Left Ventricular Mechanoreceptors Research Articles

Vasovagal syncope is associated with poor prognosis in patients with left ventricular dysfunction

Vasovagal syncope (VVS) is known to have a benign prognosis and be associated with enhanced contraction and activation of the left ventricular (LV) mechanoreceptors. However, a little is known about VVS in patients with LV dysfunction. The present study aimed to investigate the prevalence and prognosis of VVS in patients with LV dysfunction. We enrolled 368 patients with unexplained syncope. In 7 of these patients, LV ejection fraction was lower than 40%. The results of a head-up tilt test (HUT) and the recurrence of syncope were compared between these 7 patients with LV dysfunction and the remaining patients. Positive HUT was obtained in the 6 patients (86%) with LV dysfunction; this rate tended to be higher as compared with normal cardiac function (192/361, 53%, P=0.069). In patients with LV dysfunction, response in HUT was mostly vasodepressor type (62%); however, most of HUT responses were mixed type in patients with normal LV function (67%). Among patients with positive HUT, the recurrent rate of syncope after HUT was higher in those with LV dysfunction than in those with normal LV function (67 vs. 21%, P=0.008). VVS in patients with LV dysfunction may be refractory to treatment and could be associated with poor prognosis.

Vasovagal syncope in patients with reduced left ventricular function

Vasovagal syncope (VVS) is mediated by arterial mechanoreceptors, resulting in reflexive changes in heart rate and vascular tone. The Bezold-Jarisch reflex was originally described as enhanced contraction and activation of left ventricular mechanoreceptors, but later studies implicated other triggers, including coronary, carotid, and cerebral arterial mechanoreceptors. VVS is uncommon in patients with left ventricular dysfunction. We hypothesized that VVS could occur in this subset and examined patient characteristics and hemodynamic responses during tilt table testing. From 1996 through 1998, 128 consecutive patients with ejection fraction <40% underwent tilt table testing (70 degrees , 45 min). A total of 15 patients (11.7%) had a positive neurocardiogenic response thought to be the cause of syncope. Clinical data and hemodynamic responses were reviewed. Mean patient age (+/-SEM) was 70.1 +/- 12.2 years. Nine patients were male. Mean ejection fraction was 27.7% +/- 7.1%. Thirteen had electrophysiologic studies with normal findings or abnormal findings insufficient to account for syncope. Hemodynamic analysis of 14 patients who had a vasovagal response during passive tilt table testing showed a mean time to positive response of 17.6 +/- 12.7 min. Cardioinhibitory responses (pauses >3 sec or heart rate < 40 beats/min for > or =10 sec) were not observed. Five responses were classified as mixed type (>10% decrease in heart rate without a cardioinhibitory response) and 9 as vasodepressor type (< or =10% decrease in heart rate). VVS occurs in patients who have clinically significant left ventricular dysfunction. Although this study had a small cohort size, the predominantly vasodepressor response without a cardioinhibitory component warrants further investigation into mechanisms of VVS in these patients.

Reversal of Inappropriate Peripheral Vascular Responses in Hypertrophic Cardiomyopathy

We assessed the frequency of abnormal forearm vasodilator responses during lower body negative pressure (LBNP) in 21 non-obstructive hypertrophic cardiomyopathy (HCM) patients (31 +/- 8 [20 to 43] years) with abnormal blood pressure response (ABPR) to exercise and the effects of three drugs used to treat vasovagal syncope (propranolol, clonidine, and paroxetine) in a double-blind crossover study. Some HCM patients have an ABPR to exercise, which may be due to paradoxical peripheral vasodilatation. A similar proportion has paradoxical forearm vasodilatation during central volume unloading using LBNP. These abnormal reflexes may be caused by left ventricular mechanoreceptor activation. Similar mechanisms may also contribute to some cases of vasovagal syncope. Blood pressure changes were assessed during exercise, and forearm vascular responses and baroreceptor sensitivity were assessed during LBNP using plethysmography. Nine (43%) patients (group A) had paradoxical vasodilator responses (forearm vascular resistance [FVR] fell by 7.5 +/- 4.6 U), and 12 (57%) patients (group B) had normal vasoconstrictor responses during LBNP (FVR increased by 7.7 +/- 4.9 U). Paroxetine augmented systolic blood pressure (SBP) during exercise in group A (21 +/- 6 mm Hg vs. 14 +/- 11 mm Hg at baseline, p = 0.02); no effect was detected in group B. Paroxetine reversed paradoxical vascular responses during LBNP in seven (78%) patients from group A. Propranolol and clonidine had no significant effect on SBP during exercise but reversed paradoxical vascular responses in some patients from group A (n = 5 and n = 3). Paradoxical vasodilatation during LBNP occurs in 40% of patients with ABPR during exercise and is reversed by propranolol, clonidine, and paroxetine. Paroxetine also improved SBP response to exercise.

