Influence of substance P on carotid sinus nerve baro- and chemoreceptor activity in rabbits.

Substance P (SP) is abundant in the carotid sinus nerve (CSN) and has been implicated in baro- and chemoreceptor reflexes. We examined the effect of SP on blood pressure, heart rate, phrenic nerve activity, hindlimb perfusion pressure, and cardiac contractile strength in urethane-anesthetized rabbits with bilaterally cut cervical sympathetic, vagus, and aortic depressor nerves. Retrograde simultaneous injection of SP (0.5-2.7 micrograms/kg in 0.2-0.3 ml saline) into both carotid sinus areas via the internal carotid arteries decreased blood pressure (by 56%), heart rate (by 13%), cardiac contractility (by 25%) and phrenic nerve activity (by 77%). The effect on hindlimb perfusion pressure was variable. There was both a reflex effect and direct hindlimb vasodilation. In another group of rabbits, the carotid sinus areas were vascularly isolated and perfused with SP (0.19 micrograms/min dissolved in Locke's solution) or Locke's solution alone for 5 min. While carotid sinus perfusion pressure was maintained in the range of 80-120 mmHg, mean arterial blood pressure, heart rate, and unit activity from the CSN were recorded. SP increased the activity of 11 of 18 baroreceptor fibers and inhibited all of 20 chemoreceptor fibers. SP decreased mean arterial blood pressure and heart rate, but the changes were less than those obtained with injection of SP into nonisolated carotid sinus arteries because systemic effects of SP, which in some cases counteracted the reflex effects, were eliminated.     

Respiratory effects of brief baroreceptor stimuli in the anesthetized dog

To quantify the immediate isocapnic respiratory response to baroreceptor stimulation, pressure in the isolated externally perfused carotid sinuses (CS) of 24 vagotomized alpha-chloralose-anesthetized dogs was increased selectively during either inspiration or expiration as a step (from time of onset to end of respiratory phase) or a pulse (500 ms). The rise time (150 ms), base-line pressure (80 mmHg), and stimulus magnitude (40 mmHg) were similar for the two stimuli. The time of stimulus onset (delay), expressed as a percent of control time of inspiration (TI) or expiration (TE), was varied. TI, TE, and tidal volume (VT) were expressed as percent changes from control. Stimuli delivered early in inspiration lengthened TI [23.5 +/- 6.4% (SE) for step and 11.7 +/- 6.3% for pulse stimuli at 5% delay] more effectively than late stimuli. VT was essentially unaltered. In contrast, step stimuli delivered during expiration caused a lengthening of TE (32.7 +/- 6.3% at 5% delay) that did not depend on the delay (up to 75%). Very late (85%) pulse stimuli lengthened TE (15.2 +/- 5.7%) more effectively than early stimuli. For both stimuli, the expiratory VT was unaltered. When the responses are compared before and after separation of the blood supply of the carotid bodies from the CS region and when they are compared before and after inhibition of reflex systemic hypotension by ganglionic blockade, the observed responses were shown to be due solely to CS baroreceptor stimulation and not to alterations in carotid body blood flow or reflex changes in systemic cardiovascular variables.     

颈动脉窦内压的变化速率对反射性降压效应的影响

在成年狗身上制备右侧孤离颈动脉窦,借助灌流装置用饱和氧的任氏液对其进行灌流。灌流压为搏动性的。通过改变每搏泵出量、灌流管道的阻力和弹性来调节灌流压及其变化速率。用多导生理记录仪同步记录股动脉血压、窦内灌流压及其变化速率。本文主要观察窦内压的变化速率对降压反射的影响。在8只狗身上共进行了93次实验。结果表明,在窦内压相同的情况下,灌流压的上升速率愈快,降压效应愈明显,而其下降速率则无显著作用。已有资料证明搏动性窦内压所引起的降压效应较非搏动性压力更为明显。由此可见,狗的颈动脉窦压力感受器不仅对搏动性压力而且对其上升的变化速率也很敏感。     

Maintaining hypertension in negative emotional exposures as one of the functions of the baroreceptor reflex

Changes in the heart rate and blood pressure induced by different emotiogenic influences were studied in rats with intact and denervated baroreceptor afferents of the carotid sinuses and aortic arch. Aversive emotiogenic stimuli failed to induce hypertension in rats with denervated baroreceptor areas, while self-stimulation in these rats caused a profound rise in arterial pressure. It is concluded that maintenance of hypertension induced by aversive emotiogenic influences is a manifestation of baroreceptor reflex.     

