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Biomedical subjects

Naoyuki Hayashi

Publications and source records attributed to Naoyuki Hayashi.

At least 19 recordsLinked to original sources

Temperature-sensitive defects of the GSP1gene, yeast Ran homologue, activate the Tel1-dependent pathway.

RanGTPase is involved in many cellular processes. It functions in nuclear-cytosolic transport and centrosome formation. Ran also localizes to chromatin as RCC1 does, its guanine nucleotide exchange factor, but Ran's function on chromatin is not known. We found that gsp1, a temperature-sensitive mutant of GSP1, a Saccharomyces cerevisiae Ran homologue, suppressed the hydroxyurea (HU) and ultra violet (UV) sensitivities of the mec1 mutant. In UV-irradiated mec1 gsp1 cells, Rad53 was phosphorylated despite the lack of Mec1. This suppression depended on the TEL1 gene, given that the triple mutant, mec1 gsp1 tel1, was unable to grow. The gsp1 mutations also suppressed the HU sensitivity of the rad9 mutant in a Tel1-dependent manner, but not the HU sensitivity of the rad53 mutant. These results indicated that Rad53 was activated by the Tel1 pathway in mec1 gsp1 cells, suggesting that Gsp1 helps regulate the role switching the ATM family kinases Mec1 and Tel1.

Cell Proliferation↗

Cardiovascular responses to static extension and flexion of arms and legs.

This study compared cardiovascular responses to static extension and flexion exercises at four upper and lower limb joints. Eight males performed a 2 min static contraction at 30% of maximal voluntary torque followed immediately by 2 min post-exercise muscle ischaemia (PEMI) using each of four joints: the wrist, elbow, ankle, and knee. In the PEMI, an occlusion cuff placed around the proximal portion of the exercising muscle was inflated to 250 mmHg immediately before the cessation of exercise. Mean arterial pressure (MAP), heart rate (HR), calf blood flow, and calf vascular conductance (CVC) in the non-exercised calf were measured. There was a significant interaction for direction of movement (extension vs. flexion) and limb (upper vs. lower) in HR and CVC during both exercise and PEMI; extension in the wrist and elbow evoked a greater increase in HR and a greater decrease in CVC than flexion, whereas flexion in the ankle and knee elicited a greater increase in HR and a greater decrease in CVC than extension. These results suggest that the cardiovascular responses to extension and flexion differ between arms and legs, partly arising from the activation of the muscle metaboreflex.

Adult↗

Effects of femoral vascular occlusion on ventilatory responses during recovery from exercise in human.

We investigated the effect of occluding of femoral blood flow on the post-exercise ventilatory response of both the sub- and supra-anaerobic threshold (AT) leg cycling in humans. Seven healthy subjects (aged 21-44 years) volunteered to participate in this study. The protocol consisted of 6 min constant-load upright cycling at either a sub-AT (80% of AT) or supra-AT (midway between AT and VO(2)max) work rate and a subsequent 6 min rest period either with or without femoral blood flow being occluded by a rapid cuff inflation to 250 Torr during the first 2 min of recovery. Blood lactate levels at the cessation of the sub- and supra-AT exercise averaged 1.8+/-0.2 and 4.9+/-0.4 mequiv.l(-1) (mean+/-S.E.M.), respectively. Compared to spontaneous recovery, the circulatory occlusion significantly reduced ventilation irrespective of the intensity of the preceding exercise. The relative contribution of the ventilatory deficit to the total spontaneous ventilation (defined as the difference between the cumulative ventilation with and without cuff inflation during the first 2 min of recovery) was significantly greater supra-AT (18.0+/-3.9%) than sub-AT (9.3+/-2.9%, P<0.05). The subsequent release of occlusion was accompanied by a rapid increase in ventilation that began on the first breath after release. We concluded that the relatively greater speeding of ventilatory decline with occlusion during the first 2 min of recovery from supra-AT exercise argues against a significant role for an intramuscular chemoreflex-induced hyperpnoea. Rather, mechanisms related to the hemodynamic effects of suddenly altered muscle perfusion seem more consistent with this phenomenon.

Adult↗

Suppressor analysis of the mpt5/htr1/uth4/puf5 deletion in Saccharomyces cerevisiae.

