Maintained depressor responses evoked by continuous and intermittent stimulation of aortic nerve in the rabbit

Stability of depressor responses evoked by long-lasting continuous and intermittent stimulation of the aortic nerve was studied in rabbits anaesthetized with urethane. Continuous stimulation produces blood pressure falls whose stability at low frequencies (1-10 cycles/sec) ranges from 91 to 86%. With rise of the stimulation frequency stability is decreased : at 500 cycles/sec, it amounts to 19%. Intermittent stimulation consisting in switching excitation on and off every 10 sec increases stability of depressor responses and at 500 cycles/sec, it is significantly higher than stability of effects produced by continuous stimulation. Following transection of aortic nerves, stability is increased at all frequencies of continuous stimulation and at all but the lowest frequency of intermittent stimulation. Vagotomy performed after section of the aortic nerves does not significantly affect the changes in stability observed after severing the aortic afferents. It is suggested that at high frequencies of stimulation, stability of depressor responses is reduced by homosynaptic depression. During intermittent stimulation, its effect is counteracted by post-tetanic changes occurring at intervals when the stimulation is switched off. The increase in stability after section of aortic nerves is probably related to its effect on excitability of the vasomotor centres.     

Effect of changing the frequency of conditioning tetanus on depressor responses evoked by stimulation of the aortic nerve.

The effect of changes in frequency of the conditioning tetanus on the magnitude of the testing depressor response was studied in rabbits anaesthetized with urethane. Conditioning and testing stimulations were applied to the same aortic nerve. The duration of the conditioning tetani was set at 3 and 60 sec and the interval between stimulations amounted to 40 and 120 sec. At the testing interval of 40 sec the increase in frequency both of short and long conditioning tetani reduces the magnitude of the testing response which attains a minimum at frequency of about 30 cycles/sec. Conditioning stimulations of higher frequency are gradually less effective and cause the testing response to increase. Similar depression is observed at the testing interval of 120 sec but only following long-lasting conditioning tetanus. Short conditioning trains at the testing interval of 120 sec facilitate the testing response. The frequency of the conditioning stimulation which produces the greatest reduction of the depressor response indicates the range of control exerted by the conditioning tetanus over the testing blood pressure effect. The size of this control is determined by the lowest level of depression and the highest value of facilitation of the testing response.     

Cardiovascular responses to electrical stimulation of the recurrent laryngeal nerve in conscious toads (Bufo marinus)

Summary Cardiovascular responses to electrical stimulation of the cut central end of the recurrent laryngeal nerve (rLN) were recorded in 19 conscious toads (Bufo marinus). Low intensity stimulation of the rLN (3.4±0.5 V, 1 ms, 10 Hz) elicited a slow 18–22% fall in heart rate and systolic and diastolic aortic arterial blood pressures (N=18), but had little or no effect upon ventilation (N=6). This low threshold depressor response (LTDR) was considered to represent the expression of the previously demonstrated pulmocutaneous baroreflex. Bilateral stimulation of the rLNs elicited greater LTDRs than did either left or right unilateral rLN stimulation. Blood pressure and heart rate responses to bilateral stimulation were 69–77% of the sum of responses to unilateral stimulation, and the mean summation was significant for the reduction in heart rate. Stimulus intensities of >4.7±0.7 V caused an immediate cessation of cardiac activity for up to 6.5±1.3 s (N=17) and a concomitant apnoea (N=6), which were followed by a lesser bradycardia and hypotension. This response was termed a high threshold depressor response (HTDR). During continued stimulation at intensities of >9.1±1.4 V, aortic blood pressure (Pa) and ventilation were rapidly restored, and aortic blood pressure continued to rise above control values (N=14). In some cases this high threshold pressor response (HTPR) was associated with an increase in heart rate. All responses to rLN stimulation were abolished by pithing (N=9) or by pentobarbital (40 mg/kg, i.p.,N=4), but LTDS and HTPRs could be elicited in urethanized (1.5–2.0 g/kg,N=4) toads.During depressor responses, aortic arterial resistance fell by 18% in 18 of 20 trials in 5 toads, whereas pulmocutaneous arterial resistance increased by 76% in 12 of 15 trials in 4 toads. During the HTPR, aortic arterial resistance increased 40%, while pulmocutaneous arterial resistance remained unchanged. We suggest that depressor responses may actively redistribute blood flow from the pulmocutaneous to the aortic circulation, whereas the reverse should occur during HTPRs.Abbreviations HTDR high threshold depressor response - HTPR high threshold pressor response - rLN recurrent laryngeal nerve - LTDR low threshold depressor response - Pa aortic blood pressure - PCA pulmocutaneous artery - Pd diastolic aortic pressure - Ppca pulmocutaneous blood pressure - PRU peripheral resistance unit - Ps systolic aortic pressure - Pv venous blood pressure - Ra aortic arterial resistance - Rpca pulmocutaneous arterial resistance     

