Does prostacyclin sensitize arterial baroreceptors?
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Arteries↗
Biomedical subjects
M W Chapleau
Publications and source records attributed to M W Chapleau.
Suppression of baroreceptor discharge by endothelin at high carotid 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.
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Are arterial pressure and deformation the sole determinants of baroreceptor activity? Importance of humoral and endothelial modulation in normal and disease states.
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Aldosterone↗
Aggregating human platelets in carotid sinus of rabbits decrease sensitivity of baroreceptors.
Aggregating platelets release factors that act in a local paracrine manner to alter vascular tone. The purpose of the present study was to explore the possibility that factors released from aggregating platelets may alter the sensitivity of arterial baroreceptors. Baroreceptor activity was recorded from the vascularly isolated carotid sinus of rabbits anesthetized with sodium pentobarbital. The carotid sinus was filled with oxygenated Krebs-Henseleit buffer and distended with slow ramp increases in nonpulsatile pressure. Sensitivity of baroreceptors to increased pressure was determined before and during intraluminal exposure of the sinus to washed human platelets suspended in Krebs' buffer. Platelets activated with thrombin (0.4 units/ml) decreased baroreceptor activity and the slope of the pressure-activity curve significantly (n = 6). The platelet-induced decrease in baroreceptor sensitivity was related to the duration of exposure to platelets with no change in baroreceptor activity after 4 minutes and a progressive decrease in activity over the next 12 minutes. The slope of the pressure-nerve activity relation averaged 1.26 +/- 0.08 %/mm Hg during control and decreased to 0.97 +/- 0.22, 0.80 +/- 0.19, and 0.53 +/- 0.15 %/mm Hg after 12-16 minutes of exposure to 10(7), 10(8), and 3-6 x 10(8) activated platelets/ml, respectively (p less than 0.05). Baroreceptor sensitivity was restored after removal of platelets from the carotid sinus. Thrombin alone had no effect on baroreceptor sensitivity. Activated platelets did not alter the carotid pressure-diameter relation, suggesting a direct inhibitory effect on baroreceptors. The slope of the pressure-activity curve and maximum baroreceptor activity were not decreased by the stable thromboxane analogue U46619, serotonin, or ADP.(ABSTRACT TRUNCATED AT 250 WORDS)
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Increase in sympathetic activity with age. I. Role of impairment of arterial baroreflexes.
The purpose of this study was to evaluate changes in arterial baroreflex function with aging. Mean arterial pressure (MAP) obtained in the awake state was 110 +/- 7 mmHg in the young animals (1 yr; n = 5) and 128 +/- 6 mmHg in the old beagles (11 yr; n = 11) (P less than 0.05). In response to bolus administration of varying doses of phenylephrine and nitroglycerin in the conscious state, the slope relating heart rate (HR) to MAP was attenuated significantly in the old animals compared with the young (-0.87 +/- 0.30 vs. -2.35 +/- 0.44 beats.min-1.mmHg-1; P less than 0.05). After atropine, the baroreflex control of HR was abolished in both groups. After anesthesia and sectioning of the aortic depressor nerves, and with isolated carotid sinus pressures (CSP) held at 50 mmHg, absolute renal sympathetic nerve activity (RSNA) was significantly greater in the old (368 +/- 40 Hz) vs. the young animals (41 +/- 9 Hz). In the old, the gains of baroreflex inhibition of MAP (0.78 +/- 0.09) and normalized RSNA (0.38 +/- 0.14%/mmHg) during increases in CSP were decreased significantly compared with the young (MAP, 1.16 +/- 0.17 mmHg, and RSNA, 0.72 +/- 0.06%/mmHg). In a subgroup of old normotensive animals (n = 5), the baroreflex gain of RSNA was still attenuated (0.43 +/- 0.11%/mmHg) compared with the young. The reflex reduction in absolute RSNA as a function of baseline RSNA was also impaired in old vs. young beagles.(ABSTRACT TRUNCATED AT 250 WORDS)
Aging↗
Increase in sympathetic activity with age. II. Role of impairment of cardiopulmonary baroreflexes.
