Suppression of baroreceptor discharge by endothelin at high carotid sinus pressure

1992 ◽  
Vol 263 (1) ◽  
pp. R103-R108 ◽  
Author(s):  
M. W. Chapleau ◽  
G. Hajduczok ◽  
F. M. Abboud
Keyword(s):  
Endothelial Cells ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
High Dose ◽  
Nerve Activity ◽  
Local Exposure ◽  
Potent Vasoconstrictor ◽  
Alpha Chloralose ◽  
Vasoconstrictor Peptide ◽  
Sinus Pressure

Endothelin is a potent vasoconstrictor peptide released from endothelial cells capable of producing marked and prolonged increases in arterial pressure. The purpose of this study was to determine whether endothelin alters the sensitivity of arterial baroreceptors. Multifiber baroreceptor activity was recorded from the vascularly isolated, endothelium-denuded carotid sinus in dogs anesthetized with alpha-chloralose. Local exposure of baroreceptors to endothelin at a concentration of 10(-8) M produced vasoconstriction of the carotid sinus as measured with sonomicrometer crystals but did not alter baroreceptor discharge significantly. A higher concentration of endothelin (10(-7) M) markedly suppressed baroreceptor activity, particularly at pressures greater than 100 mmHg (n = 7, P less than 0.05). The magnitude of the decrease in activity was dependent on the duration of exposure to endothelin. Baroreceptor activity measured at carotid pressures of 60, 100, and 200 mmHg averaged 23 +/- 4, 65 +/- 6, and 100 +/- 0% of maximum during control; 38 +/- 12, 61 +/- 9, and 74 +/- 15% after exposure to endothelin (10(-7) M) for 2 min; and 27 +/- 8, 53 +/- 12, and 56 +/- 19% after 12 min, respectively. The suppression of nerve activity with the high dose of endothelin was not accompanied by additional vasoconstriction, suggesting a direct effect of endothelin on nerve endings. We speculate that endothelin released from endothelial cells may act in a paracrine manner to suppress activity of baroreceptors, particularly at high levels of arterial pressure. Such an action would interfere with the buffering capacity of the baroreflex and promote hypertension.

Pulsatile activation of baroreceptors causes central facilitation of baroreflex

1989 ◽  
Vol 256 (6) ◽  
pp. H1735-H1741 ◽  
Author(s):  
M. W. Chapleau ◽  
G. Hajduczok ◽  
F. M. Abboud
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve Activity ◽  
Static Pressure ◽  
Carotid Sinus ◽  
Pulse Frequency ◽  
The Other ◽  
Carotid Sinus Nerve ◽  
Nerve Activity ◽  
Pulsatile Pressure ◽  
Sinus Pressure

The reflex decrease in arterial pressure is greater and more sustained with elevated pulsatile than with elevated static carotid sinus pressure. The purpose of this study was to relate afferent baroreceptor activity (BRA) and efferent sympathetic nerve activity (SNA) during static and pulsatile pressure to evaluate the influence of pulsatile pressure on the central mediation of the baroreflex. The carotid sinuses were isolated in 11 dogs anesthetized with chloralose. Both vagosympathetic trunks were cut and both carotid sinuses exposed to static and pulsatile pressures over a range of mean carotid sinus pressures (40-180 mmHg). BRA was recorded from one carotid sinus nerve, and the other intact carotid sinus served to initiate reflex changes in lumbar or renal SNA and arterial pressure. For the same mean carotid sinus pressure, pulsatile pressure caused significantly greater inhibition of SNA than static pressure. More importantly, for the same or lesser levels of baroreceptor activity per second, pulsatile pressure caused significantly greater inhibition of SNA than static pressure. The inhibition of SNA was not sustained (i.e., there was "adaptation") with continuous baroreceptor input during static pressure, whereas the inhibition of SNA was sustained (i.e., there was no significant adaptation) with the phasic input during pulsatile pressure. Increases in pulse frequency from 1.4 to 2.5 and 3.7 Hz caused progressively less inhibition of SNA.(ABSTRACT TRUNCATED AT 250 WORDS)