Responses to stimulation of coronary and carotid baroreceptors and the coronary chemoreflex at different ventricular distending pressures in anaesthetised dogs.

Stimulation of left ventricular mechanoreceptors was believed not only to exert important effects on the circulation, but also to influence the responses to baroreceptor reflexes. However, most previous work is flawed due to inadequate localisation of stimuli to specific reflexogenic areas. In this study, we applied a discrete stimulus to left ventricular mechanoreceptors to examine other reflexes known to effect the circulation. Dogs were anaesthetised, artificially ventilated and a cardiopulmonary bypass established. The pressure distending the left ventricle was controlled through an apical cannula with the aortic valve obstructed by a balloon. Changes in ventricular systolic and end-diastolic pressure had only a small effect on vascular resistance, assessed as perfusion pressure in the systemic circulation (flow constant). Responses to changes in carotid or coronary pressure or to stimulation of chemosensitive afferents by injecting veratridine into the coronary circulation were always much larger. Responses to stimulation of these reflexes were little affected by the level of stimulus to the ventricular receptors. These experiments confirm that responses to stimulation of ventricular mechanoreceptors are very small and show that they remain small at different levels of input to other baroreceptive regions. There was no evidence of interaction between ventricular mechanoreceptor reflexes and carotid or coronary baroreceptors or ventricular chemosensitive reflexes.

Current issues in spinal anesthesia.

Spinal anesthesia is an old, simple, and popular anesthetic technique, yet much remains unknown regarding pertinent anatomy, physiology, and pharmacology. Investigations into physiologic effects of spinal anesthesia reveal complex actions on multiple organ systems. New local anesthetics, analgesic additives, and techniques are being investigated for different applications as the practice of medicine focuses on outpatient care. Safety of spinal agents and complications from spinal anesthesia continue to be examined and re-examined to improve safety. Further study will be needed to fully resolve these issues and to further understand and improve the clinical use of spinal anesthesia.

Reflex effects of independent stimulation of coronary and left ventricular mechanoreceptors in anaesthetised dogs

Previous studies which have indicated that the stimulation of ventricular mechanoreceptors induces significant reflex responses can be criticised because of the likelihood of concomitant stimulation of coronary arterial baroreceptors. We therefore undertook this investigation to examine the coronary and ventricular mechanoreflexes in a preparation in which the pressure stimuli to each region were effectively separated. Dogs were anaesthetised, artificially ventilated and placed on cardiopulmonary bypass. A balloon at the ventricular outflow separated pressure in the left ventricle from that perfusing the coronary arteries. Ventricular pressures were changed by varying inflow and outflow of blood entering and leaving the ventricle through an apical cannula, and coronary pressure by changing pressure in a reservoir connected to a cannula tied in the aortic root. Pressures distending carotid and aortic baroreceptors were controlled. Changes in descending aortic perfusion pressure (flow constant) were used to assess systemic vascular responses. Large changes in carotid sinus and coronary pressures decreased vascular resistance by 35+/-1.9 and 40+/-2.5%, respectively. Intracoronary injections of veratridine (30-60 microg) decreased vascular resistance by 31+/-2.5%. However, large increases in ventricular pressure decreased resistance by only 9+/-2.2%. Significant changes in vascular resistance were obtained with increases in coronary arterial pressure from 60 to 90 mmHg. However, ventricular pressures had to increase to 152/18 mmHg (systolic/end-diastolic) before there was a significant response. These results show that coronary mechanoreceptors are likely to play an important role in cardiovascular control. If ventricular receptors have any function at all, it is as a protective mechanism during gross distension, possibly associated with myocardial ischaemia.