Interaction between depressor and pressor reflexes arising from the aorta in dogs

In 18 dogs anesthetized with morphine-chloralose the interaction between the aortic nerve (AN) pressor and depressor reflexes was studied. Low-intensity, high-frequency electrical stimulation of the AN causes large decreases in heart rate and systemic pressure characteristic of baroreflex responses. High-intensity, low-frequency stimulation of the AN causes modest increases in heart rate and systemic pressure similar to the responses observed to intraaortic nicotine. Simultaneous electrical stimulation of these antagonistic reflexes results in much smaller (P less than 0.001) reductions in heart rate and systemic pressure that can be explained on the basis of simple addition of the individual responses. Similarly the AN depressor reflexes are suppressed during intraaortic infusions of nicotine (40 micrograms/min). The results suggest that the inhibitory effects of the AN baroreflexes are suppressed by the aortic chemoreflexes . This interaction occurs in the CNS rather than at the level of the heart or vascular smooth muscle.     

The Gigantocellular Depressor Area Revisited

1. In studies conducted with Dr Donald Reis we described a functionally distinct region of the rat medullary reticular formation that we called the Gigantocellular Depressor Area (GiDA). The GiDA was defined as a region from which vasodepressor and sympathoinhibitory responses were evoked by nanoinjections of glutamate. We later showed that cells in the GiDA project to autonomic nuclei in the medulla, brainstem, and spinal cord, including the intermediolateral cell column. We also showed that kainic acid lesions of the GiDA induce hypertension and block the baroreceptor reflex evoked by electrical stimulation of the aortic depressor nerve. The present studies describe the effects of muscimol nanoinjections into the GiDA.2. Nanoinjections of muscimol were made in the GiDA of anesthetized rats and changes in arterial pressure, heart rate, and responses to aortic depressor nerve stimulation were measured.3. Bilateral nanoinjections of muscimol into the GiDA evoke an increase in arterial pressure and lead to fulminating hypertension. Unilateral injections of muscimol into the GiDA block the baroreflex response evoked by electrical stimulation of the ipsilateral aortic depressor nerve. However, these unilateral injections of muscimol into the GiDA evoked profound falls in arterial pressure to nearly spinal levels. In spite of this fall in blood pressure, heart rate also decreased significantly and there was not a compensatory tachycardia. Both the arterial pressure and baroreceptor responses required several hours to recover following the muscimol injections.4. Although these data are consistent with the proposal that the GiDA is critical for the baroreflex, the opposing effects on blood pressure of unilateral and bilateral injections of muscimol are difficult to reconcile with our current models of central sympathetic regulation.     