The MPT5/HTR1/UTH4/PUF5 gene encodes an RNA-binding Puf-family protein in Saccharomyces cerevisiae. The Deltampt5 cells exhibit pleiotropic phenotypes, including the G2/M arrest of the cell cycle and weakened cell wall at high temperatures. The Deltampt5 disruptant was also hydroxyurea (HU) sensitive. In this study we screened deletion suppressors to rescue the temperature sensitivity of Deltampt5, and identified dsf1 (YEL070W), dsf2 (YBR007C), sir2, sir3, sir4 and swe1. Multicopy suppressors identified were PKC1 and its upstream genes, but not the downstream MAPK cascade genes. The overexpression of PKC1, however, did not suppress the HU sensitivity of Deltampt5. In contrast, both the HU- and temperature-sensitivities of a-type Deltampt5 cells were suppressed by each sir deletion or a multicopy of MATalpha2, suggesting that a diploid-type expression is involved. We found that a diploid-specific IME4 gene encoding an RNA-modifying protein was responsible for the suppression of the temperature sensitivity, but not of the HU sensitivity. Furthermore, the suppression of the HU sensitivity depended on PUF4, another Puf-family gene, and overexpression of PUF4 suppressed only the HU sensitivity of Deltampt5. The protein level of Puf4 was not affected by the sir mutation. Thus, these Ime4 and Puf4 proteins play complementary roles to rescue the defects in Deltampt5 Deltasir cells.

Cell Cycle Proteins↗

Vasoconstriction and blood flow responses in visceral arteries to mental task in humans.

The vascular responses to mental task in visceral arteries in humans have not been elucidated. We observed the responses in the renal (RA) and superior mesenteric (SMA) arteries to mental stress, using simultaneous pulsed and echo Doppler ultrasound flowmetry. Nine healthy females performed a computerized colour word conflict test (CWT) for 3 min. The mean blood velocity (MBV) in the right RA and SMA, heart rate (HR) and blood pressure were measured. The mean arterial pressure (MAP) was divided by the flow velocity to assess the vascular resistance (VR). The CWT significantly increased the MAP, HR and VR in both arteries from the first minute. During the CWT, flow in the RA decreased significantly at the third minute relative to baseline, while flow in the SMA showed no significant change from the first to the third minute. The degree of vasoconstriction in the RA bed was greater than that in the SMA bed. These results suggest that the mental task causes vasoconstriction in visceral arteries, and imply that it induces differential blood flow and vascular responses in visceral arteries.

Adult↗

Renal sympathetic and circulatory responses to activation of the exercise pressor reflex in rats.

We investigated the role played by the exercise pressor reflex in sympathetic regulation of the renal circulation in rats. In mid-collicular decerebrate rats, mean arterial pressure (MAP), heart rate (HR), left renal cortical blood flow (RCBF) and left renal sympathetic nerve activity (RSNA) were recorded before and during 30 s of static contraction of the left triceps surae muscles evoked by electrical stimulation of the tibial nerve, which activates both metabo- and mechanosensitive muscle afferents, and during 30 s of passive stretch of the left Achilles tendon, which selectively activates mechanosensitive muscle afferents. Static contraction (n = 17, +344 +/- 34 g developed tension) significantly (P < 0.05) increased MAP (+14 +/- 3 mmHg), HR (+6 +/- 1 beats min(-1)) and RSNA (n = 11, +19 +/- 5%) and significantly decreased renal cortical vascular conductance (RCVC, n = 11, -11 +/- 2%). Passive stretch (n = 20, +378 +/- 11 g) also significantly increased MAP (+11 +/- 2 mmHg), HR (+7 +/- 2 beats min(-1)) and RSNA (n = 15, +14 +/- 4%) and significantly decreased RCVC (n = 11, -12 +/- 3%). RCBF showed no significant changes during static contraction or passive stretch. Renal denervation abolished the decrease in RCVC during contraction (n = 12) or stretch (n = 13). These data indicate that both the exercise pressor reflex and its mechanically sensitive component, the muscle mechanoreflex, induced renal cortical vasoconstriction through sympathetic activation in rats.

Achilles Tendon↗

Differential sympathetic outflow and vasoconstriction responses at kidney and skeletal muscles during fictive locomotion.

