Carotid Sinus Baroreceptor Reflex Research Articles

Carotid Artery Revascularization Improves Cardiac Sympathetic Nerve Activity in Patients With Carotid Artery Stenosis.

The carotid sinus baroreceptor reflex controls the neural regulation of blood pressure. Baroreceptor disorders due to carotid sinus atherosclerosis have detrimental cardiovascular effects. This study investigated the medium-term effects of carotid artery revascularization (CAR) on sympathetic and cardiac function and systemic blood pressure variability in patients with carotid artery stenosis. This study included 21 consecutive patients (median age 70 years, 18 men) with carotid artery stenosis scheduled for CAR. 123I metaiodobenzylguanidine (MIBG) scintigraphy, echocardiography, brain natriuretic peptide levels, 24-h Holter electrocardiography (ECG), and ambulatory blood pressure monitoring assessed approximately 3 months postoperatively were compared to preoperative data. All 21 enrolled patients underwent CAR. Carotid artery stenting was done in three patients with cardiovascular risk or anatomical difficult for carotid endarterectomy. The mean common carotid artery end-diastolic velocity improved significantly (P < 0.01) by 1.6-fold, from 10.8 ± 3.2 to 16.1 ± 7.1 cm/s. In 123I-MIBG scintigraphy, the heart-to-mediastinum (H/M) count ratio was significantly higher than preoperatively (from 2.66 ± 0.48 to 2.86 ± 0.56, P = 0.03). Holter ECG analysis revealed a significant decrease in the low-frequency/high-frequency (LF/HF) ratio compared to preoperatively (from 2.17 ± 1.20 to 1.62 ± 0.68, P = 0.04). These findings suggest decreased myocardial sympathetic activation. In echocardiography, the tissue Doppler-derived e' increased, and E/e' decreased significantly (P < 0.05) from 11.7 ± 5.1 to 10.1 ± 4.0, suggesting an improved left ventricular diastolic capacity. The mean 24-h and nighttime blood pressures were unchanged. CAR in patients with carotid stenosis may provide medium-term improvement in cardiac sympathetic nerve activity and left ventricular diastolic dysfunction.

P94 Hydrogen sulfide facilitates carotid sinus baroreceptor reflex and activity of renovascular hypertensive rats

To explore the role and possible mechanism of hydrogen sulfide (H 2 S) in modulating carotid sinus baroreceptor reflex and activity of renovascular hypertensive rats. Renovascular hypertension was induced in male Sprague–Dawley rats by placing renal artery clip (two-kidney, one-clip; 2K1C).The functional curve of the carotid sinus baroreflex was measured by recording changes in arterial pressure with perfused carotid sinus. The functional curve of carotid baroreceptor (FCCB) was constructed by recording sinus nerve afferent discharge with perfused isolated carotid sinus. The expression of SUR2B and Kir6.1 of carotid sinus was examined. The systolic blood pressure (SBP) was significantly increased in the 2K1C group (172 ± 6.32 mmHg) comparing with the NaHS-treated group (134 ± 5.74 mmHg) ( P < 0.01). The plasma H 2 S concentration was decreased in the 2K1C group comparing with other groups. Perfusing the left carotid sinus with K-H solution and elevating the ISP from 0 to 250 mmHg. The reflexly decreased extent of blood pressure was obviously decreased in 2K1C group compared with other groups. The 2K1C group induced obvious changes in baroreflex parameters, marked decrease in RD and PS, and increased in TP, EP and SP, shifting the functional curve of the baroreflex to the right and upward. At the same time, the 2K1C group induced obvious changes in carotid sinus baroreceptor parameters, decreased PIV and PS, and increased TP and SP, shifting FCCB to the right and downward. All of these results were changed after the treatment of NaHS. SUR2B protein expression was higher in carotid sinus of the 2K1C + NaHS group than that of the 2K1C group. These data suggested that exogenous H 2 S exerted a facilitatory role on isolated baroreceptor reflex and activity in renovascular hypertensive rats through opening K ATP channels in vascular smooth muscle cells.

