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• W1498348401 abstract "Exaggerated cardiovascular responses to stress increase risk for hypertension and cardiovascular disease, but the mechanisms controlling the magnitude of this response are not understood. Catecholaminergic neurons located in the hindbrain area termed the nucleus of the solitary tract (NTS) modulate the control of blood pressure and are activated by psychological stress, but their role in modulating the cardiovascular response to stress is unknown. In this study we lesioned these NTS catecholaminergic neurons and measured the cardiovascular and hormonal responses to psychological stress in rats. We showed that lesioning these neurons increases baseline blood pressure and causes an exaggerated blood pressure response to acute or repeated psychological stress, suggesting that physiological or pathophysiological inhibition of these neurons could lead to exaggerated stress responses and hypertension. These results help us understand the mechanisms that contribute to enhanced cardiovascular responses to psychological stress. Abstract Catecholaminergic neurons within the central nervous system are an integral part of stress-related neurocircuitry, and the nucleus of the solitary tract (NTS) plays a critical role in cardiovascular regulation. We tested the hypothesis that NTS catecholaminergic neurons attenuate psychological stress-induced increases in blood pressure and promote neuroendocrine activation in response to psychological stress. Anti-dopamine-β-hydroxylase antibody conjugated to the neurotoxin saporin (DSAP) or saline vehicle was microinjected into the NTS to lesion catecholaminergic neurons in male Sprague–Dawley rats, and 17 days later the rats were subjected to 60 min of restraint stress for five consecutive days. DSAP treatment significantly enhanced the integrated increase in mean arterial pressure during restraint on the first (800 ± 128 and 1115 ± 116 mmHg (min) for saline- and DSAP-treated rats) and fifth days (655 ± 116 and 1035 ± 113 mmHg (min) for saline- and DSAP-treated rats; P < 0.01 for overall effect of DSAP treatment) of restraint. In contrast, after 60 min of restraint plasma corticosterone concentration was significantly lower in DSAP-treated compared with saline-treated rats (25.9 ± 7 compared with 46.8 ± 7 μg dl−1 for DSAP- and saline-treated rats; P < 0.05). DSAP treatment also significantly reduced baseline plasma adrenaline concentration (403 ± 69 compared with 73 ± 29 pg ml−1 for saline- and DSAP-treated rats), but did not alter the magnitude of the adrenaline response to restraint. The data suggest that NTS catecholaminergic neurons normally inhibit the arterial pressure response, but help maintain the corticosterone response to restraint stress. Noradrenergic and adrenergic neurotransmission within the brain can modulate the cardiovascular, neuroendocrine, behavioural and metabolic responses to psychological stress (Koepke & DiBona, 1986; Pacak et al. 1995; Morilak et al. 2005; Rauls et al. 2005; Ritter et al. 2006; Rinaman, 2007). Previous work indicates that neuronal cell bodies which synthesize noradrenaline and adrenaline are found in a limited number of brain regions, all of which are involved in cardiovascular regulation. These regions include the A2 noradrenergic and C2 adrenergic neurons within the nucleus of the solitary tract (NTS), the A5 noradrenergic neurons in the ventrolateral pons and the A1 noradrenergic and C1 adrenergic neurons of the ventral medulla (Sawchenko & Swanson, 1982; Nieuwenhuys, 1985; Cunningham & Sawchenko, 1988). Lesioning the A5 and C1 neurons does not modulate the cardiovascular response to psychological stress such as restraint (Vianna & Carrive, 2010). However, the contribution of NTS catecholaminergic neurons to this response is unknown. NTS catecolaminergic neurons are activated in response to both physiological (systemic) and psychological (emotional) stressors (Pacak et al. 1995; Dayas et al. 2001a), and could influence the physiological response to stress by way of projections to forebrain regions including the paraventricular nucleus and the amygdala (Cunningham & Sawchenko, 1988; Riche et al. 1990). The physiological response to stress includes increases in blood