We compared sympathetic and circulatory responses between kidney and skeletal muscles during fictive locomotion evoked by electrical stimulation of the mesencephalic locomotor region (MLR) in decerebrate and paralyzed rats (n = 8). Stimulation of the MLR for 30 s at 40-microA current intensity significantly increased arterial pressure (+38 +/- 6 mmHg), triceps surae muscle blood flow (+17 +/- 3%), and both renal and lumbar sympathetic nerve activities (RSNA +113 +/- 16%, LSNA +31 +/- 7%). The stimulation also significantly decreased renal cortical blood flow (-18 +/- 6%) and both renal cortical and triceps surae muscle vascular conductances (RCVC -38 +/- 5%, TSMVC -17 +/- 3%). The sympathetic and vascular conductance changes were significantly dependent on current intensity for stimulation at 20, 30, and 40 microA. The changes in LSNA and TSMVC were significantly less than those in RSNA and RCVC, respectively, at all current intensities. At the early stage of stimulation (0-10 s), decreases in RCVC and TSMVC were significantly correlated with increases in RSNA and LSNA, respectively. These data demonstrate that fictive locomotion induces less vasoconstriction in skeletal muscles than in kidney because of less sympathetic activation. This suggests that a neural mechanism mediated by central command contributes to blood flow distribution by evoking differential sympathetic outflow during exercise.

Animals↗

Sympathetically induced renal vasoconstriction during stimulation of mesencephalic locomotor region in rats.

Central command, which is a neural drive originating in the brain during exercise, regulates the sympathetic nervous system and evokes cardiovascular responses to exercise. To examine the role of the central command on sympathetic regulation of renal circulation, we compared responses in renal cortical blood flow and vascular conductance to electrical stimulation of mesencephalic locomotor region (MLR) for 30 s in decerebrate and paralyzed rats between renal nerves that were intact (n=8) and denervated (n=8). In rats with renal nerves intact, stimulation of the MLR at 40 microA current intensity significantly (p<0.05) decreased renal cortical blood flow (-17+/-5%, means+/-S.E.M.) and vascular conductance (-43+/-4%) and the decrease in renal vascular conductance was dependent on current intensity (between 20 and 60 microA). In renal denervated rats, in contrast, there were no significant changes in either renal cortical blood flow or vascular conductance during stimulation at all current intensities. In a subset of rats (n=8), the response in renal sympathetic nerve activity to 30 s stimulation of the MLR was investigated. Stimulation of the MLR significantly increased renal sympathetic nerve activity (+57+/-14% at 40 microA) and the response was dependent on current intensity (between 20 and 60 microA). These data provide evidence that central command induces renal vasoconstriction by increasing sympathetic activity, depending on central command intensity.

Adrenergic Fibers↗

Disuse atrophy increases the muscle mechanoreflex in rats.

We investigated the effect of disuse atrophy on the magnitude of the muscle mechanoreflex. The left leg of eight rats (6-7 wk, male) was put in a plaster cast for 1 wk. The rats were decerebrated at the midcollicular level. We recorded the pressor and cardioaccelerator responses to 30-s stretch of the calcaneal tendon, which selectively stimulated the muscle mechanosensitive receptors in the left atrophied and right control triceps surae muscles. Atrophied muscles showed significantly lower mass control muscles (1.0 +/- 0.1 vs. 1.4 +/- 0.1 g; P < 0.05). At the same stretch tension (229 +/- 20 g), the pressor response to stretch was significantly greater in the atrophied muscles than in the control muscles (13 +/- 3 vs. 4 +/- 2 mmHg, P < 0.05). The cardioaccelerator response was not significantly different (8 +/- 4 vs. 4 +/- 2 beats/min). Comparing responses at the same relative tension (57 +/- 6 vs. 51 +/- 8% of maximal tension), the pressor response was still significantly greater in the atrophied triceps surae than in the control (14 +/- 4 vs. 4 +/- 2 mmHg; P < 0.05). These results suggest that disuse atrophy increases the magnitude of muscle mechanoreflex.

Animals↗

The SIT4 gene, which encodes protein phosphatase 2A, is required for telomere function in Saccharomyces cerevisiae.