Mechanism of loss of consciousness during vascular neck restraint

Vascular neck restraint (VNR) is a technique that police officers may employ to control combative individuals. As the mechanism of unconsciousness is not completely understood, we tested the hypothesis that VNR simply compresses the carotid arteries, thereby decreasing middle cerebral artery blood flow. Twenty-four healthy police officers (age 35 ± 4 yr) were studied. Heart rate (HR), arterial pressure, rate of change of pressure (dP/dt), and stroke volume (SV) were measured using infrared finger photoplethysmography. Bilateral mean middle cerebral artery flow velocity (MCAVmean) was measured by using transcranial Doppler ultrasound. Neck pressure was measured using flat, fluid-filled balloon transducers positioned over both carotid bifurcations. To detect ocular fixation, subjects were asked to focus on a pen that was moved from side to side. VNR was released 1-2 s after ocular fixation. Ocular fixation occurred in 16 subjects [time 9.5 ± 0.4 (SE) s]. Pressures over the right (R) and left (L) carotid arteries were 257 ± 22 and 146 ± 18 mmHg, respectively. VNR decreased MCAVmean (R 45 ± 3 to 8 ± 4 cm/s; L 53 ± 2 to 10 ± 3 cm/s) and SV (92 ± 4 to 75 ± 4 ml; P < 0.001). Mean arterial pressure (MAP), dP/dt, and HR did not change significantly. We conclude that the most important mechanism in loss of consciousness was decreased cerebral blood flow caused by carotid artery compression. The small decrease in CO (9.6 to 7.5 l/min) observed would not seem to be important as there was no change in MAP. In addition, with no significant change in HR, ventricular contractility, or MAP, the carotid sinus baroreceptor reflex appears to contribute little to the response to VNR.

285 Hemodynamic effects of a vascular neck restraint

BACKGROUND: Vascular neck restraint (VNR) is a technique that police officers often employ to control combative individuals. As the mechanism of unconsciousness is not completely understood, we conducted a study to measure middle cerebral artery flow velocity (VelMCA), bilateral external neck pressures and multiple hemodynamic variables in healthy volunteers during the application of VNR. METHODS: Twenty-four healthy police officers (age 35 4 [SD] years) were studied. Heart rate (HR), arterial pressure, rate of change of pressure (dP/dt) and stroke volume (SV) were measured using infrared finger photo-plethysmography. Bilateral VelMCA was measured using transcranial Doppler ultrasound. Neck pressure was measured using 4 flat, fluid-filled balloon transducers positioned over both carotid bifurcations and the largest portion of both sternocleidomastoid muscles (n 12). To detect ocular fixation, subjects were asked to focus on a pen that was moved from side to side. VNR was released 1-2 sec after ocular fixation. Data were collected for 60 sec at baseline and duration of VNR. VNR was applied by the same right-handed officer in all subjects. RESULTS: Ocular fixation occurred in 16 subjects (time 9.5 0.4 [SEM] sec). Application of VNR significantly (P 0.001) decreased mean VelMCA (R 45 3 to 8 4 cm/s; L 53 2 to 10 3 cm/s) and SV (92 4 to 75 4 ml). Mean arterial pressure, dP/dt and HR did not change significantly. External pressures over the R and L carotid arteries were 257 22 and 146 18 mmHg, respectively and R and L sternocleidomastoid muscles were 429 23 and 526 36 mmHg, respectively. CONCLUSION: The most important mechanism in causing unconsciousness was decreased cerebral flow. As arterial pressure did not change, the small decrease in SV did not cause unconsciousness. Since there were no significant changes in HR, dP/dt or mean arterial pressure, the carotid sinus baroreceptor reflex does not appear to contribute to the response to VNR.

Reflexes from pulmonary arterial baroreceptors in dogs: interaction with carotid sinus baroreceptors