Rabbit carotid sinus reflex under pentobarbital, urethan, and chloralose anesthesia

1984 ◽  
Vol 246 (5) ◽  
pp. H696-H701 ◽  
Author(s):  
N. Ishikawa ◽  
C. H. Kallman ◽  
K. Sagawa
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Logistic Function ◽  
Systemic Arterial Pressure ◽  
Open Loop ◽  
Specific Effects ◽  
Reflex Control ◽  
Alpha Chloralose ◽  
Sinus Pressure

To determine the effects of different anesthesias on the performance of the arterial baro-reflex, the open-loop characteristic of the carotid sinus reflex was analyzed in 24 rabbits under anesthesia with pentobarbital (30 mg/kg), urethan (800 mg/kg), alpha-chloralose (80 mg/kg), or a mixture of alpha-chloralose (40 mg/kg) and urethan (0.4 g/kg). For each rabbit and anesthesia, mean systemic arterial pressure and heart rate were measured as carotid sinus pressure was changed in 10-mmHg steps between 40 and 150 mmHg. This set of measurements was repeated four times at 1-h intervals. A logistic function curve was fitted to the carotid sinus pressure-arterial pressure relationship. The parameters of this curve were then analyzed to delineate the specific effects of the anesthesias on the relationship. The main finding was that the response range and the slope parameters under alpha-chloralose anesthesia were significantly smaller than those obtained under the other anesthesias. Propylene glycol, used as the solvent for chloralose, did not affect the reflex control of arterial pressure or heart rate. The reflex under chloralose-urethan anesthesia showed characteristics similar to those under urethan anesthesia. We conclude that although alpha-chloralose has traditionally been used in the dog to obtain strong reflex responses, it weakens the reflex control of arterial pressure in the rabbit.

Prostaglandins in carotid sinus enhance baroreflex in rabbits

1989 ◽  
Vol 257 (2) ◽  
pp. R445-R450 ◽  
Author(s):  
T. S. McDowell ◽  
T. S. Axtelle ◽  
M. W. Chapleau ◽  
F. M. Abboud
Keyword(s):  
Arachidonic Acid ◽  
Arterial Pressure ◽  
Sympathetic Nerve Activity ◽  
Carotid Sinus ◽  
Arterial Baroreflex ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Maximum Inhibition ◽  
Endogenous Prostaglandins ◽  
Sinus Pressure

The purpose of this study was to examine the possible influence of endogenous prostaglandins in the carotid sinus on the arterial baroreflex. Lumbar sympathetic nerve activity (LSNA) and arterial pressure were recorded during step increases in isolated carotid sinus pressure in rabbits anesthetized with chloralose. Baroreflex responses were facilitated after intrasinus administration of prostacyclin (PGI2; 5 and 10 microM, n = 6) or arachidonic acid (10 microM, n = 12). PGI2 (10 microM) increased the slope of the carotid sinus pressure-LSNA relation (gain) from -0.32 +/- 0.09 to -1.19 +/- 0.38 spikes.s-1.mmHg-1 and decreased the pressure at which 50% of the maximum inhibition of LSNA occurred (EP50) from 127 +/- 5 to 98 +/- 4 mmHg (P less than 0.05). Similar responses were observed with arachidonic acid. Baroreflex responses were attenuated after intrasinus administration of indomethacin (40 and 80 microM, n = 5) or aspirin (1 and 2 mM, n = 7). Indomethacin (80 microM) decreased the gain of the baroreflex from -1.02 +/- 0.24 to -0.47 +/- 0.16 spikes.s-1.mmHg-1 and increased the EP50 from 121 +/- 6 to 133 +/- 7 mmHg (P less than 0.05). Both indomethacin (80 microM) and aspirin (2 mM) reduced the maximum percent inhibition of LSNA significantly. The results indicate that prostaglandins within the carotid sinus facilitate the baroreflex control of LSNA. The attenuation of the baroreflex after inhibition of cyclooxygenase suggests that endogenous prostaglandins contribute to the activation of baroreceptors during increases in carotid sinus pressure.