刺激肾神经传入纤维的降压反应与颈动脉窦压力感受性反射的相互作用

在麻醉兔,研究了刺激肾神经传入纤维与颈动脉窦压力感受性反射在减压反射中的相互作用。电刺激肾神经传入纤维引起平均动脉压(MAP)下降,下降程度在一定范围有赖于刺激频率。当颈动脉窦被隔离和主动脉神经切断后,随着颈动脉窦内压逐渐升高,刺激肾神经传入纤维引起的减压反应不断减弱。在45至135mmHg 之间的7个颈动脉窦内压(ISP)水平,刺激肾神经传入纤维,并画出刺激前和刺激时的 ISP-MAP 关系曲线。在颈动脉窦内压为75至105mmHg 之间,刺激肾神经传入纤维显著降低 ISP-MAP 关系曲线的斜率和对ISP 的平均动脉压反应范围。这些结果提示:(1)颈动脉窦压力感受器的传入冲动可调制刺激肾神经传入纤维的降压反应,在一定范围内与颈动脉窦内压呈反比;(2)刺激肾神经传入纤维明显减弱颈动脉窦的压力感受性反射。     

Analysis of hemodynamic reactions induced by stimulation of the hypothalamus in alert animals

Electrical stimulation on the hypothalamus in alert cats increases the blood pressure and inhibits the baroceptor reflexes. In animals with extirpated sinocarotid and aortic nerves the pressor reactions are perversed to depressor ones at threshold stimulation of the hypothalamus. Meanwhile suprathreshold stimulation of this organ leads to emergence of depressor-pressor responses. It is suggested that inhibition of the baroceptor reflexes is one of the mechanisms of the hypertensive reaction emergence at stimulation of the hypothalamus.     

刺激家兔腹部迷走神经外周端降压效应中枢机制的研究

应用电解损毁和脑室内注射药物的方法研究了刺激家兔腹部迷走神经外周端所致降压效应的中枢机制。结果表明:1.电刺激延脑闩部尾侧1.5—2mm、中线旁开0.25mm、深1—2mm 处主要引起降压反应。2.电解损毁该部位可以使刺激腹部迷走神经外周端所引起的降压效应显著减弱(n=20,P<0.001),但对刺激减压神经所致降压反应无影响。3.在延脑闩部水平电解损毁减压神经纤维在孤束核的主要投射区可以使刺激减压神经所致降压反应显著减弱,而对刺激腹部迷走神经外周端所致降压反应无影响。4.第四脑室注射5,6-双羟色胺的动物较之注射人工脑脊液的动物颈、胸髓5-羟色胺含量明显降低、动物动脉压增高、心率明显增快、刺激减压神经所致降压反应未见减弱,而刺激腹部迷走神经外周端所致降压反应却明显减小。因此,我们认为家兔腹部迷走神经外周端所致降压效应依赖于延脑闩下部的中缝隐核及连合核等结构,而与减压神经的投射部位无关。延脑中缝核至脊髓的下行性5-HT能神经纤维抑制脊髓交感节前神经元的活动,是这个降压效应的中枢机制之一。     

Possible correlation between binding of muscle type AMP deaminase to myofibrils and ammoniagenesis in rat skeletal muscle on electrical stimulation

Contraction of rat skeletal muscle by electrical stimulation of the sciatic nerve caused remarkable increase in binding of AMP deaminase (EC 3.5.4.6) to myofibrils, but did not change the total enzyme activity. After 30 sec stimulation, the ratio of bound to free enzyme was about 5 times that in resting muscle. This treatment also increased the ammonia content of the muscle to 5 times that in resting state. From these findings, we suggest that there is a correlation between the binding of muscle type AMP deaminase to myofibrils and ammoniagenesis in the muscle.     

Central inhibition of the aortic baroreceptors-heart rate reflex at the onset of spontaneous muscle contraction.