We have previously shown that arterial baroreflex function is significantly impaired in a group of old beagles [G. Hajduczok, M. W. Chapleau, S. L. Johnson, and F. M. Abboud. Am. J. Physiol. 260 (Heart Circ. Physiol. 29): H1113-H1120, 1991]. In the present study, we determined whether the neural limb of the cardiopulmonary baroreflex control of renal sympathetic nerve activity (RSNA) and the interaction between the arterial and cardiopulmonary reflexes is also impaired with senescence. In the anesthetized state, the aortic nerves were sectioned and carotid sinuses were isolated bilaterally with carotid sinus pressures held at 50 mmHg in both young (1 yr) and old animals (11 yr). In response to graded volume expansion (VE) with 3% dextran (0 to 30 ml/kg iv), the gain of cardiopulmonary baroreflex control of RSNA was significantly lower in the old (5.1 +/- 3%/mmHg) compared with the young (13.4 +/- 3%/mmHg) animals. There were no significant differences in systemic vascular compliance or left ventricular mass index between the two groups. The gain of the carotid sinus baroreflex inhibition of RSNA was significantly attenuated by VE in the young group but was not affected in the old group. Bilateral vagotomy (VX) resulted in a 182 +/- 74% increase in RSNA in the young (P less than 0.05), but VX did not significantly increase RSNA in the old (12 +/- 17%). After VX, the carotid sinus baroreflex gain markedly increased by nearly eightfold in the young group (P less than 0.05) but was not altered in the old dogs.(ABSTRACT TRUNCATED AT 250 WORDS)
Aging↗
Rapid baroreceptor resetting in chronic hypertension. Implications for normalization of arterial pressure.
The purpose of this study was to examine the ability of baroreceptors of renal hypertensive rabbits to reset rapidly during acute changes in arterial pressure. The carotid sinus (CS) was vascularly isolated and baroreceptor activity was recorded during slow ramp increases in CS pressure in hypertensive (one-kidney, one wrap; 127 +/- 3 mm Hg) and normotensive (one-kidney, no wrap; 85 +/- 3 mm Hg) rabbits anesthetized with chloralose. Control measurements were made after holding pressure for 10-15 minutes at the level of arterial pressure recorded before each experiment. Baroreceptor threshold pressure (Pth) was higher in hypertensives (78 +/- 4 mm Hg) compared with normotensives (55 +/- 3 mm Hg, p less than 0.05), and nerve activity was less in hypertensives over a wide range of pressure. CS distensibility (sonomicrometers) was not significantly different in the two groups. After increasing holding pressure from control by 30 and 60 mm Hg for 10-15 minutes, the extent of baroreceptor resetting (delta Pth/delta holding pressure x 100%) in normotensives was 39 +/- 6% and 33 +/- 2%, respectively, but only 14 +/- 5% and 9 +/- 3% in hypertensives (p less than 0.05). After decreasing holding pressure by 30 and 60 mm Hg, resetting was similar in normotensives (32 +/- 6% and 28 +/- 3%) and hypertensives (34 +/- 3% and 30 +/- 4%). In hypertensive rabbits, acute (10-15 minutes) exposure of baroreceptors to normotension (71 +/- 4 mm Hg) decreased Pth to 62 +/- 4 mm Hg and increased nerve activity to levels not significantly different from those of normotensive animals without altering CS distensibility.(ABSTRACT TRUNCATED AT 250 WORDS)
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Types of baroreceptor afferent neurons.
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Animals↗
Paracrine role of prostanoids in activation of arterial baroreceptors: an overview.
Baroreceptors located in carotid sinuses and aortic arch are activated with increases in arterial pressure. The increased afferent nerve activity triggers reflex adjustments that buffer the rise in pressure. Mechanical deformation of baroreceptor nerve endings is considered the primary mechanism of receptor activation. Recent studies in our laboratory have demonstrated that prostanoids, most likely released from endothelial cells during stretch, contribute--as paracrine factors--to the activation of baroreceptors. Exposure of the isolated carotid sinus in anesthetized rabbits to prostacyclin (PGI2) or arachidonic acid increases baroreceptor sensitivity whereas inhibition of endogenous formation of prostanoids with indomethacin or aspirin decreases sensitivity. Baroreceptor sensitivity is also decreased after endothelial denudation and restored after adding PGI2 back to the denuded sinus suggesting that endothelium is the source of prostanoids that sensitize baroreceptors. Pathologic states such as chronic hypertension and atherosclerosis are associated with both endothelial cell dysfunction and decreased baroreceptor sensitivity. The endothelial cell dysfunction and impairment of prostanoid formation contribute to the decreased baroreceptor sensitivity in these diseases.
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Prostaglandins contribute to activation of baroreceptors in rabbits. Possible paracrine influence of endothelium.