Tilt testing for syncope

Vasovagal syncope is a common cause of sudden collapse. It results from inappropriate activation of left ventricular mechanoreceptors causing sudden vasodilation with bradycardia. Tilt testing is an inexpensive and non-invasive way of establishing a vasovagal diagnosis in unexplained syncope. If critical care nurses improve their understanding of the pathophysiology of vasovagal syncope and the procedure of tilt testing, their care of syncopal patients will be enhanced. This literature review discusses the pathophysiology and clinical presentation of vasovagal syncope. The procedure of tilt testing is explained and the treatment of vasovagal syncope is briefly reviewed.

Left ventricular geometry and function preceding neurally mediated syncope.

Neurally mediated syncope has been associated with increased left ventricular (LV) fractional shortening (FS) during tilt testing, which is consistent with the hypothesis that the stimulation of LV mechanoreceptors leads to reflex hypotension and/or bradycardia. However, FS does not represent true LV contractility because of its dependence on afterload and preload. To elucidate the role of increased contractility in the mediation of neurally mediated syncope, we compared echocardiographic measures of LV performance corrected for end-systolic stress (ESS) in 21 patients (13 women and 8 men) with unexplained syncope who had either positive (n=10) or negative (n=11) responses to a tilt-table test. Two-dimensional echocardiographic LV imaging was performed at baseline and during the initial 5 minutes of upright tilt. In the supine position, both groups had similar LV end-diastolic volume indexes, stroke volumes, FS, circumferential ESS, and afterload-independent measures of LV performance (stress-corrected midwall and FS). However, after 5 minutes of upright tilt, patients who subsequently had a positive test had a lower stroke volume, lower stress-corrected midwall shortening, and endocardial FS. The tilt-positive group also had a greater fall in ESS and FS early during upright tilt. Reduced ESS, LV volume, and chamber function during initial upright tilt are associated with a subsequent positive tilt response in patients with unexplained syncope. These data suggest that if paradoxic activation of LV mechanoreceptors has a role in mediating neurally mediated syncope, it is not triggered by LV hypercontractility or increased systolic wall stress during the initial period of upright tilt.

The role of diastolic ventricular interaction in abnormal cardiac baroreflex function in chronic heart failure.

Baroreflex abnormalities have been well documented in both patients with chronic heart failure and experimental animal models of heart failure. These abnormalities are associated with increased mortality and probably contribute to neurohumoral activation. While it is likely that several mechanisms contribute to reduced baroreflex sensitivity, it has been difficult to explain why baroreflex control mechanisms during acute volume unloading in patients with severe chronic heart failure should be directionally opposite to those in normal subjects. Volume unloading normally causes a reduction in baroreceptor activity, and hence an increase in sympathetic outflow; however, patients with chronic heart failure develop attenuated increases or paradoxical reductions in forearm vascular resistance, muscle sympathetic nerve activity, and noradrenaline spillover. It has been suggested that this probably represents paradoxical activation of left ventricular (LV) mechanoreceptors, but why LV receptors should behave in such a fashion has not been determined. In the setting of diastolic ventricular interaction, the filling of the left ventricle is constrained by the surrounding pericardium and right ventricle. In these patients, the reduction in right ventricular (RV) volume that normally occurs during acute volume unloading allows for an increase in LV end-diastolic volume (as opposed to the reduction in LV volume that normally occurs). We have demonstrated this to be important in some patients with chronic heart failure, and observed that baroreflex control of forearm vascular resistance was markedly impaired in these patients. We propose that the increase in LV volume that occurred during volume unloading would increase LV mechanoreceptor activity, and could therefore explain the paradoxical reductions in sympathetic outflow. As discussed, this has important therapeutic implications.