Tachyphylaxis to the vasopressor effects of endothelin in rat aortic rings

1993 ◽  
Vol 264 (2) ◽  
pp. H352-H356 ◽  
Author(s):  
S. M. Hollenberg ◽  
J. H. Shelhamer ◽  
R. E. Cunnion
Keyword(s):  
Endothelial Cells ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Pressor Effect ◽  
Endothelin Receptor ◽  
Surface Receptors ◽  
Receptor Complexes ◽  
High Affinity ◽  
Potent Vasoconstrictor ◽  
Vasoconstrictor Peptide

Endothelin-1 (ET-1), a potent vasoconstrictor peptide released by endothelial cells, binds with high affinity to surface receptors and is highly resistant to dissociation. We observed tachyphylaxis to the pressor effects of a second application of ET-1 in rat aortic rings and investigated the mechanism of this effect. Developed tension increased progressively with doses of ET-1 ranging from 1 to 500 nM (P < 0.001), and tensions with rechallenge were correspondingly decreased (P < 0.001). In response to 500 nM ET-1, tension increased 1,599 +/- 72 (SE) mg/mg ring wt. Rechallenge with 500 nM ET-1 led to contraction of only 33 +/- 40 mg/mg ring wt. Tachyphylaxis was seen up to 6 h after initial challenge. Pretreatment with nicardipine, lidoflazine, nitroglycerin, and sphingosine did not affect tachyphylaxis. Pretreatment with 500 microM dansylcadaverine (an inhibitor of endothelin internalization) markedly inhibited ET-1-induced contraction and also inhibited tachyphylaxis to ET-1. Further studies with radiolabeled ET-1 suggested that subsequent ET-1 binding is markedly decreased after an initial ET-1 challenge. Dansylcadaverine inhibited ET-1 internalization and also inhibited the decreased binding seen with ET-1 rechallenge. Rat aortic rings demonstrate tachyphylaxis to the pressor effect of a second dose of ET-1. The mechanism appears to be related to binding and subsequent internalization of endothelin-receptor complexes. This effect suggests a possible mechanism for sustained decreases in systemic vascular resistance.

Carotid sinus control of pulsatile hemodynamics in halothane-anesthetized dogs

1980 ◽  
Vol 238 (3) ◽  
pp. H294-H299
Author(s):  
R. H. Cox ◽  
R. J. Bagshaw
Keyword(s):  
Arterial Pressure ◽  
Carotid Sinus ◽  
Open Loop ◽  
Hydraulic Power ◽  
Set Point ◽  
Hemodynamic Variables ◽  
Vascular Impedance ◽  
Mean Pressure ◽  
Anesthetized Dogs ◽  
Sinus Pressure

The open-loop characteristics of the carotid sinus baroreceptor reflex control of pulsatile arterial pressure-flow relations were studied in halothane-anesthetized dogs. Pressures and flows were measured in the ascending aorta, the celiac, mesenteric, renal, and iliac arteries and were used to compute values of regional vascular impedance and hydraulic power. The carotid sinuses were bilaterally isolated and perfused under conditions of controlled mean pressure with a constant sinusoidal component. Measurements were made with the vagi intact and after bilateral vagotomy. Maximum values of open-loop gain averaged -0.78 +/- 0.08 before and -1.42 +/- 0.20 after vagotomy. Vagotomy produced significant increases in the variation of all hemodynamic variables with carotid sinus pressure that were nonuniformly affected in the various regional vascular beds. Aortic and regional vascular impedance showed significant variations with carotid sinus pressure that were augmented by vagotomy. Aortic impedance exhibited a minimum at the normal set point. These results indicate that a) carotid sinus baroreflexes are well preserved with halothane anesthesia, b) thoracic baroreceptor-mediated reflexes exert significant hemodynamic effects on systemic hemodynamics around normal set point values of arterial pressure, c) systemic baroreceptors exert control over large as well as small vessel properties, and d) the baroreceptor-mediated reflexes produce significant influences on hydraulic power and its components.