Both central command and exercise pressor reflex reset carotid sinus baroreflex

In decerebrate unanesthetized cats, we determined whether either "central command," the exercise pressor reflex, or the muscle mechanoreceptor reflex reset the carotid baroreflex. Both carotid sinuses were vascularly isolated, and the carotid baroreceptors were stimulated with pulsatile pressure. Carotid baroreflex function curves were determined for aortic pressure, heart rate, and renal vascular conductance. Central command was evoked by electrical stimulation of the mesencephalic locomotor region (MLR) in cats that were paralyzed. The exercise pressor reflex was evoked by statically contracting the triceps surae muscles in cats that were not paralyzed. Likewise, the muscle mechanoreceptor reflex was evoked by stretching the calcaneal tendon in cats that were not paralyzed. We found that each of the three maneuvers shifted upward the linear relationship between carotid sinus pressure and aortic pressure and heart rate. Each of the maneuvers, however, had no effect on the slope of these baroreflex function curves. Our findings show that central command arising from the MLR as well as the exercise pressor reflex are capable of resetting the carotid baroreflex.     

Nonalgebraic interaction between pressor and depressor reflexes in dogs: evidence for a central site of action

In a previous study (Kendrick, JE and Matson, G 1979, Amer J Physiol 327:H662-H667) we demonstrated that the vascular responses in dogs to electrical stimulation of aortic nerve (AN) pressor and carotid sinus nerve (CSN) depressor afferents did not sum algebraically. We suggest this results from a reflex interaction which occurs in the central nervous system. The present study extends earlier studies by recording sympathetic vasomotor in chloralose-anesthetized dogs. Stimulation of the CSN reduced sympathetic activity by 51 +/- 20 (SD)%. AN stimulation (2 Hz) caused a 17 +/- 12% increase in sympathetic activity. Combined stimulation of the ipsilateral CSN and AN caused 0 +/- 28% change rather than a 34% decrease expected by an additive interaction. The interaction recorded in this study from the sympathetic outflow is therefore consistent with the previously reported vascular responses (cited above) and implicates central nervous site(s) of action. A conditioning stimulus train to CSN inhibited sympathetic discharges to AN test stimuli. This inhibition was prevented by pairing an AN stimulus with the CSN stimulus train. The AN pressor reflexes act in part by increasing sympathetic activity and in part by suppressing the baroreflexes.     

充胀犬胸部降主动脉所致的升压效应

在17只麻醉开胸犬,观察局部充胀胸部降主动脉(TDA)对心血管活动的影响。主要结果如下:1.充胀 TDA 引起心率、心肌收缩力、肾及股薄肌灌注压和全身动脉血压增加;TDA 局部去神经后反应消失,表明上述心血管效应系 TDA 受牵张刺激引起的正反馈性神经反射现象。2.切断动物两侧颈迷走神经和窦神经后,充胀 TDA 引起的心血管效应增大。3.用心得安(1mg/kg)消除心脏的β-效应后,充胀 TDA 引起的升压反应有所减小;用酚妥拉明(3mg/kg)阻断血管的α-受体效应后,多数动物即不再出现血压增高,从而提示充胀TDA 时的血压升高主要是反射性外周阻力增加所致。在缓冲神经完整的条件下,上述 TDA加压效应是存在的,但主动脉弓和颈动脉窦缓冲反射对其有对抗作用。     

Relations between changes of the pulmonary and systemic hemodynamics following neurogenic stimuli