Animals decerebrated at the precollicular-premammillary body level exhibit spontaneous locomotion without any artificial stimulation. Our laboratory reported that the cardiovascular and autonomic responses at the onset of spontaneous locomotor events are evoked by central command, generated from the caudal diencephalon and the brain stem (Matsukawa K, Murata J, and Wada T. Am J Physiol Heart Circ Physiol 275: H1115-H1121, 1998). In this study, we examined whether central command and/or a reflex resulting from muscle afferents modulates arterial baroreflex function using a decerebrate cat model. The baroreflex was evoked by stimulating the aortic depressor nerve (ADN) at the onset of spontaneous muscle contraction (to test the possible influence of central command) and during electrically evoked contraction or passive stretch (to test the possible influence of the muscle reflex). When the ADN was stimulated at rest, heart rate and arterial blood pressure decreased by 40 +/- 2 beats/min and 11 +/- 1 mmHg, respectively. The baroreflex bradycardia was attenuated to 55 +/- 4% at the onset of spontaneous contraction. The attenuating effect on the baroreflex bradycardia was not observed at the onset and middle of electrically evoked contraction or passive stretch. The depressor response to ADN stimulation was identical among resting and any muscle interventions. The inhibition of the baroreflex bradycardia during spontaneous contraction was seen after beta-adrenergic blockade but abolished by muscarinic blockade, suggesting that the bradycardia is mainly evoked through cardiac vagal outflow. We conclude that central command, produced within the caudal diencephalon and the brain stem, selectively inhibits the cardiac component, but not the vasomotor component, of the aortic baroreflex at the onset of spontaneous exercise.     

Leptin in nucleus of the solitary tract alters the cardiovascular responses to aortic baroreceptor activation

Recent data suggests that neurons expressing the long form of the leptin receptor form at least two distinct groups within the caudal nucleus of the solitary tract (NTS): a group within the lateral NTS (Slt) and one within the medial (Sm) and gelantinosa (Sg) NTS. Discrete injections of leptin into Sm and Sg, a region that receives chemoreceptor input, elicit increases in arterial pressure (AP) and renal sympathetic nerve activity (RSNA). However, the effect of microinjections of leptin into Slt, a region that receives baroreceptor input is unknown. Experiments were done in the urethane-chloralose anesthetized, paralyzed and artificially ventilated Wistar or Zucker obese rat to determine leptin's effect in Slt on heart rate (HR), AP and RSNA during electrical stimulation of the aortic depressor nerve (ADN). Depressor sites within Slt were first identified by the microinjection of l-glutamate (Glu; 0.25 M; 10 nl) followed by leptin microinjections. In the Wistar rat leptin microinjection (50 ng; 20 nl) into depressor sites within the lateral Slt elicited increases in HR and RSNA, but no changes in AP. Additionally, leptin injections into Slt prior to Glu injections at the same site or to stimulation of the ADN were found to attenuate the decreases in HR, AP and RSNA to both the Glu injection and ADN stimulation. In Zucker obese rats, leptin injections into NTS depressor sites did not elicit cardiovascular responses, nor altered the cardiovascular responses elicited by stimulation of ADN. Those data suggest that leptin acts at the level of NTS to alter the activity of neurons that mediate the cardiovascular responses to activation of the aortic baroreceptor reflex.     

Spinal GABA(A) receptors do not mediate the sympathetic baroreceptor reflex in the rat

Activation of baroreceptors causes efferent sympathetic nerve activity (SNA) to fall. Two mechanisms could account for this sympathoinhibition: disfacilitation of sympathetic preganglionic neurons (SPN) and/or direct inhibition of SPN. The roles that spinal GABA and glycine receptors play in the baroreceptor reflex were examined in anesthetized, paralyzed, and artificially ventilated rats. Spinal GABA(A) receptors were blocked by an intrathecal injection of bicuculline methiodide, whereas glycine receptors were blocked with strychnine. Baroreceptors were activated by stimulation of the aortic depressor nerve (ADN), and a somatosympathetic reflex was used as control. After an intrathecal injection of vehicle, there was no effect on any measured variable or evoked reflex. In contrast, bicuculline caused a dose-dependent increase in arterial pressure, SNA, phrenic nerve discharge, and it significantly facilitated the somatosympathetic reflex. However, bicuculline did not attenuate either the depressor response or sympathoinhibition evoked after ADN stimulation. Similarly, strychnine did not affect the baroreceptor-induced depressor response. Thus GABA(A) and glycine receptors in the spinal cord have no significant role in baroreceptor-mediated sympathoinhibition.     

