Reflex responses evoked by ventricular mechano and chemo-sensitive afferents (original) (raw)
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The Journal of physiology, 1993
1. Previous work has shown that physiological increases in mean aortic root pressure, which change the pressure in both the coronary circulation and the left ventricle, result in reflex vasodilatation. This study was undertaken to attempt to localize the reflexogenic area mainly responsible for the reflex. 2. In anaesthetized, artificially ventilated dogs, cannulae connected to perfusion systems were inserted in the ascending aorta, left ventricular apex and left atrium. This allowed us to change the pressures in: (a) the aortic root including both the coronary arteries and the left ventricle; (b) aortic root and coronary arteries, at constant ventricular pressure; and (c) in the ventricle, with mean (although not pulse) aortic pressure constant. Aortic and carotid baroreceptors were perfused at constant pressure and reflex responses were determined from changes in perfusion pressures (flows constant) to a vascularly isolated hindlimb and to the remainder of the systemic circulation...
Afferent discharges from coronary arterial and ventricular receptors in anaesthetized dogs
The Journal of physiology, 1993
1. Previous work has shown that increases in aortic root pressure result in reflex vasodilation, and that this response is likely to result mainly from stimulation of receptors in the coronary arteries, although contribution from left ventricular receptors was not excluded. This investigation was undertaken to resolve this question and to determine the afferent nerve fibres likely to be involved in this reflex. 2. In chloralose-anaesthetized dogs a perfusion circuit was used which allowed us to change the pressures in: (a) the aortic root, coronary arteries and the left ventricle; (b) aortic root and coronary arteries at constant ventricular pressure; and (c) the left ventricle with mean (although not pulse) aortic pressure constant. Electrophysiological recordings were made from slips dissected from the vagus nerve which responded with an increase in discharge to either combined increases in the pressures, or to aortic root injections of veratridine. 3. Recordings were made from tw...
Peripheral vascular responses to changes in left ventricular pressure in anaesthetized dogs
Quarterly journal of experimental physiology (Cambridge, England), 1987
In dogs anaesthetized with chloralose, cardiac receptors were stimulated by increases in left ventricular systolic pressure effected by changes in aortic root pressure. Left atrial and carotid sinus pressures were controlled. A large step increase in ventricular pressure resulted in transient decreases in heart rate, systemic arterial perfusion pressure and perfusion pressure to a vascularly isolated hind limb. The magnitudes of these responses were about three-quarters of those to either a large change in carotid sinus pressure or aortic root injection of 20 micrograms veratridine. Steady-state responses were smaller. There was no significant change in perfusion pressure to a perfused cutaneous vein. Graded changes in ventricular systolic pressure showed that the most sensitive pressure range was between 20 and 24 kPa. These results indicate that changes in left ventricular pressure result in significant vasodilation in the hind limb and in other regions and that responses are obta...
Experimental physiology, 1992
Dogs were anaesthetized with chloralose, artificially ventilated and the chests widely opened. Left ventricular mechanoreceptors, including those in or near the coronary arteries, were stimulated by changing the pressure in the aortic root. The pressures distending the left atrium and the aortic and carotid baroreceptors were controlled. Reflex vascular responses were assessed from changes in perfusion pressures to a hind limb and to the rest of the systemic circulation, which were perfused independently at constant flows. Physiological increases in peak left ventricular and coronary arterial pressures resulted in vasodilatation in both regions. These responses were not influenced by changes in the heart rate. Stimulation of the left cardiac sympathetic nerves resulted in increases in peak ventricular pressure and in the maximal rate of change of pressure (dP/dtmax). This also resulted in increases in perfusion pressures (vasoconstriction) at all levels of peak ventricular pressure ...
A Sympathetic Hypertensive Reflex from the Heart of Conscious Dogs
Clinical science. Supplement (1979), 1981
The aim of the present experiments was to study in conscious animals the effect of chemical stimulation of cardiac sensory innervation by bradykinin, a physiological substance known to activate both vagal and sympathetic cardiac sensory nerve endings, at doses devoid of systemic haemodynamic effects. 2. In conscious dogs with implanted catheters bradykinin (100 ng/kg) injected into a cannulated branch of the left coronary artery induced significant (P < 0.01, II = 5) reflex increases in mean arterial pressure and heart rate as well as increases in left ventricular pressure, left ventricular dP/dt max. and coronary blood flow. 3. These changes were obtained in the absence of pain reactions. 4. The concept, derived from experiments on anaesthetized animals, that chemical stimulation of the intact sensory supply of the heart always elicits a cardiovascular depressor reflex mediated by cardiac vagal afferents has to be modified, as pressor sympathetic reflexes may occur after an appropriate stimulus to the fully innervated heart of conscious dogs.