The character and values of changes of the pulmonary and systemic hemodynamics following neurogenic stimuli application on the cardiovascular system were studied in acute experiments on the anesthetized cats. Vagus nerve stimulation reduced the heart rate and decreased myocardial contractility in result, right and left atrial pressure increased, whereas pulmonary pressure and flow, venous return, cardiac output and venous return decreased. Pulmonary pressure reached maximal level and returned to the initial value earlier than the pulmonary flow. On the contrary, pulmonary pressure, following neurogenic pressor stimuli, reached maximal level and returned to the initial value later than the pulmonary flow; the sign of the changes of the pulmonary pressure could be positive or negative, whereas pulmonary flow were always increased. The venous return did not change, and for this reason it could not cause the increasing of pulmonary flow which was elevated following increasing of the heart rate and myocardial contractility. The shifts of the pulmonary pressure were correlated with the pulmonary resistance those, which were increased after the stellate ganglion stimulation and decreased following carotid reflex; they did not change in case of sciatic nerve stimulation. The shifts of the pulmonary pressure did not depended on the decreased right and left atrial pressures. When the pulmonary flow was always increased, the cardiac output following electrical stimulation of the stellate ganglion and sciatic nerve was elevated, and it was decreased following carotid reflex, i. e. linear correlation between these parameters were not found. Pulmonary and systemic arterial pressure changes were more obvious in case of direct neurogenic stimuli application comparing with reflectory ones; in both cases, the positive chrono- and inotropic cardiac effects were similar.     

链霉素对颈动脉窦压力感受器反射的抑制作用

在 2 3只隔离灌流颈动脉窦区的麻醉大鼠 ,观察了链霉素对颈动脉窦压力感受器反射的影响。结果如下 :(1)以链霉素 (10 0 μmol/L)隔离灌流大鼠左侧颈动脉窦区时 ,压力感受器反射机能曲线向左下方移位 ,曲线最大斜率 (PS)由 0 40± 0 0 1kPa降至 0 33± 0 0 1kPa (P <0 0 0 1) ,血压反射性下降 (reflexdecrease ,RD)幅度由 6 2 2±0 13kPa降至 5 0 2± 0 11kPa (P <0 0 0 1) ,阈压 (TP)、平衡压 (EP)和饱和压 (SP)则分别从 8 2 7± 0 2 5 ,12 71± 0 2 1和 2 4 41± 0 14kPa增至 10 33± 0 32 (P <0 0 1) ,13 33± 0 30 (P <0 0 1)和 2 6 11± 0 2 8kPa (P <0 0 1)。其中RD ,PS和TP的变化呈明显的剂量依赖性。 (2 )应用腺苷隔离灌流大鼠颈动脉窦区 ,引起颈动脉窦压力感受器反射的易化 ;在用链霉素预处理后 ,此易化效应不仅完全被阻断 ,且可使反射效应小于应用腺苷前的对照值。以上结果表明 ,链霉素对大鼠颈动脉窦压力感受器反射有明显的抑制作用。     

Differential effect of central command on aortic and carotid sinus baroreceptor-heart rate reflexes at the onset of spontaneous, fictive motor activity

Our laboratory has reported that central command blunts the sensitivity of the aortic baroreceptor-heart rate (HR) reflex at the onset of voluntary static exercise in conscious cats and spontaneous contraction in decerebrate cats. The purpose of this study was to examine whether central command attenuates the sensitivity of the carotid sinus baroreceptor-HR reflex at the onset of spontaneous, fictive motor activity in paralyzed, decerebrate cats. We confirmed that aortic nerve (AN)-stimulation-induced bradycardia was markedly blunted to 26 ± 4.4% of the control (21 ± 1.3 beats/min) at the onset of spontaneous motor activity. Although the baroreflex bradycardia by electrical stimulation of the carotid sinus nerve (CSN) was suppressed (P < 0.05) to 86 ± 5.6% of the control (38 ± 1.2 beats/min), the inhibitory effect of spontaneous motor activity was much weaker (P < 0.05) with CSN stimulation than with AN stimulation. The baroreflex bradycardia elicited by brief occlusion of the abdominal aorta was blunted to 36% of the control (36 ± 1.6 beats/min) during spontaneous motor activity, suggesting that central command is able to inhibit the cardiomotor sensitivity of arterial baroreflexes as the net effect. Mechanical stretch of the triceps surae muscle never affected the baroreflex bradycardia elicited by AN or CSN stimulation and by aortic occlusion, suggesting that muscle mechanoreflex did not modify the cardiomotor sensitivity of aortic and carotid sinus baroreflex. Since the inhibitory effect of central command on the carotid baroreflex pathway, associated with spontaneous motor activity, was much weaker compared with the aortic baroreflex pathway, it is concluded that central command does not force a generalized modulation on the whole pathways of arterial baroreflexes but provides selective inhibition for the cardiomotor component of the aortic baroreflex.     