Specific baroreceptor control of vertebral and cardiac sympathetic activity.

The effect of bilateral carotid occlusion (BCO) on the activity of the vertebral and cardiac sympathetic efferent nerves was studied in gallamine-immobilized and artificially ventilated cats under chloralose-urethane anaesthesia. Electrical activity of the vertebral and cardiac nerves (VNA and CNA), their integram, arterial blood pressure and respiration were recorded. BCO led to an increase in VNA persisting throughout the occlusion period, while merely a transient increase took place in CNA. When blood pressure was kept at a constant level or the depressor nerves was transected, CNA responded to BCO with a lasting increase. Electrical stimulation of the central stump of the left depressor nerve inhibited CNA much more than VNA. It is assumed that the selective inhibition of CNA, after a transient increase, arises as a consequence of a rise in blood pressure, i.e. of consecutive aortic baroreceptor excitation.     

The freezing threshold of the peripheral motor nerve: an electrophysiological and light-microscopical study on the sciatic nerve of the rabbit.

Fifty sciatic nerves of 39 rabbits are treated at different temperatures (+5, +1, 0, ?3, ?5, ?10, ?15 and ?20 °C), for different freezing times (10, 20, 30, 60 and 120 sec), and for different numbers of freeze-thaw cycles (1, 2 and 4). After electric supramaximal stimulation (3.8 V) action potentials of the sciatic nerve are measured before, immediately after, and 1, 3, 5, 10, 20, 30, 60, 90 min, 2, 5 and 10 days after freezing. Two or ten days after freezing, the nerves are examined in a light microscope. The cold threshold of the sciatic nerve was determined, i.e., the temperature at which after supramaximal stimulation it is still possible to measure an action potential within 1.5 hr after freezing. On application of one freeze-thaw cycle, the cold threshold is ?15 °C after a freezing time of 10 sec, ?10 °C after 20 sec and 30 sec, and ?5 °C after 60 and 120 sec. After application of two and four freeze-thaw cycles, the cold threshold is elevated, and after a super-cooling time of 10 sec it is ?10 °C, after 30 sec ?5 °C. The longer the freezing time and the more freeze-thaw cycles, the higher is the cold threshold. At ?20 °C (superthreshold temperature) an action potential can no longer be measured and all myelinated nerve fibres have decayed, except some small-caliber ones.Electrophysiologically, it is evident that some of the myelinated nerve fibres become functionally damaged for 1.5 hr, while other parts of the nerve fibres will degenerate and later regenerate. The amplitudes of the measured action potentials correlate with the decay of myelin sheaths and axons of large- and medium-caliber nerve fibres. Action potentials between 0 and 40% show a gradual paresis, above 40% a physiological motor function. The pathophysiological mechanism of this reversible functional loss after super-cooling and freezing may be a consequence of a disturbed membrane permeability.It is of clinical importance that, if the cold threshold of a peripheral motor nerve is known, the nerve can be frozen concomitantly for a short time at application of low temperatures without suffering any functional loss. This is achieved by controlling during freezing the motor function of the corresponding nerve situated on the periphery of cryolesion, and, if there is a loss of motor function, the freezing process has to be interrupted immediately.     