Diastolic ventricular interaction: a possible mechanism for abnormal vascular responses during volume unloading in heart failure.

Baroreflex dysfunction is common in chronic heart failure and contributes to the associated sympathoexcitation. Baroreceptor activity normally decreases during volume unloading, causing an increase in sympathetic outflow and resulting in forearm vasoconstriction. Some heart failure patients develop attenuated vasoconstriction or paradoxical vasodilation. The mechanism for this is unknown. We have recently demonstrated diastolic ventricular interaction in some patients with chronic heart failure as evidenced by increases in left ventricular (LV) end-diastolic volume in association with decreases in right ventricular (RV) volume during volume unloading. We reasoned that such an increase in LV volume, by increasing LV mechanoreceptor activity, would decrease sympathetic outflow and could therefore explain the abnormal vascular responses seen in such patients. We assessed changes in forearm vascular resistance (FVR) during application of -20 and -30 mm Hg lower-body negative pressure (LBNP) in 24 patients with chronic heart failure and 16 control subjects. Changes in LV and RV end-diastolic volumes were assessed during -30 mm Hg LBNP in all heart failure patients. Diastolic ventricular interaction was demonstrated in 12 patients as evidenced by increases in LV end-diastolic volume in association with decreases in RV end-diastolic volume during LBNP. Changes in FVR during LBNP (-20 and -30 mm Hg) were markedly attenuated in these 12 patients (-1.6+/-11.2 and -0.9+/-12.5 U) compared with both the remaining patients (11.9+/-10.0 and 17.0+/-12.3 U) and the control subjects (16.5+/-9.5 and 23.1+/-13.9 U) (P<.01 for both comparisons at each level of LBNP). FVR decreased in 5 of these 12 patients during -30 mm Hg LBNP, a response seen in none of the remaining patients (P=.01). Diastolic ventricular interaction in patients with chronic heart failure is associated with attenuated forearm vasoconstriction or paradoxical vasodilation during LBNP. This may explain the apparent derangement in baroreflex control of sympathetic outflow during acute volume unloading in heart failure.

Effects of Pericardial Constraint on Left Ventricular Mechanoreceptor Activity in Cats

The purpose of this study was to assess the effect of pericardial constraint on the activity of left ventricular (LV) mechanoreceptors with nonmyelinated vagal afferents. Single-unit activity of cervical vagal afferents (conduction velocity, 1.6 +/- 0.5 m/s) was recorded in six cats anesthetized with alpha-chloralose. Discharge frequency during diastole (DFdiastole) and systole (DFsystole) was determined after correction for conduction delay of the nerve action potential. When the pericardium was closed and LV end-diastolic pressure (LVEDP) was approximately 5 mm Hg, DFdiastole and DFsystole were 1.3 +/- 1.0 and 0.3 +/- 0.1 impulses per second, respectively. Volume expansion increased LVEDP, LV transmural LVEDP, and segment length and was associated with a significant increase in DFdiastole. At a given LVEDP, DFdiastole was significantly greater in the absence of the pericardium than with the pericardium closed. Removal of the pericardium increased the slope of the relation between DFdiastole and intracavitary LVEDP but did not alter the slope of the relations between DFdiastole and transmural LVEDP and LV segment length. These results suggest that, rather than the absolute value of intracavitary LVEDP, transmural LVEDP and distension appear to be more important determinants of diastolic LV mechanoreceptor activity and that pericardial constraint may attenuate mechanoreceptor activity by limiting cardiac distension.