In contrast to the reflex vasodilatation occurring in response to stimulation of baroreceptors in the aortic arch, carotid sinuses and coronary arteries, stimulation of receptors in the wall of pulmonary arteries results in reflex systemic vasoconstriction. It is rare for interventions to activate only one reflexogenic region, therefore we investigated how these two types of reflexes interact. In anaesthetized dogs connected to cardiopulmonary bypass, reflexogenic areas of the carotid sinuses, aortic arch and coronary arteries and the pulmonary artery were subjected to independently controlled pressures. Systemic perfusion pressure (SPP) measured in the descending aorta (constant flow) provided an index of systemic vascular resistance. In other experiments, sympathetic efferent neural activity was recorded in fibres dissected from the renal nerve (RSNA). Physiological increases in pulmonary arterial pressure (PAP) induced significant increases in SPP (+39.1 ± 10.4 mmHg) and RSNA (+17.6 ± 2.2 impulses s(−1)) whereas increases in carotid sinus pressure (CSP) induced significant decreases in SPP (−42.6 ± 10.8 mmHg) and RSNA (−42.8 ± 18.2 impulses s(−1)) (P < 0.05 for each comparison; paired t test). To examine possible interactions, PAP was changed at different levels of CSP in both studies. With CSP controlled at 124 ± 2 mmHg, the threshold, 'set point' and saturation pressures of the PAP–SPP relationship were higher than those with CSP at 60 ± 1 mmHg; this rightward shift was associated with a significant decrease in the reflex gain. Similarly, increasing CSP produced a rightward shift of the PAP–RSNA relationship, although the effect on reflex gain was inconsistent. Furthermore, the responses to changes in CSP were influenced by setting PAP at different levels; increasing the level of PAP from 5 ± 1 to 33 ± 3 mmHg significantly increased the set point and threshold pressures of the CSP–SPP relationship; the reflex gain was not affected. These results indicate the existence of interaction between pulmonary arterial and carotid sinus baroreceptor reflexes; physiological and pathological states that alter the stimulus to one may alter the reflex responses from the other.

An investigation of vitamin B12 deficiency in elderly inpatients in neurology department

To investigate the status of vitamin B12 deficiency in elderly inpatients in the department of neurology. A total number of 827 patients in the department of neurology of Shanghai Punan hospital, from March 2007 to July 2008, were employed in the present study. They were 60 years or older, and the average age was 77.1+/-7.5 years old. All the patients were diagnosed with no severe hepatic or renal dysfunction, without any usage of vitamin B12 during the previous 3 months before the detection. The levels of serum vitamin B12, folate and homocysteine (Hcy) were evaluated. The patients with vitamin B12 deficiency were screened. The resulting symptoms, positive signs of neurological examination, and the neuroelectricphysiological results were compared between patients with or without vitamin B12 deficiency. Vitamin B12 deficiency was found in 163 patients (19.71% of the total patients), and was more prevalent in female than in male patients, also with increased incidences with aging. Patients with low levels of serum vitamin B12 exhibited higher rate of gastrointestinal diseases, while only 9.82% of the vitamin B12 deficient patients had megaloblastic anemia. Symptoms of vitamin B12 deficiency included unsteadily walking in the darkness and hypopallesthesia, and some chronic diseases such as cerebral ischemia, hypertension, Parkinson's disease (Parkinsonism), diabetes mellitus and coronary heart disease. Most of the vitamin B12 deficient patients had neuroelectricphysiological abnormalities. Vitamin B12 deficiency is remarkably common in elderly patients in neurology department, with various and atypical clinical manifestations, and the neurological symptoms are more common than megaloblastic anemia symptoms.