Carotid and aortic baroreflexes of the rat: I. Open-loop steady-state properties and blood pressure variability

To characterize the baroreflex in central nervous system-intact neuromuscular-blocked rats, we measured the vascular and cardiac responses and compared direct stimulation of the aortic depressor nerve (ADN) with a capacitance electrode (differentially activating either A or A + C fibers) to carotid sinus pressure with a micro-balloon (SINUS). One-thousand-two-hundred-ninety-seven open-loop measurements of systolic blood pressure (SBP), heart rate, venous pressure (VBP), and mesenteric (msBF), femoral (fmBF), and skin (skBF) blood flow were completed; the linear range of the effects was determined for each response and stimulus mode. The rats were sinoaortic denervated (SAD). The open-loop stimulation effect was very stable; e.g., the mean effect of 790 ADN stimulations during >7 days was -9.8 mmHg, with an average drift of +0.001 mmHg/h. In contrast, there was large variability of the SBP baseline (e.g., SD = +/-10.9), which was due to SAD (+/-6.3 to +/-16.3 mmHg, t = -13. 9, df = 4, P < 0.0002) and was reversed by ganglionic block (+/-10.8 to +/- 2.9 mmHg, t = -12.9, df = 3, P < 0.001). The ADN stimuli produced larger depressor responses than sinus stimuli (-66 vs. -45 mmHg); all component responses paralleled the magnitude of the SBP effect, except interbeat interval (IBI), for which the ADN DeltaIBI was approximately 10 times that of SINUS. For all stimuli, fmBF increased and msBF did not. Mesenteric and femoral vascular conductance both increased, whereas VBP decreased and skBF followed SBP. We found that for all baroreflex response components, with the exception of SINUS-elicited DeltaIBI, there was an orderly, substantially linear, relationship between stimulus strength and response magnitude.     

Norepinephrine reuptake, baroreflex dynamics, and arterial pressure variability in rats

This study examined the effect of norepinephrine reuptake blockade with desipramine (DMI) on the spontaneous variability of the simultaneously recorded arterial pressure (AP) and renal sympathetic nerve activity (SNA) in conscious rats. Acute DMI administration (2 mg/kg iv) depressed AP Mayer waves ( approximately 0.4 Hz) and increased low-frequency (<0.2 Hz) components of AP variability. DMI decreased renal SNA variability, especially due to the abolition of oscillations related to Mayer waves. To examine whether DMI-induced changes in AP and renal SNA variabilities could be explained by alterations in the dynamic characteristics of the baroreceptor reflex loop, the frequency responses of mean AP to aortic depressor nerve stimulation were studied in urethan-anesthetized rats. DMI accentuated the low-pass filter properties of the transfer function without significantly altering the fixed time delay. The frequency responses of iliac vascular conductance to stimulation of the lumbar sympathetic chain were studied in an additional group of anesthetized rats. DMI did not markedly alter the low-pass filter properties of the transfer function and slightly increased the fixed time delay. These results suggest that the DMI-induced decrease in the dynamic gain of the baroreceptor reflex is responsible for the decreased spontaneous renal SNA variability and the accompanying increased AP variability. The "slowing down" of baroreflex responses cannot be attributed to an effect of DMI at the vascular neuroeffector junction.     

Resetting blood pressure by a closed-loop implanted chip system in normotensive rats

A closed-loop implanted chip system was designed to control blood pressure without using drugs. The chip system instantaneously reset blood pressure by stimulating the left aortic depressor nerve according to the feedback signals of arterial blood pressure. The relationship between pressure signals and frequency of stimulation was identified in vitro and in vivo, and the efficiency of the chip system was evaluated in normal anesthetized Wistar rats. To determine whether the depressor effect of the chip was primarily independent on the bradycardia induced by the resetting, the effects of methyl atropine (1.5 g/kg, iv.) and bilateral vagotomy on depressor effect induced by the chip system were determined, respectively. The results indicated that the chip system worked well. The frequency of stimulus linearly increased following the elevation of pressure from 70 to 160 mm Hg. The frequency of the stimulus reached its maximum (100 Hz) when pressure exceeded 160 mm Hg, and the stimulation stopped when MAP was below 70 mm Hg. There were significant decreases in mean arterial pressure (MAP, -20.0+/-4.4 mm Hg) and heart rate (HR, -43.0+/-10.5 bpm) during the resetting in rats. After resetting, both MAP and HR recovered in a minute without any significant rebound. Pretreatment with either methyl atropine or bilateral vagotomy abolished the bradycardia effect but produced no significant effect on hypotension. The results demonstrated that the chip system successfully reset blood pressure in rats, and that the hypotension induced by the chip system was primarily independent on the bradycardia effect.     