Differential therapeutic responses of patients with isoproterenol-dependent and isoproterenol-independent vasodepressor syncope

Orthostatic stress during tilt table testing (TTT) is used to examine patients who may have vasodepressor syncope. This response is thought to be mediated by activation of left ventricular mechanoreceptors. Isoproterenol, by increasing the rate of discharge of these mechanoreceptors, has been proposed to increase the sensitivity of TTT without decreasing its specificity. This mechanism is not, however, totally consistent with recent observations of vasodepressor responses after cardiac transplantation in patients with denervated hearts. These reports and data showing that not all sympathomimetic agents increase the sensitivity of TTT suggest that more than one mechanism may be responsible for a positive TTT result. Therefore we hypothesized that patients with positive TTT results tests not requiring isoproterenol (iso-independent) would have a different clinical and therapeutic response than patients who required isoproterenol (iso-dependent). One hundred sixty-one consecutive patients who underwent TTT for the evaluation of unexplained syncope were included in the study. TTT was performed without and during isoproterenol infusion. A positive TTT result was defined as syncope or presyncope with a sudden decrease in systolic blood pressure and reproduction of the patient's clinical symptoms. Patients with a positive TTT result underwent a second test after 1 to 2 weeks of therapy with an oral β-blocking agent; if the result remained positive, TTT was performed again with other agents until a satisfactory therapeutic response was obtained. Sixty-six (41%) of 161 patients had a positive result; 18 (27%) were iso-independent, and 48 (73%) were iso-dependent. There were no significant differences in age, gender, or presence of underlying heart disease between these two groups. Patients with iso-dependent and underlying heart disease between these two groups. Patients with iso-dependent and iso-independent syncope had similar hemodynamic responses to treatment with β-blockers. However, the response rate to β-blockers in the iso-dependent group was 100% versus 47% in the iso-independent group ( p < 0.0001). Patients with iso-dependent and iso-independent syncope during TTT have markedly different responses to treatment with β-blockers, a differential response that is not caused by differences in hemodynamics effects of treatment. This differential response cannot be attributed solely to differences in dosing or in pharmacologic effect of the drug, because both groups had a similar fall in heart rate and no substantial differences in blood pressure after initiation of therapy. These data, experimental data in animals, and the demonstration of a vasodepressor response in humans after cardiac transplantation suggest that the presently accepted left ventricular mechanoreceptor hypothesis of vasodepressor syncope may be incomplete and not applicable to all patients.

Occurrence of presyncope in subjects without ventricular innervation.

1. To determine whether activation of the left ventricular C-fibre mechanoreceptors initiates the vasodepressor reflex that often causes syncope, we exposed six orthotopic cardiac transplant patients and six matched, healthy control subjects to progressively increasing lower body negative pressure until the onset of vasodepressor responses. 2. There was no significant difference (P = 0.78) between the central hypovolaemia tolerances of the cardiac transplant and the control groups. 3. The decrease in systolic blood pressure before the onset of vasodepressor reflexes was greater in the cardiac transplant group. The cardiac transplant group did not maintain diastolic blood pressure during central hypovolaemia. From baseline to the onset of vasodepression, there were no differences in leg circumference, forearm blood flow and forearm vascular resistance responses between the two groups. 4. We conclude that the left ventricular mechanoreceptors may not be the primary afferent trigger for syncope.

Reflex vascular responses to changes in left ventricular pressures, heart rate and inotropic state in dogs.

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 although there was little effect on the responses to changes in ventricular pressure. Sympathetic stimulation had little effect on the relationship between perfusion pressures and aortic root pressure. Increases in ventricular filling also resulted in vasoconstriction at all levels of peak ventricular pressure. Increases in filling, however, did not affect the relationship between either perfusion pressure and aortic root pressure. Conversely, decreases in left ventricular filling, by bypassing some of the left atrial blood, resulted in vasodilatation at all levels of peak ventricular pressures but had no effect on the perfusion pressures at any aortic root pressure. The combination of sympathetic stimulation with decreased ventricular filling resulted in little effect on perfusion pressures or on their responses to changes in either aortic root or ventricular systolic pressures. We conclude that the vascular responses to stimulation of left ventricular mechanoreceptors are not enhanced by sympathetic stimulation, decreases in ventricular filling or the combination of the two. The apparent effects of each of these interventions alone on the relationships between perfusion pressures and ventricular, but not aortic root, pressure, could be explained if the receptors responsible were sensitive more to changes in aortic root and coronary arterial pressures than to pressure changes in the ventricle itself.