pressure, heart rate, sympathetic nerve activity and circulating catecholamines, and activation of the hypothalamic–pituitary–adrenal (HPA) axis leading to increases in glucocorticoids (cortisol and corticosterone) (Pacak et al. 1995). NTS neurons can mediate the stress-induced activation of the HPA axis when the stress is physiological or systemic in nature (Ulrich-Lai & Herman, 2009). It is also possible that they contribute to HPA axis activation in response to a psychological stress, but this remains unconfirmed (Dayas et al. 2001b; Ulrich-Lai & Herman, 2009). Silencing NTS catecholaminergic neurons leads to an increase in baseline blood pressure, indicating that these neurons exert a tonic inhibitory influence on blood pressure (Duale et al. 2007); whether they also inhibit the cardiovascular response to psychological stress is unknown. The present study tested the hypothesis that NTS catecholaminergic neurons inhibit psychological stress-induced increases in blood pressure and heart rate and promote neuroendocrine activation in response to psychological stress. NTS catecholaminergic neurons were lesioned using an anti-dopamine-β-hydroxylase antibody conjugated to the neurotoxin saporin (DSAP), an established, selective and effective method to lesion noradrenaline- and adrenaline-synthesizing neurons within selected brain regions including the NTS (Wrenn et al. 1996; Madden et al. 1999; Rinaman & Dzmura, 2007). Rats were subsequently subjected to restraint stress on five consecutive days, which is categorized as a psychological stress in rats (Dayas et al. 2001a). All animal housing, handling, surgical and experimental procedures were conducted within an Association for the Assessment and Accreditation of Laboratory Care (AALAC) internationally accredited animal care facility at the University of Florida, in accordance with the USA's Public Health Service Policy on Humane Care and Use of Laboratory Animals and the National Institutes of Health's Guide for the Care and Use of Laboratory Animals. The Institutional Animal Care and Use Committee of the University of Florida approved all animal housing, handling and surgical and experimental procedures. Experiments were performed in 52 adult male Sprague–Dawley rats purchased from Charles River Laboratories at 275–300 g. Rats were housed in a Specific Pathogen Free animal care facility with a 12:12 h light–dark cycle. All experimental and surgical procedures were conducted within the AALAC-accredited animal care facility. General All surgical procedures were performed using a mixture of oxygen (1 litre min−1) and isoflurane (5% for induction and 2–3% for maintenance). Carprofen (5 mg kg−1, s.c.; Pfizer Inc., New York) and penicillin G were administered (s.c.) prior to surgery. Carprofen (5 mg kg−1 day−1, s.c.) was administered for 2 days after major surgery and for 1 day following femoral catheter implantation. The rats were returned to their home cages upon full recovery from anaesthesia. Implantation of telemetry transducers Telemetry transducers for the measurement of arterial pressure, heart rate and activity (model PA-C40, Data Sciences International, St Paul, MN, USA) were implanted into the descending aorta via a midline abdominal incision. The aorta was isolated and briefly occluded, and the tip of the catheter was inserted using a 21-gauge needle. Surgical glue (3M Vetbond Tissue Adhesive) and a nitrocellulose patch were applied to secure the catheter in place. The transducer was sutured to the abdominal muscle and the incision closed in layers. NTS microinjection Anti-dopamine-β-hydroxylase conjugated to saporin (DSAP) is an immunotoxin that can be used to selectively lesion catecholaminergic neurons (Wrenn et al. 1996; Madden et al. 1999; Rinaman & Dzmura, 2007). DSAP (Advanced Targeting Systems, San Diego, CA, USA) was diluted to a working concentration of 0.22 ng nl−1 in 0.1 m sterile phosphate buffered saline (pH 7.4). Rats were anaesthetized and placed in a stereotaxic frame with the head ventroflexed at an angle of approximately 40o to allow for surgical exposure of the dorsal surface of the hindbrain. Bilateral microinjections were made with a glass micropipette (1.2/0.68 mm OD/ID, World Precision Instruments Inc., Sarasota, FL, USA) pulled to obtain a tip