Respiratory responses to aortic and carotid chemoreceptor activation in the dog

Respiratory responses arising from both chemical stimulation of vascularly isolated aortic body (AB) and carotid body (CB) chemoreceptors and electrical stimulation of aortic nerve (AN) and carotid sinus nerve (CSN) afferents were compared in the anesthetized dog. Respiratory reflexes were measured as changes in inspiratory duration (TI), expiratory duration (TE), and peak averaged phrenic nerve activity (PPNG). Tonic AN and AB stimulations shortened TI and TE with no change in PPNG, while tonic CSN and CB stimulations shortened TE, increased PPNG, and transiently lengthened TI. Phasic AB and AN stimulations throughout inspiration shortened TI with no changes in PPNG or the following TE; however, similar phasic stimulations of the CB and CSN increased both TI and PPNG and decreased the following TE. Phasic AN stimulation during expiration decreased TE and the following TI with no change in PPNG. Similar stimulations of the CB and CSN decreased TE; however, the following TI and PPNG were increased. These findings differ from those found in the cat and suggest that aortic chemoreceptors affect mainly phase timing, while carotid chemoreceptors affect both timing and respiratory drive.     

Dysfunction of supramedullary alpha-adrenergic mechanisms following sino-aortic denervation in Kyoto Wistar rats

Central α-adrenergic mechanisms of blood pressure regulation were investigated by injecting norepinephrine or bradykinin into the carotid input of the cross-circulated head preparations of normotensive Wistar Kyoto rats (WKY). Rats were divided into three groups: sham-operated (sham), carotid sinuses denervated (SD) and carotid sinuses and aortic nerves debuffered (SAD). Norepinephrine, 5 μg, produced vasodepression in all rats, accompanied by corresponding decreases in sympathetic nerve activity recorded in some rats. Magnitude of vasodepression was largest in SAD rats. In sham rats, bradykinin, 1 μg, produced a biphasic response:initial vasodepression followed by a sustained pressor phase. This was accompanied by corresponding changes in peripheral sympathetic nerve activity recorded in some rats. In both SAD and SD rats bradykinin-induced vasodepression was abolished, while the magnitude of the pressor phase became more prominent. The increase in the pressor phase was greater in SAD than in SD rats. In similar studies of spontaneously hypertensive rats (SHR), responses to both α-adrenergic agonist and bradykinin are augmented, suggesting a dysfunction of hypothalamic α-adrenergic mechanisms. Since in the present study it has been shown that sino-aortic denervation produces effects similar to those seen in SHR, dysfunction of buffer nerves may account for the deficient central α-adrenergic mechanisms in SHR.     

Modulation of reflexsympathetic discharge by the cholinergic agonist oxotremorine and by clonidine

The cholinergic agonist oxotremorene can produce marked centrally-mediated cardiovascular effects. In past experiments in anesthetized cats, oxotremorine reduced blood pressure and an evoked sympathetic reflex. However, unlike other sympathetic inhibitors, it decreased sympathetic outflow selectively, did not slow heart rate but prolonged the latency of an evoked sympathetic reflex. In view of these striking differences, effects of oxotremorine on another reflex involved in cardiovascular control were assessed in anesthetized cats and compared to those produced by clonidine. Stimulation of the carotid sinus nerve with short duration pulses evoked reflex firing in the splanchnic nerve. Oxotremorine (50 – 800 ug/kg i.v.) caused a dose-related decrease in blood pressure and inhibited the evoked potential at the higher doses (200–800 ug/kg) but did not prolong its latency. Clonidine produced similar effects. Thus, attenuation by oxotremorine of an additional fundamental cardiovascular reflex was demonstrated. Seletcive inhibition of sympathetic outflow by oxotremorine as well as its differential effect on the latencies of cardiovascular reflexes indicates that the compound influences medullary and descending sympathetic pathways in a complex manner and suggests that the inhibition occurs at more than one site.     

