The control of arterial pressure during sleep was studied in 13 untreated, unsedated subjects aged 20 to 46, including 7 with hypertension. Arterial pressure was measured directly. A transient rise of arterial pressure up to 30 mm Hg was produced by the sudden intravenous injection of 0.25 to 2 µg of angiotensin. Linear plots were obtained in 10 of 13 subjects when the systolic pressures of successive pulses during the pressure rise were plotted against the pulse intervals which began the next beat. The relationship was disturbed by movement or arousal, and was better when pulse intervals falling in inspiration were discarded. The slope of the line (milliseconds of cardiac slowing per millimeter rise in systolic pressure) in the awake subject ranged from 2 to 15.5 msec/mm Hg, and from 4.5 to 28.9 during sleep. Reflex sensitivity was highest in dreaming sleep. In 7 of 10 subjects, baroreflex sensitivity increased significantly during sleep; in 6, the prevailing arterial pressure was inversely correlated wi...

Reflex Regulation of Arterial Pressure during Sleep in Man: A Quantitative Method of Assessing Baroreflex Sensitivity

The relationship of respiratory sinus arrhythmia amplitude (RSA) to tidal volume and breathing frequency was quantified during voluntarily controlled tidal volume and breathing frequency and spontaneous quiet breathing. Seventeen seated subjects breathed via mouthpiece and nose-clip, maintaining constant tidal volumes at each of several breathing frequencies. Inspiratory breath hold was zero frequency. Log RSA was plotted vs. log frequency for each tidal volume. The large stable RSA for frequencies less than 6 cycles/min was called low-frequency intercept (LFI, 20 +/- 5 beats/min). Low-frequency intercept was inversely proportional to a subject's age only to 35 yr. At higher breathing frequencies above a characteristic corner frequency (fC, 7.2 +/- 1.5 cycles/min) RSA decreased with constant slope (roll-off; 21 +/- 3.4 dB/decade). The RSA-volume relationship was linear permitting normalization of RSA-frequency curves for tidal volume to yield one curve. Spontaneous breathing data points fell on this curve. Voluntarily coupling of heart rate to breathing frequency in integer ratios reduced breath-by-breath variability of RSA without changing mean RSA. In conclusion, low-frequency intercept, corner frequency, and roll-off characterize an individual's RSA-frequency relationship during both voluntarily controlled and spontaneous breathing.

Respiratory sinus arrhythmia in humans: how breathing pattern modulates heart rate

Arterial pressure regulation: Overriding dominance of the kidneys in long-term regulation and in hypertension☆

The arterial pressure of the adult human rarely deviates from normal by more than 10 to 15 percent during each day. To achieve such constancy, the body has a network of pressure control systems. Several are based on neural receptors that respond within seconds to help correct any abnormal pressure. The activities of these systems are followed within minutes by activation of hormonal controllers. Within hours or days, a kidney pressure control system is induced that increases body fluid volume when the pressure falls (or decreases the volume when the pressure rises). This kidney-fluid system is the dominant method of establishing long-term pressure control.

https://science.sciencemag.org/content/sci/252/5014/1813.full.pdf

Blood pressure control--special role of the kidneys and body fluids.

A wide variety of tissues undergo a change of functional state on exposure to noradrenaline or adrenaline. Those molecular constituents of the effector cells of a tissue with which molecules of these catecholamines must first interact in order to produce a change of state — or response — of the tissue, are the so-called adrenoceptors (also commonly called adrenergic receptors). For convenience, we refer to noradrenaline, adrenaline and other agents which produce responses in tissues by interacting with adrenoceptors, as adrenergic agonists. An agent which specifically inhibits a response produced by an adrenergic agonist is referred to as adrenergic blocking agent or adrenergic antagonist.

The Classification of Adrenoceptors (Adrenergic Receptors). An Evaluation from the Standpoint of Receptor Theory

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

IF the isolated head of a dog B is perfused from the vessels of a dog A, and the only connections between the head of B and the isolated heartlung preparation of B are the vagus-depressor nerves, one observes(1) that an increase or a decrease of the arterial blood-pressure in the cardioaortic vascular area of B produces respectively a reflex inhibition, a reflex apncea, or a reflex stimulation, a reflex hyperpncea, of the respiratory centre of head B. The vagus-depressor nerves are the centripetal paths of these respiratory reflexes, in relation with the cardio-aortic bloodpressure. It is known that the occlusion of the common carotid arteries stimulates and that an increase of blood-pressure, or blood flow, in the carotid cephalic circulation inhibits the activity of the respiratory centre (Magendies and Cooperv2), Kussmaul and Tenner(3), Rosenthal(4), Hill(5), Lumsden(6), J. F. and C. Heymans(l, Gesell(7m, C. F. Schmidt(s)). These facts are taken by several authors as evidence that \" the respiratory centre is influenced directly by changes in the blood supply ... respiration is depressed by an increase in cerebral blood flow, stimulated by a decrease no matter how produced\" (C. F. Schmidt). However, as early as 1900, Siciliano(9 pointed out that the respiratory reactions are more marked after the occlusion of the carotids than after occlusion of the vertebral arteries, although the latter are more important for the blood supply of the circle of Willis, and Siciliano concludes in favour of respiratory reflexes of carotid origin. In 1912, Sollmann and Brown(lo) demonstrated that traction on the cephalic end of the common carotid produced respiratory reflexes. More recent investigations have shown that electric stimulation of the bifurcation of the common carotid (sinus caroticus) and the increase of

Heymans C

Papers

Reflexogenic Areas of the Cardiovascular System

Sinus caroticus and respiratory reflexes

Les Chémo-récepteurs du Sinus Carotidien

Survival and revival of nervous tissues after arrest of circulation

Le sinus carotidien et la zone homologue cardio-aortique