Comparison of carotid sinus baroreceptors in dogs, cats, monkeys, and rabbits

1984 ◽  
Vol 247 (1) ◽  
pp. R52-R56
Author(s):  
J. P. Gilmore ◽  
E. Tomomatsu
Keyword(s):  
Arterial Pressure ◽  
Single Unit ◽  
Static Pressure ◽  
Carotid Sinus ◽  
Lower Threshold ◽  
Threshold Pressure ◽  
Experimental Conditions ◽  
Single Unit Recordings ◽  
Sinus Pressure

Single-unit recordings were obtained from the vascularly isolated Krebs-Henseleit-perfused carotid sinus of the rabbit and cat, and the results were compared with those obtained previously from the monkey and dog. Carotid sinus pressure was altered using static pressure steps. There was a highly significant correlation between resting arterial pressure and carotid sinus baroreceptor threshold pressure. The baroreceptors of the monkey and rabbit had a significantly lower threshold than those of the dog and cat. The baroreceptors of the monkey had a significantly lower gain than those of the three nonprimates. This is the first study in which baroreceptor activity has been studied under the same experimental conditions in four different species.

Inhibition of NO synthesis minimally affects the dynamic baroreflex regulation of sympathetic nerve activity

1997 ◽  
Vol 272 (5) ◽  
pp. H2446-H2452 ◽  
Author(s):  
H. Miyano ◽  
T. Kawada ◽  
T. Shishido ◽  
T. Sato ◽  
M. Sugimachi ◽  
...  
Keyword(s):  
Transfer Function ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Carotid Sinus ◽  
Function Analysis ◽  
Corner Frequency ◽  
Nerve Activity ◽  
Carotid Sinus Baroreflex ◽  
Transfer Function Analysis

The purpose of this investigation was to examine the role of nitric oxide (NO) in the dynamic baroreflex regulation of cardiac sympathetic nerve activity. In anesthetized rabbits, we imposed random pressure perturbations on the isolated carotid sinuses before and after the intravenous administration of NG-monomethyl-L-arginine. We characterized the dynamic properties relating carotid sinus pressure input to sympathetic nerve activity by means of a transfer function analysis. NG-monomethyl-L-arginine decreased the corner frequency of the transfer function (0.100 +/- 0.054 vs. 0.074 +/- 0.035 Hz; P < 0.05), whereas other parameters such as the steady-state gain and transmission lag time remained unchanged. Although cursory examination of these findings would suggest a possible contribution of NO in the dynamic baroreflex regulation of sympathetic nerve activity, quantitative assessment of the transfer function reveals only a minimal effect on the baroreflex regulation of arterial pressure, particularly under closed-loop conditions. We conclude that NO noticeably affects the dynamic baroreflex regulation of sympathetic nerve activity. However, it may not significantly affect arterial pressure regulation through central modulation of the carotid sinus baroreflex.

Occlusive summation of carotid and aortic baroreflexes in control of renal nerve activity

1984 ◽  
Vol 246 (6) ◽  
pp. H851-H857 ◽  
Author(s):  
M. D. Thames ◽  
B. J. Ballon
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Baroreflex Control ◽  
Full Control ◽  
Carotid Baroreflex ◽  
Renal Nerve Activity ◽  
Vascular Beds ◽  
Alpha Chloralose

We recently reported that denervation of aortic or carotid baroreceptors impaired baroreflex control of heart rate but not of hindlimb vascular resistance or lumbar sympathetic nerve activity. Since baroreflex control of sympathetic outflow to different vascular beds is nonuniform, we determined whether carotid or aortic baroreceptor denervation would impair baroreflex control of renal nerve activity. Experiments were performed in 23 alpha-chloralose-anesthetized rabbits. Phenylephrine and nitroglycerin were infused to raise or lower arterial pressure. Pressure elevation inhibited and pressure reduction increased renal nerve activity. The linear regression relationships between changes in arterial pressure and percent change in renal nerve activity were determined with baroreflexes intact and after aortic or carotid denervation. Neither carotid nor aortic denervation alone impaired baroreflex control of renal nerve activity. In nine experiments responses were determined first with vagi sectioned. The results were comparable to those obtained without prior vagotomy. Our data indicate that one group of baroreceptors (aortic or carotid) exerts full control of renal nerve activity and that aortic and carotid baroreflex influences on renal nerve activity add by occlusive or mutual inhibitory summation.