Stimulation of atrial natriuretic peptide and vasopressin during retrograde mitral valvuloplasty

Acute mitral obstruction may lead to an increase in atrial natriuretic peptide (ANP) due to increased atrial pressure and a large increase in arginine vasopressin (AVP) due to simultaneous arterial and ventricular baroreceptor unloading. We measured ANP and AVP concentration after transseptal puncture and during percutaneous retrograde mitral balloon valvuloplasty (PRMV) in 11 patients (mean age 57 ± 12 years; nine women) with mitral stenosis and congestive heart failure. Atrial septal puncture per se resulted in a significant increase in ANP and AVP without a significant change in aortic pressure. Subsequent PRMV led to a further increase in ANP, a transient decrease in aortic pressure from 89 ± 7 to 45 ± 4 mm Hg, and a large (fivefold) increase in AVP. ANP and AVP were no longer different from baseline values 18 to 24 after the procedure. This study suggests that transseptal puncture and acute mitral obstruction are major stimuli to ANP release and that combined unloading of arterial and left ventricular mechanoreceptors is a very potent vasopressinergic stimulus.

Left ventricular reflex control of venous return and systemic vascular capacitance in dogs.

The reflex effects of left ventricular distension on venous return, vascular capacitance, vascular resistance, and sympathetic efferent nerve activity were examined in dogs anesthetized with sodium pentobarbital. In addition, the interaction of left ventricular distension and the carotid sinus baroreflex was examined. Vascular capacitance was assessed by measuring changes in systemic blood volume, using extracorporeal circulation with constant cardiac output and constant central venous pressure. Left ventricular distension produced by balloon inflation caused a transient biphasic change in venous return; an initial small increase was followed by a late relatively large decrease. Left ventricular distension increased systemic blood volume by 3.8 +/- 0.6 mL/kg and decreased systemic blood pressure by 27 +/- 2 mmHg (1 mmHg = 133.3 Pa) at an isolated carotid sinus pressure of 50 mmHg. These changes were accompanied by a simultaneous decrease in sympathetic efferent nerve activity. When the carotid sinus pressure was increased to 125 and 200 mmHg, these responses were attenuated. It is suggested that left ventricular mechanoreceptors and carotid baroreceptors contribute importantly to the control of venous return and vascular capacitance.

Modulation of cardiovascular reflexes by arginine vasopressin.

Arginine vasopressin (AVP), a potent vasoconstrictor, does not raise arterial pressure in normal humans or neurally intact animals, even during infusions that achieve pathophysiological plasma concentrations. It has been proposed that this is because AVP facilitates the baroreflex control of the circulation. We performed a series of investigations to test this hypothesis, and to determine sites at which AVP might act to augment the baroreflex. In anesthetized rabbits, vasopressin (36 pmol.kg-1.min-1) increased discharge from both medullated and nonmedullated single fibres from aortic baroreceptor nerves during elevations in aortic arch pressure. Similarly, vasopressin (36 pmol.kg-1.min-1) increased the response of left ventricular mechanoreceptor single fibre discharge to elevations of left ventricular end-diastolic pressure. These observations suggest that sensitization of high and low pressure baroreceptors is one mechanism by which vasopressin may facilitate baroreflexes. In a further series of experiments in sinoaortic denervated anesthetized rabbits, vasopressin (18 pmol.kg-1.min-1) facilitated vagally mediated reflex inhibition of renal sympathetic nerve activity during volume expansion. In humans, AVP (0.37 pmol.kg-1.min-1) raised plasma AVP to an antidiuretic level (22 +/- 4 fmol/mL), but did not change blood pressure or the baroreflex control of heart rate or forearm vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

Does digoxin sensitize left ventricular mechanoreceptors?