REBUTTAL FROM DR. ROTHE

POINT-COUNTERPOINTREBUTTAL FROM DR. ROTHEPublished Online:01 Oct 2006https://doi.org/10.1152/japplphysiol.00561b.2006MoreSectionsPDF (43 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat Hainsworth and Drinkhill (2) concluded that active venoconstriction is not important in raising end-diastolic volume (EDV) or stroke volume during exercise and orthostasis. They do admit that active venoconstriction exists, but in their last paragraph, they conclude that it only provides a small venous return enhancement. I fully agree with the following. 1) The skeletal muscle pump during exercise can provide the major part of the maintenance or increase in EDV (7). 2) Active venoconstriction occurs primarily in the abdominal splanchnic bed. 3) Skin and skeletal muscle venous responses are minimal. 4) The spleens of dogs are much larger than that of humans. 4) In response to changes in flow and venous distending pressure, passive changes in venous volume are indeed important.However, Hainsworth and Drinkhill did not support the assumption that constant pressure perfusion eliminates concurrent active venoconstriction in assessing the magnitude of the passive venous responses. Changing the carotid sinus pressure between 60 and 195 mmHg, Hainsworth and Drinkhill (2) claim a 3 ml/kg change in effective circulatory volume (the total stressed volume) of the liver and intestinal bed. In conjunction with a total body compliance of 2.5 ml·kg−1·mmHg−1, this would change the Pmcf by 1.2 mmHg. Assuming that the Pra at equilibrium would be increased by the same amount, they then claim, using “Guyton's curves,” that this would increase the cardiac output by only 20%. Herndon and Sagawa (Ref. 3, Fig. 7) suggest that the sensitivity of cardiac output to changes in Pra is 52 ml·min−1·kg−1 change in flow per millimeter mercury change in Pra. Thus a change in cardiac output from a 1.2 mmHg change in Pra would be a much larger increase of 60 ml·min−1·kg−1. Other studies have reported much larger active venous changes than the 3 ml/kg. For example, for dogs, carotid baroreceptor changes, a 7.0 ml/kg change (1); maximum sympathetic simulation, with spleen intact 7.2 ml/kg, without spleen 4.3 ml/kg (4); carotid sinus pressure changes, with spleen 8.4 ml/kg, without spleen 7.2 ml/kg (8).They also claim (Ref. 2; Fig. 2) that the intestinal bed provides a negligible active venoconstriction response based on the data from the study by Noble et al. (4). We (6) evaluated active and passive venoconstriction in segments of dog jejunum. Norepinephrine caused an active change in intestinal blood volume of 24% and a passive change of 62%. Active venoconstriction is important.REFERENCES1 Brunner MJ, Shoukas AA, and MacAnespie CL. The effect of the carotid sinus baroreceptor reflex on blood flow and volume redistribution in the total systemic vascular bed of the dog. Circ Res 48: 274–285, 1981.Crossref | PubMed | ISI | Google Scholar2 Hainsworth R and Drinkhill MJ. Counterpoint: Active venoconstriction is not an important adjunct to maintaining or raising end-diastolic volume and stroke volume during exercise and orthostasis. J Appl Physiol. In Press.Google Scholar3 Herndon CW and Sagawa K. Combined effects of aortic and right atrial pressure on aortic flow. Am J Physiol 217: 65–72, 1969.Link | ISI | Google Scholar4 Karim F and Hainsworth R. Responses of abdominal vascular capacitance to stimulation of splanchnic nerves. Am J Physiol 231: 434–440, 1976.Link | ISI | Google Scholar5 Noble BJ, Drinkhill MJ, Myers DS, and Hainsworth R. Reflex control of splanchnic blood volume in anesthetized dogs. J Physiol 513: 363–272, 1998.Google Scholar6 Rothe CF, Johns BL, and Bennett TD. Vascular capacitance of dog intestine using mean transit time of indicator. Am J Physiol Heart Circ Physiol 234: H7–H13, 1978.Link | ISI | Google Scholar7 Sheriff D. Point: The muscle pump raises muscle blood flow during locomotion. J Appl Physiol 99: 371–372, 2005.Link | ISI | Google Scholar8 Shoukas AA, MacAnespie CL, Brunner L, and Watermeier MJ. The importance of the spleen in blood volume shifts of the systemic vascular bed caused by the carotid sinus baroreceptor reflex in the dog. Circ Res 49: 759–766, 1981.Crossref | PubMed | ISI | Google Scholar Download PDF Previous Back to Top Next FiguresReferencesRelatedInformation More from this issue > Volume 101Issue 4October 2006Pages 1265-1266 Copyright & PermissionsCopyright © 2006 the American Physiological Societyhttps://doi.org/10.1152/japplphysiol.00561b.2006History Published online 1 October 2006 Published in print 1 October 2006 Metrics

The following letters are in response to the Point:Counterpoint series “Hypoxic pulmonary vasoconstriction is/is not mediated by increased production of reactive oxygen species” that appears in this issue.

