increased activity in receptors located in the left ventricle and signalling in non-medullated afferents. The receptors were found to be activated also by obstructions of the ascending aorta and mechanical stimulation of the heart, and therefore seem to operate as mechanorecepton, stimulated by a “distortion” of the myocardium. - It is conceivable that with rapid bleeding or pooling of blood, the receptors are excited by an improper squeezing of the myocardium when the ventricles contract vigorously around an almost empty chamber, and then induce a reflex bradycardia. This reflex mechanism, resembling the so-called vaso-vagal syncope reaction in man, may therefore serve as a protective system causing a break on the heart and allowing for an improved diastolic filling in situations when venous return is critically reduced.

Increased Activity in Left Ventricular Receptors during Hemorrhage or Occlusion of Caval Veins in the Cat. ‐ A Possible Cause of the Vaso‐vagal Reaction

Studies were performed on 11 healthy men to evaluate the role of low pressure baroreceptors in the reflex forearm vasoconstrictor responses (plethysmography) to venous pooling produced by lower body negative pressure. Lower body negative pressure (LBNP) at - 5, - 10, - 20, and - 40 mm Hg lowered central venous pressure by 42, 59, 74, and 93%, respectively, and decreased forearm vascular conductance by 24, 29, 34, and 40%, respectively. The decreases in forearm blood flow and conductance during the low levels of venous pooling (LBNP - 5 and - 10 mm Hg) occurred without significant changes in arterial pressure, arterial dP/dt. and heart rate. These results with the low levels indicate that maneuvers which decrease venous return and central venous pressure in man can influence forearm vascular tone without significant changes in the determinants of carotid and aortic baroreceptor activity. During high levels of venous pooling (LBNP - 20 and - 40 mm Hg), significant decreases in arterial pressure and dP/dt and significant increases in heart rate accompanied the further reductions in central venous pressure, forearm blood flow, and forearm vascular conductance. About 73% of the decrease in conductance during venous pooling at LBNP - 40 mm Hg, which was sufficient to decrease arterial pressure and activate high pressure baroreceptor reflexes, occurred during low levels of venous pooling at LBNP - 10 mm Hg without changes in arterial pressure. This suggests that much of the forearm vasoconstriction with the high levels of venous pooling, which were sufficient to decrease arterial pressure, may be accounted for by reflexes originating in areas other than high pressure baroreceptors. The results of these studies suggest that low pressure baroreceptors exert an important influence on forearm vascular tone during decreases in venous return and central venous pressure in man.

/pdf/the-role-of-low-pressure-baroreceptors-in-reflex-a9vsjdcx0e.pdf

The role of low pressure baroreceptors in reflex vasoconstrictor responses in man

The satisfactory recording of impulses in afferent fibres from receptors in the great veins and atria has been accomplished by a number of investigators (Amann & Schaifer, 1943; Walsh, 1947; Whitteridge, 1948; Jarisch & Zotterman, 1948; Dickinson, 1950; Neil & Zotterman, 1950), and it has been shown that their frequency of discharge is related to the pressure in the great veins and atria (Whitteridge, 1948; Dickinson, 1950). The receptors so far described are known to arise from the atria and are characterized by the presence of an a volley of impulses in time with the a wave of the venous pressure curve. Hereafter these will be referred to as type A atrial receptors. The existence of another kind of cardiovascular fibre in the vagus was reported by Walsh & Whitteridge (1944) and confirmed by Whitteridge (1948). It was shown that this fibre differed in many ways from venous and depressor fibres and, for several reasons, it was believed that it arose from receptors in the small vessels of the lung. Later, Pearce & Whitteridge (1951) showed that a linear relationship existed between the activity of these 'pulmonary vascular' fibres and the pulmonary arterial pressure. The blocking temperature of these fibres was shown to be about 8 to 40 C (Torrance & Whitteridge, 1948) which corresponded well with their conduction velocity (Paintal, 1952). However, no experiments with the view to locating these pulmonary vascular receptors had been undertaken with the open chest so far. This was recently achieved, and in this paper the results of these experiments will be described. It will be shown that all such receptors encountered so far arose in the right and left atria of the heart; these will be referred to as type B atrial receptors. METHODS

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1113/jphysiol.1953.sp004920

A. S. Paintal

Papers

A study of right and left atrial receptors.