Life span and number of cell divisions in eukaryotes are limited. The accumulation of stress-associated damage due to ageing may cause irreversible cell cycle arrest, so-called "cellular senescence". Although many genes have been implicated in determining life span, regulatory systems that counteract age-related stress have not yet been clarified. We examined senescence during a stress of Saccharomyces cerevisiae strains carrying disruptions in protein phosphatase (PPase)-encoding genes in order to identify the system counteracting senescence. Among these strains, short telomeres were found in the sit4 disruptant that lacks one form of protein phosphatase 2A (PP2A). Silencing ability in the subtelomeric region was impaired and hyperphosphorylation of Sir3 was also observed in this mutant. The sit4 mutant was found to have altered nucleoli and a life span as short as an sgs1 mutant. These observations suggest that the PP2A pathway regulates life span in yeast.

Cell Cycle↗

Mutational analysis of human RNA polymerase II subunit 5 (RPB5): the residues critical for interactions with TFIIF subunit RAP30 and hepatitis B virus X protein.

RNA polymerase II (RNAPII) subunit 5 (RPB5) is positioned close to DNA downstream of the initiation site and is the site of interaction with several regulators. Hepatitis B virus X protein (HBx) binds the central part of RPB5 to modulate activated transcription, and TFIIF subunit RAP30 interacts with the same part of RPB5 that is critical for the association between TFIIF and RNAPII. However the residues necessary for these interactions remain unknown. Here we report systematic mutagenesis of the central part of RPB5 using two-step alanine scanning libraries to pinpoint critical residues for its binding to RAP30 in the TFIIF complex and/or to HBx, and identified these residues in both mammalian cells and in an in vitro binding assay. Four residues, F76, I104, T111 and S113, are critical for both TFIIF- and HBx-binding, indicating the overlapping nature of the sites of interaction. In addition, V74 and N98 are required for HBx-binding, and T56 and L58 are needed for RAP30-binding. Interestingly the residues exposed to solvent, T111 and S113, are very close to the DNA, implying that two factors may modulate the interaction between DNA and RPB5.

Amino Acid Sequence↗

Nucleolin interacts with telomerase.

Telomerase is a specialized reverse transcriptase composed of core RNA and protein subunits which plays essential roles in maintaining telomeres in actively dividing cells. Recent work indicates that telomerase shuttles between subcellular compartments during assembly and in response to specific stimuli. In particular, telomerase colocalizes with nucleoli in normal human fibroblasts. Here, we show that nucleolin, a major nucleolar phosphoprotein, interacts with telomerase and alters its subcellular localization. Nucleolin binds the human telomerase reverse transcriptase subunit (hTERT) through interactions with its RNA binding domain 4 and carboxyl-terminal RGG domain, and this binding also involves the telomerase RNA subunit hTERC. The protein-protein interaction between nucleolin and hTERT is critical for the nucleolar localization of hTERT. These findings indicate that interaction of hTERT and nucleolin participates in the dynamic intracellular localization of telomerase complex.

Catalytic Domain↗

Mutational Analysis of Hepatitis C Virus NS5B in the Subgenomic Replicon Cell Culture.

The hepatitis C virus (HCV) NS5B is an RNA-dependent RNA polymerase (RdRP), a central catalytic enzyme of HCV RNA replication. We previously identified five novel residues of NS5B in a JK-1 isolate indispensable for RdRP activity in vitro (Qin, W., Yamashita, T., Shirota, Y., Lin, Y., Wei, W., and Murakami, S. (2001) Hepatology 33, 728-737). We addressed the role of these residues in HCV RNA replication using a HCV replicon system derived from an M1LE isolate (Kishine, H., Sugiyama, K., Hijikata, M., Kato, N., Takahashi, H., Noshi, T., Nio, Y., Hosaka, M., Miyanari, Y., and Shimotohno, K. (2002) Biochem. Biophys. Res. Commun. 293, 993-999). The five residues of NS5B in M1LE were found to be critical for HCV replication in vivo and also indispensable for RdRP activity in vitro along with purified bacterial recombinant proteins. We also found a chimeric replicon of JK-1 and M1LE in which only the NS5B sequence derived from JK-1 could not replicate in Huh-7 cells. The residues responsible for the phenomenon were mapped by several chimeric and substituted forms of NS5B M1LE and/or JK-1 isolates in the HCV RNA replicon. Two residues, amino acids 220 and 288, were critical, and two residues, amino acids 213 and 231, were important for efficient HCV replication. Mutant JK-1 NS5B harboring all four residues of M1LE was replication-competent in the chimeric replicon and was as efficient as the original M1LE replicon. By comparing the replication competence in vivo and RdRP activity in vitro with various chimeric and mutated versions of NS5B, the HCV replication ability was found to correlate well with the RdRP activity. However, heat- and dilution-sensitive NS5Bs exhibiting weaker RdRP activity in vitro were found to be replication-incompetent, suggesting that HCV replication requires RdRP activity higher than a certain critical threshold.