Afferent nerve fibre activity from left ventricular mechanoreceptors was recorded in 10 anaesthetized cats before and after two intravenous injections of 15 micrograms/kg digoxin at 1 hour interval. These receptors are activated by coronary artery occlusion and induce a depressor cardiovascular reflex resulting in bradycardia and hypotension. Neither the spontaneous activity of the receptor's afferent nerve fibres nor their maximum activity during temporary coronary artery occlusion was affected by digoxin. The results show that digoxin in therapeutic doses has no sensitizing effect on left ventricular mechanoreceptors with vagal afferent fibres. The sensitization of cardiopulmonary baroreflexes by digitalis glycosides shown in previous investigations is thus more likely to be mediated by a central nervous effect of the drug.

Sensitization of aortic and cardiac baroreceptors by arginine vasopressin in mammals.

Vasopressin facilitates the baroreflex control of the circulation. The peptide may act at several sites to augment the baroreflex. In this study we examined the effect of vasopressin on aortic baroreceptors in anaesthetized rabbits and on left ventricular mechanoreceptors in anaesthetized cats. Vasopressin (16 mu./kg. min) did not change resting nerve discharge in single fibres from aortic baroreceptors. Vasopressin (16 mu./kg. min) significantly enhanced the response of single aortic nerve fibre discharge to elevation in arterial pressure. The slope relating nerve activity to mean arterial pressure increased from 0.24 +/- 0.05 (mean +/- S.E. of mean) to 0.50 +/- 0.16 impulses/cardiac cycle. mmHg (P less than 0.05) in ten aortic medullated fibres and from 0.06 +/- 0.03 to 0.18 +/- 0.04 impulses/cardiac cycle. mmHg (P less than 0.05) in three non-medullated fibres. Vasopressin (16 mu./kg. min) did not change resting nerve discharge in single fibres from left ventricular mechanoreceptors. Vasopressin (16 mu./kg. min) significantly enhanced the response of single nerve fibre discharge from left ventricular mechanoreceptors in response to elevation of left ventricular end-diastolic pressure. The slope relating nerve activity to left ventricular end-diastolic pressure increased from 0.24 +/- 0.07 to 0.32 +/- 0.07 impulses/cardiac cycle. mmHg (P less than 0.05) in six medullated fibres and from 0.10 +/- 0.01 to 0.15 +/- 0.02 impulses/cardiac cycle. mmHg (P less than 0.05) in four non-medullated fibres. These data show that vasopressin sensitizes high and low pressure baroreceptors and suggest a mechanism by which vasopressin may facilitate the baroreflex control of the circulation.

Increased left ventricular pressure attenuates the baroreflex in unanesthetized dogs.

To determine whether stimulation of left ventricular mechanoreceptors alters the baroreflex control of heart rate (HR), dogs were instrumented with a vascular occluder around the ascending aorta and appropriate instrumentation for the recording of left ventricular pressure (LVP), aortic pressure, left atrial pressure, HR, and left ventricular dP/dt. Baroreflex sensitivity (pulse interval or HR vs. aortic systolic pressure linear-regression slopes to infusions of phenylephrine or nitroprusside) was determined in the conscious state a minimum of 7 days postoperatively. After control responses were determined with both phenylephrine and nitroprusside, the experiment was repeated during inflation of the ascending aortic occluder so as to significantly raise left ventricle systolic pressure from 127.9 +/- 8.4 to 178.5 +/- 11.3 mmHg (P less than 0.01) and left ventricle end-diastolic pressure from 3.5 +/- 0.7 to 8.9 +/- 1.0 mmHg (P less than 0.01). There were no changes in mean arterial blood pressure, pulse pressure, or HR during elevation of LVP. The baroreflex sensitivity was reduced only during the infusion of nitroprusside from a control of 11.03 +/- 1.9 to 4.80 +/- 1.2 ms/mmHg (P less than 0.01) for the pulse interval relationship and from -2.51 +/- 0.53 to -1.14 +/- 0.32 beats . min-1 . mmHg-1 (P less than 0.05) for the HR relationship. Cholinergic blockade with atropine abolished the depression in the baroreflex sensitivity during nitroprusside infusion when LVP was increased. beta 1-Adrenergic blockade with metoprolol did not significantly reduce the baroreflex sensitivity during increased LVP.(ABSTRACT TRUNCATED AT 250 WORDS)