The purpose of this study was to test the hypothesis that prostaglandins released from vascular endothelial cells contribute to activation of baroreceptors during increases in arterial pressure. Baroreceptor activity was recorded from the vascularly isolated carotid sinus in rabbits anesthetized with chloralose. Baroreceptor activity was measured during ramp or step increases in nonpulsatile carotid sinus pressure over a range of 0-175 mm Hg. Exposure of the isolated carotid sinus to inhibitors of prostaglandin formation (indomethacin [n = 10] or aspirin [n = 6]) decreased baroreceptor activity significantly (p less than 0.05). The slope of the pressure-activity relation averaged 0.80 +/- 0.07 %/mm Hg (mean +/- SEM) during control measurements and 0.72 +/- 0.06 and 0.63 +/- 0.05 %/mm Hg during exposure to 10 and 20 microM indomethacin, respectively. Exposure of the carotid sinus to exogenous prostacyclin (PGI2 [n = 11]) increased baroreceptor activity significantly. The slope of the pressure-activity relation averaged 0.89 +/- 0.10, 1.09 +/- 0.09, and 1.26 +/- 0.16 %/mm Hg during control and during exposure to 10 and 20 microM PGI2, respectively. Activity returned to control after removal of PGI2 (0.89 +/- 0.12 %/mm Hg). Removal of endothelium with either a balloon catheter (n = 4) or a jet of a 95% O2-5% CO2 gas mixture (n = 6) decreased the slope of the pressure-activity relation from 0.92 +/- 0.09 to 0.56 +/- 0.08 %/mm Hg (p less than 0.05). Exposure of the denuded sinus to exogenous PGI2 (20 microM [n = 4]) restored activity (slope = 1.09 +/- 0.24 %/mm Hg). Neither indomethacin (n = 5) nor PGI2 (n = 5) nor denudation (n = 5) significantly altered the pressure-diameter relation of the carotid sinus (sonomicrometers), suggesting that the effects on baroreceptor discharge are not caused by altered stretch of the carotid sinus at a given pressure. The results suggest that prostaglandins (e.g., PGI2) released from endothelium contribute in a paracrine manner to activation of baroreceptors during increases in arterial pressure.
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Mechanism of decreased baroreceptor activity in chronic hypertensive rabbits. Role of endogenous prostanoids.
We examined the contribution of endogenous prostanoids to baroreceptor activation in chronic renal hypertension. Baroreceptor activity was recorded from the vascularly isolated carotid sinus during slow ramp increases in pressure in rabbits anesthetized with pentothal and chloralose. Mean arterial pressure averaged 133 +/- 4 mmHg in hypertensive rabbits (one kidney, one wrap, n = 12) and 85 +/- 3 mmHg in normotensive rabbits (one kidney, no wrap, n = 13). Baroreceptor activity was decreased significantly (P less than 0.05) in the hypertensive compared with the normotensive rabbits. The decreased baroreceptor activity could not be explained by decreased distensibility of the carotid sinus (sonomicrometers). Inhibition of the endogenous formation of prostanoids with intrasinus administration of indomethacin (50 microM) decreased baroreceptor activity in normotensive (P less than 0.05) but not in hypertensive rabbits over a wide range of pressures. At a pressure of 120 mmHg, activity declined from 61 +/- 14 spikes/s before indomethacin to 47 +/- 12 spikes/s with indomethacin, i.e., a drop of 24 +/- 4%. In contrast, corresponding values in hypertensive rabbits averaged 41 +/- 13 and 40 +/- 12 spikes/s (-1 +/- 2%). Intrasinus prostacyclin, on the other hand, increased activity in both groups: at 120 mmHg activity increased from 62 +/- 9 to 92 +/- 15 spikes/s (51 +/- 17%) in normotensive rabbits and from 29+/- 7 to 47 +/- 14 spikes/s (68 +/- 23%) in hypertensive rabbits. Neither indomethacin nor prostacyclin (n = 5) influenced the pressure-diameter relation of the carotid sinus. The increase in prostacyclin (6-keto-PGF 1 alpha) formation by the sinus in response to its exposure to arachidonic acid (10 microM) was significant (P less than 0.05) in the normotensives (1,627 +/- 344%; n = 5) but not in the hypertensives (583 +/- 353%; n = 5). We conclude that the decreased baroreceptor activity in chronic hypertension may not be caused by decreased distensibility of the vascular wall of the sinus and that endogenous prostanoids that contribute to baroreceptor activation in normotensive rabbits fail to do so in hypertensive rabbits. This appears to be due to decreased formation of prostacyclin rather than decreased sensitivity of the baroreceptors to prostacyclin. The results suggest a new mechanism that contributes to chronic baroreceptor resetting in hypertension.