Amino Acid Sequence↗

Subcellular localization of RPB5-mediating protein and its putative functional partner.

We previously identified a novel cellular protein, RPB5-mediating protein (RMP), that retains corepressor activity and functionally antagonizes transcriptional modulation via hepatitis B virus X protein. The subcellular localization of RMP was examined using green fluorescent protein-fused protein forms. We found that a nuclear localization signal (NLS) and a coiled-coil (CC) domain functioning as a cytoplasmic localization signal (CLS) are important for the subcellular localization of RMP. The CLS apparently acts dominantly, since RMP was mostly localized in the cytoplasm with weak and diffuse signals in the nucleus, and the NLS was indispensable for the nuclear localization of RMP only in the absence of the CLS. Using a yeast two-hybrid method, we isolated a putative corepressor, DNA methyltransferase 1-associating protein (DMAP1), which was found to bind to the CC domain of RMP. DMAP1 facilitated the nuclear localization of RMP and the corepressor activity of RMP in a dose-dependent manner by interacting with the CC domain of RMP. These results are discussed in light of a recent paper showing a novel evolutionarily conserved role of URI in the TOR signaling pathway.

Animals↗

[Pharmacological and clinical profile of telmisartan, a selective angiotensin II type-1 receptor blocker].

Telmisartan (Micardis) is a potent, long-lasting, nonpeptide angiotensin II type-1 (AT(1)) receptor blocker (ARB) that is indicated for the treatment of essential hypertension. In receptor binding studies, telmisartan showed a high affinity and selectivity for the human AT(1) receptors compared with AT(2) receptors and a slower dissociation rate from the human AT(1) receptor than those of ARBs. In isolated aorta rings, telmisartan was shown to be an insurmountable antagonist of AII-induced contractions. The inhibitory effects of telmisartan on AII-induced contraction persisted even after wash-out procedures. In animal models such as spontaneous hypertension rats and renovascular hypertensive rats, telmisartan produced the consistent reduction of blood pressure. Furthermore, there were no rebound phenomenon and no tolerance to the drug developed in the repeated oral administration. Telmisartan has a longer terminal elimination half-life (about 24 h) than the other ARBs. In patients with mild-moderate hypertension, trough/peak ratios for telmisartan were above 80%. In Japanese patients with mild-moderate hypertension, telmisartan produced a significant reduction in blood pressure (effective rate: 76.0%) with a good safety profile. Therefore, telmisartan is expected to be effective in the treatment of hypertension, producing sustained 24-h blood pressure control.

Adult↗

Pressor response to static and dynamic knee extensions at equivalent workload in humans.

Static exercise has been thought to induce greater pressor response than dynamic exercise, but in contrast it has been recently reported that repetitive muscle contraction recruiting small muscles evokes greater response than sustained contraction. It remained unknown whether sustained contraction induces greater pressor response if large muscles were recruited. Nine subjects performed three types of isometric knee extensions recruiting the large muscle group, i.e., 2-min sustained (20% and 40% maximal voluntary contraction [MVC]) and 4-min repetitive (40% MVC, duty cycle = 1:1 s) muscle contractions. Compared under the equivalent TTI and exercising duration (2 min), the changes in femoral arterial blood flow and VO(2) from baseline (Delta BF, Delta VO(2)) were significantly less during sustained contraction than during repetitive contraction (sustained vs. repetitive; Delta BF: +92 +/- 195 vs. +1,174 +/- 269 ml.min(-1), Delta VO(2): +53 +/- 12 vs. +180 +/- 32 ml.min(-1), mean +/- SE, p < 0.05), although the change in mean arterial pressure (Delta MAP) was greater during sustained contraction (+24 +/- 3 vs. +19 +/- 3 mmHg). Compared under the equivalent TTI and peak tension (40% MVC), Delta BF and Delta VO(2) were less and Delta MAP was greater during sustained contraction (Delta BF: -296 +/- 176 vs. +868 +/- 272 ml.min(-1); Delta VO(2): +104 +/- 16 vs. + 212 +/- 46 ml.min(-1); Delta MAP: +37 +/- 8 vs. +20 +/- 4 mmHg). Moreover Delta MAP during postexercise occlusion of the active limb was significantly greater after sustained contraction than after repetitive contraction (+17.0 +/- 2.8 vs. +9.5 +/- 4.4 mmHg). These results demonstrated that pressor response is greater during sustained than during repetitive contraction, recruiting a large muscle group. This finding should be mainly due to the greater accumulation of metabolites in active muscles during sustained contraction.