diameter of 30–50 μm. The micropipette tip was positioned at calamus scriptorius (rostral–caudal), 250 μm lateral to midline, and 500 μm ventral to the dorsal surface of the medulla. These coordinates were selected to target the region of the NTS that expresses c-Fos in response to restraint stress (Dayas et al. 2001a). DSAP (22 ng in 100 nl) or sterile 0.9% saline (100 nl) was delivered bilaterally into NTS by micro syringe pump over 60 s (Stoelting Co., Wood Dale, IL, USA). The incision was sutured closed. Rats continued to gain weight following the surgery, and body weight at the conclusion of the studies averaged 467 ± 6 g and 481 ± 11 g for saline- and DSAP-treated rats, respectively. Arterial catheter implantation Indwelling arterial catheters were implanted to obtain blood samples for the measurement of plasma corticosterone and catecholamine concentrations. A small skin incision was made and a Teflon-tipped catheter was introduced into the femoral artery, and then advanced to the descending aorta. The catheter was tunnelled subcutaneously to exit between the scapulae, sutured in place, filled with sterile heparin (1000 U ml−1), and closed with a sterile plug. The incision was sutured in layers. Protocol 1: immunohistochemistry to characterize the efficacy of DSAP Microinjection of saline (n= 6) or DSAP (n= 7) was performed as described above, except that three of the DSAP-treated rats received a higher dose of DSAP (27.5 ng in 125 nl per side). Rats were humanely killed 23–26 days later and the brain tissue processed for immunohistochemistry as described below. Protocol 2: cardiovascular data Rats recovered from the telemetry surgery for a minimum of 2 weeks, and then control baseline arterial pressure and heart rate measurements were recorded for 7 days. NTS microinjections were performed on day 8 (saline n= 12, DSAP n= 12), and then the animals were subjected to 60 min of restraint stress on days 21–25. Restraint stress was performed in the morning between 08.00 and 12.00 h and consisted of placing each rat in a Plexiglas tube that provided ample circulation of air. Protocol 3: neuroendocrine data A second set of experiments was performed to determine if lesioning NTS catecholaminergic neurons also modulates the neuroendocrine response to restraint stress. Since DSAP had similar effects on the arterial pressure response to restraint on the first and fifth days of restraint, the neuroendocrine response was determined only for day 1 of stress (novel restraint). NTS microinjections were performed on day 1 (saline n= 8, DSAP n= 7), arterial catheters were implanted on day 13, and then the animals were subjected to 60 min of restraint stress on day 17. Blood samples (600 μl each) for the measurement of plasma corticosterone, adrenaline and noradrenaline were obtained 5 min prior to restraint and at 10 and 60 min of restraint. The volume was replaced with sterile isotonic saline after each sample was obtained. Samples were drawn while the rat remained in his home cage by connecting the arterial catheter to a long piece of tubing at least 2 h prior to the collection of any blood. Thus, the rats could move freely (except while restrained) and were unaware of the sampling procedure. Blood samples were aliquoted into separate tubes containing either 0.5 μl of heparin for measurement of corticosterone or 6 μl of glutathione-EGTA for measurement of catecholamines. The samples were kept on ice then centrifuged at 4°C, and the plasma was stored at −80°C until being assayed. Immunohistochemistry All DSAP-treated rats, all the saline-treated rats from protocol 1, and five of the saline-treated rats from protocols 2 and 3 were deeply anaesthetized with isoflurane and perfused with ice cold 0.1 m phosphate-buffered saline (PBS; pH 7.4) followed with 4% paraformaldehyde. The remaining saline-treated rats were humanely killed with an overdose of isoflurane and death was then ensured with a bilateral thoracotomy. Perfused brains were post-fixed in 4% paraformaldehyde and cryoprotected in 30% sucrose. The hindbrains were sectioned at 40 μm and deposited in series into four wells, then stored in cryoprotectant at −20°C. Brains from protocols 2 and 3 were sectioned from approximately −14.6 mm through −12.8 mm relative to Bregma while