To the Editor : The underlying issue being discussed ([1a][1], [4][2]) seems much broader than simply the role of venoconstriction. It is really about the regulation of the magnitude of cardiac output. Thus while the argument put forth by Hainsworth and Drinkhill is fine as far as it goes, it fails

Gender differences in carotid sinus baroreceptor reflexes in healthy young normal subjects and in ASCOT patients with treated essential hypertension

Gender differences in carotid sinus baroreceptor reflexes in healthy young normal subjects and in ASCOT patients with treated essential hypertension

Modulation of the carotid baroreceptor reflex by substance P in the nucleus tractus solitarius

Previous studies have shown that administration of substance P (SP) into the nucleus tractus solitarius (NTS) can evoke a depressor response similar to that produced by activation of the arterial baroreceptors. In addition, some studies have suggested that SP increases the reflex responses to activation of baroreceptor input. The present study was performed to determine the effects of SP on the carotid sinus baroreceptor reflex at the level of the NTS by examining the effects of both exogenous SP microinjected into different rostrocaudal locations in the NTS and blockade of the effects of endogenous SP, through the microinjection of a substance P antagonist (SPa; [ d-Pro, d-Trp]-substance P). Changes in pressure in an isolated carotid sinus in anesthetized dogs were used to evoke baroreflex changes in arterial blood pressure (BP) before and after microinjection of SP (0.5 μM) or SPa (10 μM) into barosensitive regions of the NTS. Microinjection of SP or its antagonist did not alter baseline, resting BP but did produce significant changes in baroreflex sensitivity. Microinjection of SP into different rostrocaudal regions of the NTS produced different responses, with rostral and caudal NTS microinjections producing significant increases in sensitivity. No effects on baroreflex sensitivity were obtained in response to SP microinjections into the intermediate NTS. Unlike SP, microinjection of the SPa significantly decreased baroreflex sensitivity at all rostrocaudal levels of the NTS. These data demonstrated that SP has the capability to modulate the carotid baroreflex at the level of the NTS and support a physiological role for endogenously released SP.

Chronic isolation of carotid sinus baroreceptor region in conscious normotensive and hypertensive rats.

We have developed a chronic technique to isolate the carotid sinus baroreceptor region in the conscious rat model. Our technique, when used in conjunction with other methods, allows for the study of the control of arterial pressure, heart rate, and cardiac output by the carotid sinus baroreceptor reflex in conscious, unrestrained rats. The performance of our technique was evaluated in two strains: normotensive Sprague-Dawley (SD) rats and spontaneously hypertensive rats (SHR). Each rat was instrumented with an aortic flow probe and a catheter placed in the right femoral artery to monitor cardiac output and arterial pressure, respectively. The cervical sympathetic trunk and aortic depressor nerve were ligated and cut bilaterally, leaving vagus nerves intact. The right and left carotid sinuses were isolated using our new technique. We tested the open-loop function of the carotid sinus baroreceptor reflex system in the conscious rat after recovery from the isolation surgery. We found that changes in nonpulsatile carotid sinus pressure caused significant changes in arterial pressure, heart rate, and total peripheral resistance in both rat strains. However, the cardiac output responses differed dramatically between strains. Significant changes were seen in the cardiac output response of SHR, whereas no significant changes were observed in normotensive SD rats. We have found this technique to be a highly reliable tool for the study of the carotid sinus baroreceptor reflex system in the conscious rat.

Central ANG II Receptor Involved in Carotid Sinus Reflex Resetting in Chronically Stressed Rats

Qian, Z. M., D. S. Xiao, W. Q. Huang, P. L. Tang and B. Xu. Central ANG II receptor involved in carotid sinus reflex resetting in chronically stressed rats. Physiol Behav 62(2) 241–247, 1997.—The performance of carotid sinus baroreceptor reflex (CSR) was characterized in chronically stressed rats by changing intracarotid sinus pressure (ISP) and constructing ISP-MAP (mean arterial pressure) relationship curve. The role of central angiotensin II (ANG II) receptors in the changes of CSR performance induced by chronic stress was determined. Rats were subjected to foot-shock stress for two weeks. The carotid sinus was isolated from the systemic circulation and the ISP changed in a stepwise manner. The results showed that in chronically stressed rats, ISP-MAP relationship curve shifted upward, the set point was significantly higher than that obtained from the unstressed group, and the reflex gain and the MAP range were significantly smaller than those in unstressed rats. After intracerebroventricular injection of saralasin (20 ng), MAP range was augmented and the set point decreased significantly. Injection of vehicle did not lead any significant differences between the parameters of the reflex measured before or after injection in either the stressed or the unstressed rats. Furthermore, administration of ANG II (10 μg) induced a significant increase in the set point and decrease in the reflex gain in the unstressed rats. The responses of CSR to ANG II were completely blocked by pretreatment of saralasin. These findings suggest that chronic stress could induce the decreased CSR function in the normotensives and central ANG II receptors involved in the resetting of CSR in the chronically stressed rats.