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Peripheral and central mechanisms of baroreflex resetting.
1. A change in the arterial pressure-sympathetic activity or heart rate relation (baroreflex resetting) can result from resetting of baroreceptors ('peripheral' resetting) or from an altered coupling within the central nervous system of afferent baroreceptor to efferent nerve activities ('central' resetting). 2. 'Peripheral' resetting involves a shift in the pressure-baroreceptor activity curve in the direction of the prevailing level of arterial pressure, e.g. after elevations in pressure, the baroreceptor pressure threshold (Pth) is increased and activity reduced at equivalent pressures and vascular strains. 3. 'Peripheral' resetting occurs during the diastolic phase of a cardiac cycle (instantaneous resetting), after brief exposure to elevated pressure (acute resetting), and during chronic hypertension or when chronic structural changes in the vasculature have occurred (chronic resetting). 4. Mechanisms include: (i) changes in the mechanical properties of the vessel wall that may alter the tension on the receptors; (ii) ionic mechanisms operating at the neuronal membrane such as activation of Na+,K+-ATPase; and (iii) release of endothelial factors that may modulate baroreceptor sensitivity. 5. Acute resetting of baroreceptors can be prevented or attenuated when the sustained elevations in pressure are pulsatile rather than static. Increases in flow increase carotid sinus nerve activity at constant pressure and strain and decrease the Pth of baroreceptors. 6. 'Central' resetting can involve neural-humoral interactions or an altered responsiveness of central neurons mediating the baroreflex to changes in afferent baroreceptor activity. 7. During static pressure, the continuous baroreceptor discharge causes significant 'central' resetting, i.e. sympathetic activity escapes from baroreflex inhibition. In contrast, during pulsatile pressure, the pulse phasic baroreceptor discharge minimizes 'central' resetting causing sustained sympathetic inhibition.
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Pulsatile activation of baroreceptors causes central facilitation of baroreflex.
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)
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Prostaglandins in carotid sinus enhance baroreflex in rabbits.
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.
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Determinants of sensitization of carotid baroreceptors by pulsatile pressure in dogs.
The threshold pressure of single baroreceptor units is decreased after compared with before exposure to pulsatile pressure according to previous studies in our laboratory. The purpose of the present study is to characterize the determinants of sensitization of arterial baroreceptors by pulsatile pressure. Carotid sinus nerve activity was recorded in dogs anesthetized with chloralose. Two indexes of baroreceptor "sensitivity" were obtained by comparing nerve activity before and immediately after exposure of the isolated carotid sinus to pulsatile pressure for periods up to 10 minutes. Sensitization occurred 1) when the threshold pressure of single baroreceptor units determined with a slow nonpulsatile ramp decreased after as compared with before pulsing and 2) when multiple unit activity increased after as compared with before pulsing at various mean levels of static pressure. Sensitization was evident after pulsing at mean pressure of 50 and 100 mm Hg, but not at 150 and 200 mm Hg, and was caused by the pulsatile change in diameter or deformation and not by the pulsatile change in wall tension. The magnitude of the effect was directly related to the duration of the pulsing period and to the frequency and amplitude of the pressure pulses. The sensitization could not be explained by increased diameter (sonomicrometers) or strain of the carotid sinus at the same pressure after pulsing; thus, there was an increase in "strain sensitivity" that outlasted the period of pulsing by up to several minutes. In most experiments the shift from static to pulsatile pressure at 50 and 100 mm Hg caused an increase in nerve activity, yet sensitization occurred after pulsing when one would have expected postexcitatory hyperpolarization or depression of activity upon return to static pressure. The sensitization was not caused by the release of prostacyclin from the endothelium since it was not reduced after endothelial denudation or inhibition of cyclooxygenase with indomethacin (30-80 microM) or ibuprofen (250 microM). We speculate that sensitization of baroreceptors by pulsatile pressure may contribute to the decreased sympathetic activity after periods of elevated pulse pressure (e.g., after exercise). We also propose that the decreased sensitivity of baroreceptors after acute elevation of arterial pressure (acute resetting) may be offset in part by the sensitizing effect of increased pulsatile stretch.