brains from protocol 1 were sectioned from approximately −14.6 mm through −8.8 mm relative to Bregma (Paxinos & Watson, 1998). Immunohistochemical labelling of dopamine-β-hydroxlase (DβH) was performed on brain sections from protocols 2 and 3 to determine the adequacy of the lesion within the NTS and to verify that catecholaminergic neurons in the corresponding ventrolateral medulla (VLM) remained intact (Rinaman & Dzmura, 2007). Brains from protocol 1 were also used to determine if microinjection of DSAP into the NTS affected the number of catecholaminergic neurons in the rostral ventrolateral medulla (RVLM), the A5 region or the locus coeruleus. Free-floating sections were incubated with a mouse anti-DβH primary antibody (1:1000 or 1:5000, Millipore, Billerica, MA, USA) for 24 to 48 h at 4°C. Sections were then incubated with biotinylated goat anti-mouse secondary antibody and the signal was visualized using avidin–biotin complex and 3,3′-diaminobenzidine substrate (Vectastain Elite ABC kit and DAB substrate kit for peroxidase, Vector Laboratories, Burlingame, CA, USA) to produce a brown reaction product. The selectivity of DSAP for catecholaminergic neurons was verified by determining the effect of DSAP on 11β-hydroxysteroid dehydrogenase (11βHSD2)-positive neurons in the NTS, as these neurons are adjacent to the catecholaminergic neurons (Geerling et al. 2006). Hindbrain sections were mounted on slides, incubated with a sheep anti-11βHSD2 primary antibody (1:30,000, Millipore, Billerica, MA, USA) for 48 h at 4°C, followed by a fluorophore-conjugated donkey anti-sheep secondary antibody (DyLite 488, Jackson ImmunoResearch Laboratories, Inc., West Grove, PA, USA). This antibody sometimes produces non-specific nuclear staining, so only neurons with cytoplasmic and dendritic staining were counted (Geerling et al. 2006). Immunohistochemistry for choline acetyltransferase was also performed on sections from two rats to confirm previous reports that the cholinergic neurons in the adjacent dorsal motor nucleus of the vagus were not lesioned by the catecholamine-specific neurotoxin (Wrenn et al. 1996). These sections were incubated for 40–48 h at 4°C in rabbit anti-choline acetyltransferase antibody (1:400, Millipore), and then processed as described above for DβH. To count DβH-positive neurons, photomicrographs were obtained using an Olympus BX41 system microscope and DP71 digital camera (Olympus America, Melville, NY, USA). Images of the NTS and ventrolateral medulla were taken at 100× total magnification at three rostral to caudal levels (approximately at calamus scriptorius and 0.5 mm rostral and 0.4 mm caudal to this anatomical landmark according to the atlas of Paxinos & Watson (1998). DβH-positive neuronal cell bodies were counted bilaterally at all three levels in each rat. DSAP-treated rats were considered to be significantly lesioned if no more than 70% of the DβH-positive neurons remained in the NTS compared with the average number of neurons present in the saline-treated animals. The caudal ventrolateral medulla (CVLM) was considered intact if at least 70% of the neurons were present in DSAP-treated rats compared with the average number of neurons present in the saline-treated animals. DβH-positive neurons were also counted bilaterally in the RVLM (Bregma −12.7 mm), the A5 region (Bregma −10.0 and −9.7 mm) and the locus coeruleus (Bregma −9.7 mm). All locations relative to Bregma are approximate, based on Paxinos & Watson (1998). Photomicrographs were taken of all sections with 11βHSD2-positive neurons in rats from protocol 1. The total number of 11βHSD2-positive neurons in the three sections with the largest number of 11βHSD2-positive neurons in each rat was determined. Hormone assays Plasma corticosterone was measured using a commercially available double antibody 125I radioimmunoassay kit (MP Biomedicals, Solon, OH, USA). Plasma adrenaline and noradrenaline were measured by HPLC by the Vanderbilt University Hormone Assay and Analytical Services Core (Nashville, TN, USA). Data acquisition and analysis Arterial pressure (mmHg) and heart rate (beats min−1) data were collected for 20 s every 10 min for 24 h per day, except for the 2 h periods beginning 30 min prior to restraint stress on the first and last days of