Baroreceptor control of pressure-flow relationships during hypoxemia

In the absence of peripheral chemoreceptors, the effects of graded hypoxemia on the carotid sinus control of central and regional hemodynamics were studied in anesthetized mongrel dogs. Baroreceptor stimulation was effected by carotid sinus isolation and perfusion under controlled pressure. Blood flows were measured in the aorta and the celiac, mesenteric, left renal, and right iliac arteries. Carotid sinus reflex set-point pressures were well maintained until hypoxemia was severe. Carotid sinus reflex set-point gain was maximal during mild hypoxemia. Reflex operating point regional flows were unaffected by hypoxemia. A factorial analysis of overall reflex increases in mean aortic pressure, flow, and power during reduced baroreceptor stimulation showed potentiation by increasing hypoxemia. Corresponding effects of baroreceptor stimulation and hypoxemia on aortic resistance and heart rate were additive. Celiac, renal, and iliac blood flows increased during both hypoxemia and reduced baroreceptor stimulation. Only in the celiac bed were blood flow changes independent of concomitant changes in cardiac output. Thus, at maximum sympathetic stimulation (low carotid sinus pressure) during hypoxemia, the cardiovascular system maintained both central and regional blood flows at high systemic blood pressures independent of the peripheral chemoreceptors.     

Phase-linked variations in the amplitude of the digastric nerve jaw-opening reflex response during fictive mastication in the rabbit

The diagastric nerve reflex response to stimulation of the upper lip was studied in urethan-anesthetized rabbits paralysed with pancuronium bromide. Rhythmic bursts of masticatory activity were evoked in the nerve by repetitive electrical stimulation of the motor cortex. The amplitude and latency of the reflex responses during fictive mastication were compared with preceding control values. When stimuli close to threshold were given, the largest and earliest responses occurred during the digastric burst. When intense stimuli were employed, the largest responses were out of phase with the burst, although the latency was still shortest when the motoneurons were rhythmically active. Since the pattern is essentially the same as that seen during normal mastication, we conclude that the cyclical modulation of reflex amplitude and latency is not the result of sensory feedback generated by the movements themselves but is instead governed by the central motor program.     

Cervical preganglionic sympathetic nerve activity and chemoreflexes in the cat

The role of chemoreflexes originating from carotid body and central chemoreceptors in the regulation of cervical preganglionic sympathetic nerve (PSN) activity was studied in anesthetized and spontaneously breathing cats. PSN efferents which responded to hypoxia were selected for the study. The PSN activity, breath-by-breath inspiratory tidal volume, tracheal PO2 and PCO2, and arterial systemic blood pressure were recorded simultaneously. The responses of PSN efferents to transient changes in and steady-state levels of arterial PO2 and PCO2 and to graded bolus injections of intravenous sodium cyanide (50-100 micrograms), nicotine (50-100 micrograms), and dopamine hydrochloride (30-60 micrograms) were compared before and after bilateral section of carotid sinus nerves (CSN). CSN section raised the base-line PSN activity and practically eliminated the responses to brief pharmacological stimuli, but it did not eliminate the responses to transient changes in and steady-state levels of arterial PO2 and PCO2. However, CSN section diminished PSN responses and abolished ventilatory responses to hypoxia. Thus the PSN response to hypoxia was partly independent of peripheral chemoreflex and of respiratory drive. We conclude that carotid body chemoreflex elicits fast PSN responses and that a moderate decline in arterial PO2 causes an additional slow, direct excitation of sympathetic nervous system. The latter indicates O2 chemosensitivity of the system in the physiological range of arterial PO2. This O2-sensing property may allow sympathetic nervous system to initiate chemoreflex responses independent of the peripheral chemoreceptors.     

Cardiorespiratory reflexes from muscles during dynamic and static exercise in the dog

Cardiorespiratory reflex responses during the initial phase of dynamic and static contraction of hindlimb muscles were studied in anesthetized dogs. Muscle contractions were elicited by stimulating the femoral and gastrocnemius nerves at 3 and 100 Hz with the intensity of 2.0-2.5 times the motor threshold for a 20-s period. Rhythmic contractions caused a decrease in arterial pressure (Pa) and heart rate (HR) and increased pulmonary ventilation (VE) by increasing frequency (f) without significantly changing VT. Tetanic contractions provoked an increase in Pa and HR and a hyperpnea resulting from a rise in both f and VT. Similar responses were also obtained in anesthetized dogs with carotid sinuses denervated and cervical vagi cut. The abrupt increase in VE at the start of both types of exercise was not associated with immediate significant decreases in end-tidal CO2 values. These two patterns of cardiocirculatory and respiratory responses were closely similar to those reported in anesthetized rabbits in previous studies. Both patterns of responses were reflexes initiated by activation of muscle receptors verified by interrupting the afferents from the contracting muscles. It is concluded that, during dynamic and static work, two distinct muscular reflex mechanisms might exert their drives, related to the muscular metabolic rate, on the circulatory and respiratory function.     