Analysis of afferent,central, and efferent components of the baroreceptor reflex in mice

Studies of genetically modified mice provide a powerful approach to investigate consequences of altered gene expression in physiological and pathological states. The goal of the present study was to characterize afferent, central, and efferent components of the baroreceptor reflex in anesthetized Webster 4 mice. Baroreflex and baroreceptor afferent functions were characterized by measuring changes in renal sympathetic nerve activity (RSNA) and aortic depressor nerve activity (ADNA) in response to nitroprusside- and phenylephrine-induced changes in arterial pressure. The data were fit to a sigmoidal logistic function curve. Baroreflex diastolic pressure threshold (P(th)), the pressure at 50% inhibition of RSNA (P(mid)), and baroreflex gain (maximum slope) averaged 74 +/- 5 mmHg, 101 +/- 3 mmHg, and 2.30 +/- 0.54%/mmHg, respectively (n = 6). The P(th), P(mid), and gain for the diastolic pressure-ADNA relation (baroreceptor afferents) were similar to that observed for the overall reflex averaging 79 +/- 9 mmHg, 101 +/- 4 mmHg, and 2.92 +/- 0.53%/mmHg, respectively (n = 5). The central nervous system mediation of the baroreflex and the chronotropic responsiveness of the heart to vagal efferent activity were independently assessed by recording responses to electrical stimulation of the left ADN and the peripheral end of the right vagus nerve, respectively. Both ADN and vagal efferent stimulation induced frequency-dependent decreases in heart rate and arterial pressure. The heart rate response to ADN stimulation was nearly abolished in mice anesthetized with pentobarbital sodium (n = 4) compared with mice anesthetized with ketamine-acepromazine (n = 4), whereas the response to vagal efferent stimulation was equivalent under both types of anesthesia. Application of these techniques to studies of genetically manipulated mice can be used to identify molecular mechanisms of baroreflex function and to localize altered function to afferent, central, or efferent sites.     

Depressor reactions to sural nerve stimulation in intact unanesthetized cats]

Changes in the arterial pressure, in the heart and respiratory rate evoked by the gastrocnemuis nerve stimulation were studied on conscious cats before and during intravenous injection of noradrenaline. Stimulation of the gastrocnemius nerve increased the arterial pressure, the heart and respiratory rates. The same stimulation of the nerve during hypertension caused by noradrenaline injection led to the fall of arterial pressure and tachycardia. The depressor response failed to change under the effect of the beta-adrenoreceptor block and disappeared after the m-cholinoreceptor block with methylatropine. The depressor response was absent in the unanesthetized decerebrated cats. It is supposed that the depressor response of the arterial pressure depended on the strong cholinergic vasodilatation, reflexively evoked by stimulation of the motor nerve in the intact cats.     

Role of the various groups of afferent fibers of the mesenteric nerves in vasomotor reflexes

The dependence of the magnitude and character of vasomotor reflexes on the amplitude of tetanic stimulation of the mesenteric nerves was investigated in experiments on anesthetized cats. Comparison of the results of analysis of the stimulus amplitude versus reflex magnitude curves with previous data on excitability of the various groups of mesenteric nerve fibers revealed three groups of "vasomotor" afferents with different conduction velocities: fast-conducting Aδ-fibers (conduction velocity over 8 m/sec) evoking depressor or small pressor reflexes; slow-conducting Aδ-fibers (conduction velocity below 8 m/sec), evoking pressor reflexes or, by interaction with impulses of lower-threshold, fast-conducting Aδ-fibers, either reduce the magnitude of the depressor reflexes evoked by those impulses or increase the corresponding pressor reflexes; C-fibers increasing the magnitude of the pressor reflexes evoked by slow-conducting A-fibers.