stress during which time data were collected continuously at 500 Hz. Twenty-four hour baseline mean arterial pressure and heart rate values were averaged into hourly bins and divided into daytime (light) and nighttime (dark) periods for analysis. Arterial pressure and heart rate values during periods of restraint were excluded from the analysis of the 24 h baseline data shown in Fig. 3. Mean arterial pressure and heart rate responses to stress were calculated as follows. Data were averaged into 5 min bins starting at 30 min prior to restraint and continuing through to 30 min after the termination of stress. The average baseline value was calculated during the 30 min prior to stress, excluding the final 3 min. Periods during which the telemetry system recorded animal movement were excluded from the baseline data. The average baseline was then subtracted from the values measured during the 60 min of stress and the 30 min recovery period following stress. Average results are expressed as means ± SEM. The 30 min baseline data prior to stress were also used for determination of spontaneous baroreflex sensitivity and spectral analysis of blood pressure and heart rate variability using the freely available HemoLab software (http://www.haraldstauss.com/HemoLab/HemoLab.html). Blood pressure data for the baseline periods preceding restraint stresses 1 and 5 were visually inspected and artifact-free segments of at least 10 min duration were extracted. Sampling rate of the datasets was increased to 1000 Hz using spline interpolation as described by Bhatia et al. (2010). The gain of the baroreceptor reflex was determined using the sequence technique. Sequences were defined as a minimum of three consecutive (beat-by-beat) increases or decreases in systolic blood pressure that were associated with simultaneous changes in pulse interval. Sequences with increases and decreases in systolic blood pressure were pooled. No threshold for changes in systolic blood pressure or pulse interval was used. Only sequences with a correlation coefficient of >0.8 for the linear correlation between systolic blood pressure and pulse interval were included in the analysis, and the slope of the linear correlation was taken as the gain of the baroreceptor reflex (Bhatia et al. 2010). Baseline mean arterial pressure (A) and heart rate (B) measured 24 h per day and divided into the light and dark periods Bilateral NTS microinjections of saline (filled squares and continuous lines) or DSAP (open triangles and dashed lines) were performed on day 8, and rats were subjected to daily restraint stress on days 21–25. Data for day 25 are not shown because the experiments ended after the morning stress on that day. †P≤ 0.05 compared with the baseline control period for saline-treated rats. *P≤ 0.05 compared with the pre-stress period for saline-treated rats. ‡P≤ 0.05 compared with the baseline control period for DSAP-treated rats. Statistical significance was evaluated using one-way or two-way ANOVA as appropriate (SPSS software, IBM). Linear regression analysis was performed to determine the relationship between the number of DβH-positive NTS neurons and the integrated increase in mean arterial pressure in response to 60 min of restraint stress in the DSAP-treated rats. Post hoc analyses were performed using Duncan's test. When multiple one-way ANOVA was required due to significant interactions between main effects, a Bonferroni adjustment was used. Differences were considered significant at P < 0.05. Two saline-treated rats from protocol 2 were removed from the study because the quality of the signal from the telemetry transmitter diminished following the microinjection such that average pulse pressure fell below 25 mmHg, and stress data from one rat were removed due to loss of a good signal during stress. Data from three saline-treated rats are not included in the 24 h results because of a power failure that resulted in the loss of several days’ worth of data. Two DSAP-treated rats from protocol 2 had insufficient NTS lesions (greater than 70% of cells remaining) and their data were excluded from the analyses, except for the linear regression analysis described above. Data from one animal were excluded from protocol 2 due to substantial (>70%) loss of VLM neurons. The