Dynamics of sympathetic baroreflex control of arterial pressure in rats

2003 ◽  
Vol 285 (1) ◽  
pp. R262-R270 ◽  
Author(s):  
Takayuki Sato ◽  
Toru Kawada ◽  
Masashi Inagaki ◽  
Toshiaki Shishido ◽  
Masaru Sugimachi ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve Activity ◽  
Transfer Functions ◽  
Carotid Sinus ◽  
Quantitative Estimation ◽  
Systemic Arterial Pressure ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Low Pass ◽  
Compensatory Effect

By a white noise approach, we characterized the dynamics of the sympathetic baroreflex system in 11 halothane-anesthetized rats. We measured sympathetic nerve activity (SNA) and systemic arterial pressure (SAP), while carotid sinus baroreceptor pressure (BRP) was altered randomly. We estimated the transfer functions from BRP to SNA (mechanoneural arc), from SNA to SAP (neuromechanical arc), and from BRP to SAP (total arc). The gain of the mechanoneural arc gradually increased about threefold as the frequency of BRP change increased from 0.01 to 0.8 Hz. In contrast, the gain of the neuromechanical arc rapidly decreased to 0.4% of the steady-state gain as the frequency increased from 0.01 to 1 Hz. Although the total arc also had low-pass characteristics, the rate of attenuation in its gain was significantly slower than that of the neuromechanical arc, reflecting the compensatory effect of the mechanoneural arc for the sluggish response of the neuromechanical arc. We conclude that the quantitative estimation of the baroreflex dynamics is vital for an integrative understanding of baroreflex function in rats.

Aortic arch reflex control of total systemic vascular capacity

1987 ◽  
Vol 253 (3) ◽  
pp. H598-H603
Author(s):  
A. A. Shoukas ◽  
M. J. Brunner ◽  
A. S. Greene ◽  
C. L. MacAnespie
Keyword(s):  
Arterial Pressure ◽  
Aortic Arch ◽  
Carotid Sinus ◽  
Peripheral Resistance ◽  
Systemic Arterial Pressure ◽  
Reservoir Volume ◽  
Aortic Arch Pressure ◽  
Pressure Changes ◽  
Change In Mean ◽  
Sinus Pressure

The ability of the aortic arch baroreceptors to change vascular capacity was measured and, in the same animal, compared with carotid sinus reflex changes in capacity. Seven dogs were anesthetized with pentobarbital sodium and perfused with constant flow. Changes in external reservoir volume reflected reciprocal changes in total systemic vascular capacity and changes in arterial pressure parallel changes in total peripheral resistance. The aortic arch and carotid sinus baroreceptor areas were isolated, and the pressures were controlled separately. With carotid sinus pressure held constant at 125 mmHg, aortic arch pressure was increased and decreased between 225 and 50 mmHg, and the changes in reservoir volume and systemic arterial pressure were measured. Results from increasing and decreasing aortic arch or carotid sinus pressure were not significantly different and were averaged. The mean change in reservoir volume was 1.9 +/- 0.2 ml/kg and the change in mean arterial pressure was 18.7 +/- 3.7 mmHg. The changes in reservoir volume and arterial pressure caused by the aortic arch reflex were not influenced by the level of carotid sinus pressure. Carotid sinus pressure changes between 200 and 50 mmHg at a constant aortic arch pressure caused reservoir volume and arterial pressure to change by 7.2 +/- 0.9 ml/kg and 45.1 +/- 4.1 mmHg, respectively. The level of aortic arch pressure did not modify these responses.

Sign in / Sign up

Export Citation Format

Share Document