Effects of fentanyl, nitrous oxide, or both, on baroreceptor reflex regulation in the cat

We have investigated the effects of fentanyl, nitrous oxide, or both, on carotid sinus baroreceptor reflexes in cats during basal chloralose anaesthesia. The bilaterally isolated carotid sinuses were perfused at prevailing systemic arterial pressure or at predetermined levels of pump-controlled pulsatile pressures of 50-200 mm Hg in steps of 25 mm Hg. Other major baroreceptor sites were denervated by bilateral vagotomy. Fentanyl decreased arterial pressure dose-dependently when the carotid sinuses were perfused at prevailing systemic arterial pressure and when the perfusion pressure was controlled artificially. High-dose fentanyl reduced significantly baroreceptor reflex responses in the sinus perfusion pressure range 50-125 mm Hg. Nitrous oxide increased arterial pressure in the carotid sinus perfusion range 75-125 mm Hg. There was no interaction between nitrous oxide and fentanyl for baroreceptor reflex responses. Our results indicated that baroreceptor reflexes, with and without nitrous oxide, were well preserved by moderate doses of fentanyl while high doses of fentanyl depressed baroreceptor reflexes.

Effect of arterial compliance on carotid sinus baroreceptor reflex control of the circulation.

Capacitive properties of the arterial and venous segments of the peripheral circulation are important in the regulation of cardiac output and arterial blood pressure. We examined whether an acute increase in arterial compliance C(a) would alter carotid sinus baroreflex control of the circulation. Eight mongrel dogs were anesthetized with pentobarbital sodium, and the carotid sinus regions were isolated and perfused with nonpulsatile pressures. Open-loop baroreflex response curves for systemic arterial pressure (SAP), heart rate (HR), aortic blood flow (ABF), peripheral vascular resistance (PVR), and left ventricular (LV) contractility were obtained when carotid sinus pressure (CSP) was changed in 25-mmHg steps between 50 and 200 mmHg under a control condition and when C(a) was increased by including two hydraulic compliant chambers to the arterial circulation (CS 1.72 ml/mmHg and CL 5.05 ml/mmHg). The compliant chambers significantly increased C(a) and altered the ratio of arterial to venous compliance C(a)/Cv). Changes in C(a)/Cv significantly decreased the maximal open-loop baroreflex gain (Gmax) for SAP (-2.3 +/- 0.5, -1.6 +/- 0.3, and -1.1 +/- 0.2 mmHg/mmHg, control vs. CS vs. CL, P < 0.05). Gmax for ABF was decreased by CS (-0.9 +/- 0.2 vs. -0.3 +/- 0.1 ml.kg-1.min-1, control vs. CS, P < 0.05), and CL reversed the reflex changes in ABF (Gmax: +0.6 +/- 0.3 ml.kg-1.min-1). Gmax for HR, PVR, and LV contractility was not altered when C(a) was increased (P > 0.05). These findings indicate that an increase in C(a) changes C(a)/Cv and alters carotid baroreflex control of SAP by modifying the ABF response. We conclude that a change in C(a)/Cv affects the reflex control of the circulation by altering the distribution of blood volume between the arterial and venous circulations.

Effect of carotid sinus baroreceptor reflex on hepatic and splenic vascular capacitance in vagotomized dogs

Mechanisms of how baroreflex activation changes splanchnic vascular volumes were studied in eight vagotomized dogs, anesthetized by chloralose/urethan. Hepatic and splenic vascular volume changes were determined from organ dimensions by sonomicrometry. Pulsatile carotid sinus pressure (CSP) in isolated and separately perfused carotid sinuses was changed among 200, 120, and 40 mmHg. Lowering CSP from 120 to 40 mmHg significantly decreased both hepatic and splenic vascular volume (at similar portal pressure) by 1.9 +/- 0.5 and 1.8 +/- 0.6 ml/kg body wt, respectively. Increasing CSP from 120 to 200 mmHg tended to increase regional vascular volumes (P = NS). The combined volume change of liver and spleen between CSP 40 and 200 mmHg was 4.2 +/- 0.6 ml/kg body wt (P < 0.001). Pressure-volume (dimension) curves at high, low, and baseline CSP were determined to separate active and passive mechanisms of vascular volume changes. Changes in CSP did not change regional vascular compliance. Low CSP significantly decreased unstressed liver and unstressed splenic volume by 3.3 +/- 0.9 and 1.9 +/- 0.5 ml/kg body wt, respectively. These results indicate that liver and spleen both contribute to blood volume mobilization by vasoconstriction during low CSP and that the carotid sinus baroreceptor reflex modulates hepatic and splenic vascular capacitance by changing unstressed volume rather than by changing vascular compliance.