Contrasting reflex effects of chemosensitive and mechanosensitive vagal afferents
Hypertension, 1988
Previous studies have identified two distinct types of cardiac vagal afferents, mechanosensitive and chemosensitive. We tested the hypothesis that these two types of vagal afferents mediate different reflex sympathetic nerve responses. We compared effects of stimulation of chemosensitive and mechanosensitive vagal afferents on renal and adrenal sympathetic nerve activity in rats. In anesthetized, sinoaortic baroreceptor-denervated rats, we measured arterial pressure, heart rate, and renal and adrenal sympathetic nerve activity during intrapericardial administration of phenyl diguanide as a stimulus for chemosensitive afferents and during volume expansion and acute occlusion of the ascending aorta as stimuli for mechanosensitive afferents. Stimulation of chemosensitive afferents with phenyl diguanide (3,10, and 30 /^g/kg intrapericardially) caused decreases in renal sympathetic nerve activity (-3 6 ± 5,-5 2 ± 11, and-7 1 ± 5%; p<0.01) and in arterial pressure and heart rate but increased adrenal sympathetic nerve activity (+ 14 ±27, +63 ± 2 1 , and + 8 3 ± 28%;p<0.05). These responses were abolished by vagotomy. Intrapericardial injection of saline vehicle did not change renal and adrenal sympathetic nerve activity. In contrast to the effects of phenyl diguanide, activation of mechanosensitive afferents by volume expansion with intravenous infusion of 6% dextran in 0.9% saline (Dextran 75) decreased both renal and adrenal sympathetic nerve activity. Stimulation of mechanosensitive afferents by acute occlusion of the ascending aorta also decreased both renal and adrenal sympathetic nerve activity. These results indicate that chemosensitive and mechanosensitive cardiac vagal afferents produce different reflex responses: Chemosensitive afferents increase and mechanosensitive afferents decrease adrenal sympathetic outflow. (Hypertension 11: 674-679, 1988) KEY WORDS • phenyl diguanide • vagotomy • sinoaortic baroreceptor denervation S INCE the concept of vagal depressor reflexes originating in the heart was introduced by von Bezold and Hirt 1 in 1867, many studies have revealed that vagal afferent reflexes originating in cardiac sensory receptors participate in control of circulation in physiological 2 " 6 and pathological states. 7 "" These reflexes have been classified according to various characteristics including location of the receptors (e.g., atrial, ventricular, or pulmonary) and type of afferent fibers (e.g., myelinated or unmyelinated). There is substantial evidence that stimulation of unmyelinated cardiac vagal afferents produces inhibitory
Different pharmacological responses of atrium and ventricle: Studies with human cardiac tissue
European Journal of Pharmacology, 1994
It has been recently reported that 5-hydroxytryptaminc (5-HT) increases force of contraction in atrial tissue but not in ventricular tissue. In the present study with trabeculae obtained from non-diseased human hearts, we investigated whether this difference in the contractile responses is specific for 5-HT or is also observed for other substances: calcitonin gene-rclatcd peptide (CGRP), angiotensin II, adenosine, somatostatin and acetylcholine. CGRP (10-9 to 10 7 M) and angiotensin II (10 ~ to 10 5 M) caused concentration-dependent increases in force of contraction in atrial trabeculae (up to 36 _+ 8% and 42 + 8% of the response to 10-5 M noradrenaline, respectively). Similar to 5-HT, no effects were observed with CGRP and angiotcnsin II in ventricular trabeculae. Adenosine (10 s to 10-5 M) and somatostatin (10 ~ to 10 ~ M) caused concentration-dependent negative inotropic effects on baseline atrial contractility (-54 _+ 17% and-51 _+ 25%, respectively), but no response was found on baseline ventricular contractility. Adenosine, but not somatostatin, reduced force of contraction after pre-stimulation with 10 5 M noradrenaline in atrial tissue and, to a lesser extent, in ventricular tissue. Acetylcholine exhibited a biphasic concentration-response curve in the atrial tissue, consisting of an initial negative inotropic response (10 ' to 10 v M, from 120 +_ 41 mg at baseline to 48 + 16 mg at 10 7 M), followed by a positive inotropic response (10-6 to 10 .3 M, from 48 +_ 16 mg at 10-7 M to 77 + 15 rag). On the baseline ventricular force of contraction, acctylcholine (10-9 to 10-4 M) induced only a positive inotropic effect, starting at 10 9 M (from 252 _+ 65 mg at baseline to 353 + 71 mg at 10 4 M). After pre-stimulation with 10 5 M noradrenaline, acetylcholine reduced force of contraction in both tissues at 10 _3 M (atrium:-14_+ 4%, ventricle:-61 _+ 5%). The data indicate that, in atrial tissue, force of contraction can be affected by either positive or negative inotropic agents. However, in ventricular tissue only positive inotropic effects could be detected. Since atrial and ventricular tissues display different responses to the above biogenic substances, a different mechanism of regulation of contractility seems feasible.
Quarterly journal of experimental physiology (Cambridge, England), 1988
Responses of systemic arterial perfusion pressure to changes in ventricular systolic pressure were determined before and after administration of dobutamine, then after propranolol, to determine whether the effective stimulus to left ventricular receptors was the change in ventricular systolic pressure or inotropic state. The results showed that increases in ventricular systolic pressure resulted in reflex vasodilatation which was unaffected by inotropic state, indicating that changes in ventricular systolic pressure provided the more potent stimulus.