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Chemoreceptor stimulation interferes with regional hypoxic pulmonary vasoconstriction.
Hypoxemia interferes with the diversion of blood flow away from hypoxic regions of the lung, possibly through activation of the arterial chemoreceptor reflex. The purpose of this study was to determine if selective stimulation of carotid chemoreceptors reduces the diversion of flow (hypoxic vasoconstriction) when normal systemic oxygen levels are present. Chloralose anesthetized dogs were paralyzed and each lung was separately ventilated via a dual-lumen endobronchial tube. Left pulmonary artery (QL) and main pulmonary artery (QT) blood flows were measured with electromagnetic flow probes. Chemoreceptors were stimulated by perfusion of the carotid sinuses with hypoxic, hypercapnic blood. QL/QT averaged 46 +/- 4, 29 +/- 2, and 36 +/- 4% during bilateral O2 ventilation (control), left lung N2 ventilation, and left lung N2 plus chemoreceptor stimulation in dogs treated with the cyclo-oxygenase inhibitor meclofenamate. After vagotomy, QL/QT averaged 45 +/- 4, 27 +/- 3, and 28 +/- 2% during the same conditions. QL/QT decreased significantly from control (P less than 0.05) during left lung N2 alone but did not decrease during left lung N2 plus chemoreceptor stimulation in dogs with intact vagi. In contrast, QL/QT decreased significantly both before and during chemoreceptor stimulation in vagotomized dogs. The same responses were observed in dogs not treated with meclofenamate. These results indicate that selective stimulation of arterial chemoreceptors can interfere with regional hypoxic vasoconstriction and suggest that the vagus nerves may mediate this effect.
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Rheoreceptors in the carotid sinus of dog.
The arterial baroreceptors are known to be sensitive to changes in pressure but there are no known sensors in the cardiovascular system for changes in flow. We tested the hypothesis that changes in flow at constant pressure alter carotid sinus multi-unit nerve activity. In anesthetized dogs with vascularly isolated carotid sinuses, increases in flow at constant pressure resulted in increases in carotid sinus nerve activity in relation to the increase in flow. The increased activity during flow was not caused by an increase in strain of the sinus wall but was directly related to the increase in shear stress (36.6 +/- 11.7% increase in activity per dyne/cm2; 1 dyne = 0.1 MN). The pressure threshold of single baroreceptor units was determined during a slow pressure ramp with and without flow. Flow caused a significant decrease in pressure threshold from 81.1 +/- 6.1 mmHg (1 mmHg = 1.333 x 10(2) Pa) in the absence of flow to 69.3 +/- 5.7 mmHg with flow. We conclude that there are arterial "rheoreceptors" in the carotid sinus that respond to flow at constant pressure and strain. The results with single baroreceptor units indicate also that baroreceptors may be sensitized by increases in flow. Thus, changes in flow per se in addition to changes in arterial pressure may be important determinants of reflex circulatory adjustments.
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Mechanisms of resetting of arterial baroreceptors: an overview.
Arterial baroreceptors are reset when their afferent nerve activity is reduced at an equivalent arterial pressure and vascular strain. Resetting occurs as a result of stretch of the baroreceptors, usually during an acute or chronic rise in arterial pressure. It may be seen during the diastolic phase of a cardiac cycle (instantaneous resetting), after brief exposure to a sustained elevation of pressure (acute resetting), and after chronic elevation of pressure or in physiologic or pathologic states associated with structural changes in the vascular regions of baroreceptors (chronic resetting). The mechanisms reviewed here include mechanical, ionic and chemical factors. Viscoelastic properties of the carotid sinus and aortic arch may explain the instantaneous resetting that occurs with each cardiac cycle when activity begins in early systole and stops in early diastole. Viscoelastic properties and ionic mechanisms may play a role in acute resetting. Inhibition of Na+K+ ATPase reduces the magnitude of acute resetting. The release of chemicals from the endothelium may modulate baroreceptor activity. Exogenous prostacyclin suppresses and indomethacin augments acute resetting in the rabbit, suggesting that the release of endogenous prostacyclin during a rise in arterial pressure attenuates resetting. Changes in pulsatility and blood flow also may modulate baroreceptor activity. The addition of pulsatile pressure at an increased mean pressure attenuates resetting.(ABSTRACT TRUNCATED AT 250 WORDS)
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