Relative influence of carotid baroreceptors and muscle receptors in the control of renal and hindlimb circulations.

In vagotomized dogs, a comparison was made of the relative ability of the carotid baroreceptors and of the receptors in skeletal muscles to cause constriction of the renal and hindlimb resistance vessels. With kidney and hindlimb perfused at constant pressure a decrease in pressure in the carotid sinuses from 250 to 40-45 mm Hg (1 mm Hg = 133 N/m2) caused the respective blood flows to increase by 19 +/- 6% and 80 +/- 4% (mean +/- SE), and stimulating muscle receptors with capsaicin caused a further decrease of 49 +/- 9% and 4 +/- 2%, respectively. With perfusion at constant flow, the baroreflex caused an increase of 34 +/- 4 mm Hg in the renal perfusion pressure and of 99 +/- 10 mm Hg in the hindlimb; capsaicin caused further increases of 203 +/- 17 and 35 +/- 9 mm Hg; respectively. These responses were abolished by sympathectomy. Capsaicin injection increased mean renal sympathetic nerve activity by 111 +/- 16% over the maximal impulse frequency recorded when the carotid sinus pressure was 40-45 mm Hg. Thus, withdrawal of the restraint exerted by the carotid baroreceptors on the pool of central neurons controlling the vascular beds of the hindlimb and kidney leads to near maximal constriction of the resistance vessels in the former bu not the latter; with strong activation of muscle receptors, near maximal constriction occurs in both beds.     

Ca^2＋参链霉素对大鼠颈动脉窦压力感受器反射影响中的作用

在２３只隔离灌流颈动脉窦区的麻醉大鼠上,观察了链霉素（ｓｔｒｅｐｔｏｍｙｃｉｎ,ＳＭ）对动脉压力感受器反射影响的离子机制。结果：（１）用ＳＭ（２００μｍｏｌ／Ｌ）隔离灌流大鼠颈动脉窦区时,压力感受器机能曲线向右上方移位,曲线最大斜率及反射性血压下降幅度均减小（Ｐ〈０．０１）,提示ＳＭ对压力感受器反射的抑制作用;（２）预先灌流高Ｃａ＾２＋溶液（４ｍｍｏｌ／Ｌ）后,可部分消除ＳＭ（２００μｍｏｌ／Ｌ）     

Vestibulosympathetic reflex during the early follicular and midluteal phases of the menstrual cycle

Evidence suggests that both the arterial baroreflex and vestibulosympathetic reflex contribute to blood pressure regulation, and both autonomic reflexes integrate centrally in the medulla cardiovascular center. A previous report indicated increased sympathetic baroreflex sensitivity during the midluteal (ML) phase of the menstrual cycle compared with the early follicular (EF) phase. On the basis of this finding, we hypothesize an augmented vestibulosympathetic reflex during the ML phase of the menstrual cycle. Muscle sympathetic nerve activity (MSNA), mean arterial pressure (MAP), and heart rate responses to head-down rotation (HDR) were measured in 10 healthy females during the EF and ML phases of the menstrual cycle. Plasma estradiol (Delta72 +/- 13 pg/ml, P < 0.01) and progesterone (Delta8 +/- 2 ng/ml, P < 0.01) were significantly greater during the ML phase compared with the EF phase. The menstrual cycle did not alter resting MSNA, MAP, and heart rate (EF: 13 +/- 3 bursts/min, 80 +/- 2 mmHg, 65 +/- 2 beats/min vs. ML: 14 +/- 3 bursts/min, 81 +/- 3 mmHg, 64 +/- 3 beats/min). During the EF phase, HDR increased MSNA (Delta3 +/- 1 bursts/min, P < 0.02) but did not change MAP or heart rate (Delta0 +/- 1 mmHg and Delta1 +/- 1 beats/min). During the ML phase, HDR increased both MSNA and MAP (Delta4 +/- 1 bursts/min and Delta3 +/- 1 mmHg, P < 0.04) with no change in heart rate (Delta0 +/- 1 beats/min). MSNA and heart rate responses to HDR were not different between the EF and ML phases, but MAP responses to HDR were augmented during the ML phase (P < 0.03). Our results demonstrate that the menstrual cycle does not influence the vestibulosympathetic reflex but appears to alter MAP responses to HDR during the ML phase.