Bradykinin is released in the lungs in asthma and pulmonary anaphylaxis. It has negligible direct bronchoconstrictor effects in humans or dogs, but inhaled as aerosol it causes cough and reflex bronchoconstriction in asthmatics and some normal subjects. The afferent nerves responsible for these reflex effects have not been identified. We recorded vagal impulses in anesthetized dogs to determine whether lung afferents were stimulated by bradykinin. C-fiber endings in the intrapulmonary airways accessible from the systemic circulation were stimulated by bradykinin injected into the left atrium (0.5-1.0 micrograms/kg) or bronchial artery (1.5 micrograms), activity increasing 15-fold on average. C-fiber endings accessible from the pulmonary circulation were relatively insensitive to bradykinin. Bradykinin caused a small increase in firing of some rapidly adapting (irritant) receptors, but the effect appeared to be secondary to vascular changes. Bradykinin had variable effects on slowly adapting stretch receptors, but did not stimulate them directly. Thus vagally mediated sensory or reflex effects initiated by bradykinin in the lung are probably due to stimulation of "bronchial" C-fibers.
SUMMARY1. We have examined the effect of bradykinin on impulse traffic in sympathetic afferent fibres from the heart, great vessels and pleura, and have attempted to identify cardiac nociceptors that on the basis of their functional characteristics might have a role in the initiation of cardiac pain.2. In anaesthetized cats, we recorded afferent impulses from 'single-fibre' slips of the left 2nd-5th thoracic rami communicantes and associated chain, and selected fibres arising from endings in the heart, great vessels, pericardium and pleura. We applied bradykinin solution (0 1-1.0 jug/ml.) locally to the site of the ending; we also injected bradykinin (0 3-1 0 ,ug/kg) into the left atrium.3. Afferent endings excited by bradykinin (158 of 191 tested) were of two types. The larger group (140) were primarily mechanoreceptors with Ad or C fibres (mean conduction velocity, 7-5 + 0-6 m/sec). They were very sensitive to light touch. Those located in the heart, great vessels or overlying pleura had a cardiac rhythm of discharge and were stimulated by an increase in blood pressure or cardiac volume.4. Bradykinin increased mechanoreceptor firing from 0 7 + 0.1 to 5 0 + 0 3 (mean + S.E. of mean) impulses/sec. Some endings appeared to be stimulated directly by bradykinin, others sensitized by it so that they responded more vigorously to the pulsatile mechanical stimulation associated with the cardiac cycle.5. The smaller group of eighteen endings, of which ten were in the left ventricle, were primarily chemosensitive. Most had C fibres, a few had A6 fibres (mean conduction velocity, 2-3 + 0-7 m/sec). They were insensitive to light touch. With one exception they never fired with a cardiac rhythm, and even large increases in aortic or left ventricular pressure had little effect on impulse frequency. 6. Chemosensitive endings were stimulated by bradykinin, impulse activity increasing from 0.6 + 0-2 to 15-6 + 1-3 impulses/sec and remaining above the control level for 1-3 min. The evoked discharge, which was either continuous or occurred in irregular bursts, was not secondary to mechanical changes in the heart and great vessels.
SUMMARY Stimulus-response curves of aortic baroreceptors constructed by alternately increasing and decreasing pressure from a normal baseline or set-point differ from curves constructed by varying pressure in one direction only from an abnormally high or low pressure. In anesthetized dogs we recorded impulses from aortic baroreceptors with myelinated fibers, using a pressurized reservoir to control mean aortic blood pressure (MABP). After setting MABP to a baseline of 100 mm Hg (normal MABP in unanesthetized dogs), we constructed baroreceptor response curves by alternately decreasing MABP from 100 to 30 mm Hg, and increasing it from 100 to 180 mm Hg, in each case returning MABP to the baseline to obtain hysteresis loops. All baroreceptors were active at 100 mm Hg, their discharge averaging 15-16 impulses/sec. At all pressures above threshold, baroreceptors fired more when pressure was increasing than when pressure was decreasing. This hysteresis caused the steepest part of the response curve constructed in this manner to span the baseline value, demonstrating that, contrary to previous views, aortic baroreceptors signal decreases in pressure below the normal level, as well as increases above it. We also constructed response curves after holding MABP at a "hypertensive" baseline of 125 mm Hg for 20 minutes. "Hypertensive" curves demonstrated reversible resetting, shifting significantly to the right of "normotensive" curves so that baroreceptor threshold increased on average by 7 mm Hg ( P < 0.01). Both hysteresis and short-term resetting probably result from the viscoelastic behavior of wall elements with which baroreceptors are coupled. Circ Res 48: 676-684, 1981 THE ROLE of aortic baroreceptors in regulating blood pressure is controversial. From the results of an electroneurographic study in dogs, Pelletier et al. (1972) concluded that at normal arterial pressure the aortic nerve displays little baroreceptor activity and that, rather than acting as a true buffer system, aortic baroreceptors have a predominantly antihypertensive role. However, two recent studies in conscious dogs indicate that when the carotid sinus nerves are cut the aortic nerves alone can buffer decreases, as well as increases, in arterial pressure (McRitchie et al., 1976;Ito and Scher, 1978). This apparent conflict of evidence about a fundamental aspect of the functions of aortic baroreceptors in dogs suggests that a reexamination of their afferent properties is timely.In studies of the stimulus-response characteristics of arterial baroreceptors, the common practice is either to increase pressure until firing frequency is maximal and then to examine baroreceptor response as pressure is reduced (Fig. 1A), or to reduce pressure below baroreceptor threshold and then to examine the response as pressure is increased (Fig.
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