Carotid baroreflex responsiveness during dynamic exercise in humans.

We utilized 5-s changes of neck pressure and neck suction (from 40 to -80 Torr) to alter carotid sinus transmural pressure in seven men with peak oxygen uptake (VO2peak) of 41.4 +/- 3.6 ml O2.kg-1.min-1. Peak responses of heart rate (HR) and mean arterial pressure (MAP) to each carotid sinus perturbation were used to construct open-loop baroreflex curves at rest and during exercise at 25.7 +/- 1.1 and 47.4 +/- 1.9% VO2peak. The baroreflex curves were fit to a logistic function describing the sigmoidal nature of the carotid sinus baroreceptor reflex. Maximal gain for baroreflex control of HR (-0.31 +/- 0.05 beats.min-1.mmHg-1) and MAP (-0.30 +/- 0.08 mmHg/mmHg) at rest was the same as during exercise at 25 and 50% VO2peak (-0.30 +/- 0.05, -0.39 +/- 0.13 beats.min-1.mmHg-1 for HR, P = NS; -0.23 +/- 0.04, -0.60 +/- 0.38 mmHg/mmHg for MAP, P = NS). Resetting of the baroreflex occurred during exercise at 50% VO2peak. The centering point, threshold, and saturation pressures were significantly increased for baroreflex control of HR (delta pressure = 26.3 +/- 6.8, 19.6 +/- 10.4, 33.0 +/- 5.6 mmHg, P < 0.05) and MAP (delta pressure = 27.1 +/- 7.7, 16.1 +/- 14.8, 38.2 +/- 8.5 mmHg, P < 0.05). The operating point (steady-state HR and MAP) was shifted closer to threshold of the baroreflex during exercise at 50% VO2peak, as reflected by differences in HR and MAP between the centering and operating points (delta HR = 12.5 +/- 4.7 beats/min, P = 0.10; delta MAP = 7.6 +/- 1.3 mmHg, P < 0.05). These findings suggest a resetting of the carotid baroreflex during exercise with no attenuation in maximal sensitivity. A shift in operating point toward threshold of the baroreflex enables effective buffering of elevations in systemic blood pressure via reflex alterations in HR and MAP.

Effects of distension of the urinary bladder on the cardiovascular reflexes from the carotid baroreceptors in the dog.

1. The hindlimb vasoconstrictor effects of distension of the urinary bladder were studied at different levels of input from the carotid sinus baroreceptors in the dog anaesthetized with a mixture of chloralose and urethane. 2. The vascularly isolated hindlimb was perfused at constant blood flow through its femoral artery, so that a change in pressure gradient (mean femoral arterial perfusion pressure minus mean inferior vena caval pressure) indicated a similar directional change in vascular resistance. The vascularly isolated carotid sinus regions were perfused with blood at a constant pulsatile flow. 3. Raising the carotid sinus mean perfusion pressure in randomly selected steps of 30 mmHg from 60 to 210 mmHg had little effect on heart rate unless the blood pressure was controlled, when a progressive bradycardia occurred, but caused a progressive reduction in arterial blood pressure and vasodilatation in the perfused hindlimb. Distension of the bladder at each level of carotid sinus pressure resulted in tachycardia, hypertension and hindlimb vasoconstriction. 4. The cardiac responses to bladder distension were the same at all carotid sinus pressures. When the blood pressure was controlled, however, the response was reduced at high and low sinus pressures. 5. The relationship between the carotid sinus perfusion pressure and hindlimb perfusion pressure (i.e. vascular resistance) was affected by distension of the bladder in two ways. In the one, hindlimb perfusion pressure increased by approximately the same amount at all levels of carotid sinus pressure indicating resetting of the carotid sinus baroreceptor reflex control of hindlimb vascular resistance towards vasoconstriction without change in gain of the reflex. In the other, the pressure increases were diminished at the higher levels of carotid sinus pressure indicating both resetting and an increase in gain of the reflex. 6. Both types of response occurred in the spontaneously breathing animal, in animals artificially ventilated, while pacing the heart, with the arterial blood pressure maintained constant at about 100 mmHg, and after division of the cervical vagosympathetic nerves. The frequency of occurrence of each type of response, however, varied under the different conditions. 7. The possible reasons for the two types of vascular response are discussed.