Adult↗

Facial cooling-induced bradycardia does not slow pulmonary V.O2 kinetics at the onset of high-intensity exercise.

The mechanism(s) underlying the attenuation of the slow component of pulmonary O2 uptake (Vo2) by prior heavy-intensity exercise is (are) poorly understood but may be ascribed to either an intramuscular-metabolic or a circulatory modification resulting from "priming" exercise. We investigated the effects of altering the circulatory dynamics by delayed vagal withdrawal to the circulation induced by the cold face stimulation (CFS) on the Vo2 kinetics during repeated bouts of heavy-intensity cycling exercise. Five healthy subjects (aged 21-43 yr) volunteered to participate in this study and initially performed two consecutive 6-min leg cycling exercise bouts (work rate: 50% of the difference between lactate threshold and maximal Vo2) separated by 6-min baseline rest without CFS as a control (N1 and N2). CFS was then applied separately, by gel-filled cold compresses to the face for 2-min spanning the rest-exercise transition, to each of the first bout (CFS1) or second bout (CFS2) of repeated heavy-intensity exercise. In the control protocol, Vo2 responses in N2 showed a facilitated adaptation compared with those in N1, mainly attributable to the reduction of slow component. CFS application successfully slowed and delayed the heart rate (HR) kinetics (P < 0.05) on transition to exercise [HR time constant; N1: 55.6 +/- 16.0 (SD) vs. CFS1: 69.0 +/- 12.8 s and N2: 55.5 +/- 11.8 vs. CFS2: 64.0 +/- 17.5 s]; however, it did not affect the "primary" Vo2 kinetics [Vo2 time constant; N1: 23.7 +/- 7.9 (SD) vs. CFS1: 20.9 +/- 3.8 s, and N2: 23.3 +/- 10.3 vs. CFS2: 17.4 +/- 6.3 s]. In conclusion, increased vagal withdrawal delayed and slowed the circulatory response but did not alter the Vo2 kinetics at the onset of supra-lactate threshold cycling exercise. As the facilitation of Vo2 subsequent to prior heavy leg cycling exercise is not attenuated by slowing the central circulation, it seems unlikely that this facilitation is exclusively determined by a blood flow-related mechanism.

Adult↗

Exercise pressor reflex in decerebrate and anesthetized rats.

I investigated whether muscular contraction evokes cardiorespiratory increases (exercise pressor reflex) in alpha-chloralose- and chloral hydrate-anesthetized and precollicular, midcollicular, and postcollicular decerebrated rats. Mean arterial pressure (MAP), heart rate (HR), and minute ventilation (Ve) were recorded before and during 1-min sciatic nerve stimulation, which induced static contraction of the triceps surae muscles, and during 1-min stretch of the calcaneal tendon, which selectively stimulated mechanosensitive receptors in the muscles. Anesthetized rats showed various patterns of MAP response to both stimuli, i.e., biphasic, depressor, pressor, and no response. Sciatic nerve stimulation to muscle in precollicular decerebrated rats always evoked spontaneous running, so the exercise pressor reflex was not determined from these preparations. None of the postcollicular decerebrated rats showed a MAP response or spontaneous running. Midcollicular decerebrated rats consistently showed biphasic blood pressure response to both stimulations. The increases in MAP, HR, and Ve were related to the tension developed. The static contractions in midcollicular decerebrated rats (381 +/- 65 g developed tension) significantly increased MAP, HR, and Ve from 103 +/- 12 to 119 +/- 24 mmHg, from 386 +/- 30 to 406 +/- 83 beats/min, and from 122 +/- 7 to 133 +/- 25 ml/min, respectively. After paralysis, sciatic nerve stimulation had no effect on MAP, HR, or Ve. These results indicate that the midcollicular decerebrated rat can be a model for the study of the exercise pressor reflex.

Anesthetics↗