Blood volume changes in microcirculation of rat intestine caused by carotid sinus baroreceptor reflex.

This series of experiments quantified the role of the rat small intestinal arterioles in capacity changes during bilateral carotid occlusion (BCO) and compared them with previous venular studies. We also determined the role of autoregulation in arteriolar constriction during BCO. First-order, second-order, and third-order arteriolar diameter changes were measured during changes in arteriolar pressure and/or sympathetic activity (via BCO). The results indicated that an arteriolar pressure drop caused an immediate significant transient diameter decrease of 14% (P < 0.001), followed by an average steady-state diameter increase of 11% (P < 0.001) over control because of autoregulation. During BCO, the arterioles demonstrated an initial 8-22% decrease in diameter (P < 0.05). The largest first-order vessels were the least responsive to changes in pressure and BCO, while the smallest third-order vessels were the most responsive. Apparently autoregulation, and not sympathetic activity, was responsible for most of the arteriolar constriction during BCO. We also developed an anatomic model of the rat intestinal vasculature which revealed that venules hold 70% of the microcirculatory volume and are responsible for 80% of the total blood shift during BCO. Venular constriction and, to a minor degree, arteriolar constriction result in a 14% decrease in microcirculatory intestinal blood volume during BCO.

9 On the location of the defect in the carotid sinus baroreceptor reflex arc in human essential hypertension

9 On the location of the defect in the carotid sinus baroreceptor reflex arc in human essential hypertension

Neurons in the caudal ventrolateral medulla mediate the arterial baroreceptor reflex by inhibiting barosensitive reticulospinal neurons in the rostral ventrolateral medulla in rabbits

Participation of the caudal ventrolateral medulla in the arterial baroreceptor reflex was examined in urethane-anesthetized, vagotomized and immobilized rabbits whose aortic nerve was cut bilaterally. The extent of the caudal ventrolateral medulla was mapped by decreases in the renal sympathetic nerve activity and arterial pressure following a local microinjection of a neuroexcitatory amino acid, sodium glutamate (0.075-1.5 nmol). It extended between the levels 1.3 mm rostral and 3.0 mm caudal to the obex. An injection of sodium glutamate into the caudal ventrolateral medulla also diminished spontaneous activity of barosensitive reticulospinal neurons in the rostral ventrolateral medulla. In the 'split medulla preparation' in which the medulla was split along the midsagittal plane to disrupt fiber connections associating both sides, a neurotoxic agent, kainic acid, was injected unilaterally into the rostral ventrolateral medulla. This treatment markedly attenuated responses of renal sympathetic nerve activity and arterial pressure induced by a sodium glutamate injection into the ipsilateral caudal ventrolateral medulla, whereas responses to an injection into the contralateral caudal ventrolateral medulla were totally preserved. In four separate experiments, three to five injections of kainic acid were made unilaterally to cover the whole extent of the caudal ventrolateral medulla. The sympathoinhibitory and depressor responses to stimulation of the ipsilateral aortic nerve were then totally abolished. Simultaneously, the cardiac cycle-related rhythmic fluctuation of renal sympathetic nerve activity, which represented activity of the carotid sinus baroreceptor reflex, was attenuated to the noise level. These results, together with our previous electrophysiological demonstration of barosensitive caudal ventrolateral medulla neurons with axonal projections to the rostral ventrolateral medulla, strongly support the hypothesis that neurons in the caudal ventrolateral medulla mediate the arterial baroreceptor-vasomotor reflex through inhibition of barosensitive reticulospinal neurons in the rostral ventrolateral medulla.