plasma sample for the measurement of plasma catecholamines in one DSAP-treated animal was lost during processing. Microinjection of the low dose of DSAP (22 ng per side) significantly reduced the number of DβH-positive neurons at all levels of the NTS by 87%, while the higher dose (27.5 ng per side) caused a reduction of 97% (Table 1). The low dose of DSAP did not reduce the average number of DβH-positive neurons in the VLM, while the high dose reduced the number by 28% (Table 1). Low dose DSAP had no effect on the number of DβH-positive neurons in the RVLM or locus coeruleus, but significantly reduced the number of such neurons in the A5 region by 30% (Table 2 and Fig. 1). High dose DSAP significantly reduced DβH-positive neurons in all three regions (Table 2). Neither dose of DSAP diminished the number of 11βHSD2-positive neurons in the NTS; neuronal counts were 45 ± 3, 42 ± 6 and 46 ± 7 for saline-, low dose DSAP- and high dose DSAP-treated rats, respectively (see Fig. 1 for sample photomicrographs). Example photomicrographs from saline-treated (A, C, E and G) and DSAP-treated (B, D, F and H) rats for labelling of 11βHSD2-positive neurons in the NTS (A and B), or the DβH-positive neurons in the RVLM (C and D), locus coeruleus (E and F) or A5 region (G and H) As in Protocol 1, microinjection of DSAP (22 ng per side) significantly reduced the total number of DβH-positive neurons (Fig. 2, Table 3). Conversely, the number of DβH-positive neurons in the ventrolateral medulla was not altered by DSAP treatment (Fig. 2, Table 3). Cholinergic neurons appeared to be unaffected by the DSAP treatment as has been previously reported (data not shown) (Wrenn et al. 1996). DβH-positive NTS (A and B) and ventrolateral medulla (C and D) neurons in a saline-treated rat (A and C) and a DSAP-treated rat (B and D) The scale bars represent 200 μm. Average baseline mean arterial pressure during the control period prior to the microinjection of saline or DSAP (days 1–7, Fig. 3A) was not different between treatment groups (101 ± 1 mmHg and 106 ± 2 mmHg, P= 0.11, for the saline- and DSAP-treated rats, respectively, during the light period, with corresponding values of 106 ± 1 and 108 ± 2 mmHg, P= 0.23, during the dark period). Analysis of mean arterial pressure over the time course of the experiment revealed a significant interaction between time and treatment, so one-way ANOVA with a Bonferroni adjustment for multiple means comparisons was performed separately on each treatment group. Saline treatment alone (prior to any stress) had no significant effect on baseline blood pressure, while DSAP significantly increased mean arterial pressure during both the light period (P= 0.038) and the dark period (P= 0.04). Repeated restraint stress significantly increased average baseline mean arterial pressure in saline-treated rats during the light period on days 23–24, and tended to increase baseline mean arterial pressure by day 24 during the dark period, but the change was not statistically significant (P= 0.08). In contrast, repeated stress did not further increase baseline blood pressure in DSAP-treated rats. Baseline heart rate fell significantly during the 7 day control period during both the light and dark periods, so days 5–7 were used to represent baseline control values. Average baseline heart rate during the control period prior to the microinjection of saline or DSAP (days 5–7, Fig. 3B) was not significantly different between treatment groups (359 ± 3 mmHg and 368 ± 9 mmHg, P= 0.46, for the saline- and DSAP-treated rats, respectively, during the light period, with corresponding values of 419 ± 2 and 398 ± 9 mmHg, P= 0.09, during the dark period). Average baseline heart rate during the light period was similar in saline- and DSAP-treated rats throughout the experimental protocol, and there were no significant changes in heart rate relative to the control (days 5–7) or pre-stress (days 18–20) periods. (Fig. 3B). Baseline heart rate during the dark period decreased over time during the experiment in the saline-treated rats, and was significantly lower compared with both the control period and the pre-stress period on days 22–24. There was no significant change in heart rate over time in the DSAP-treated rats. During the 30 min prior to stress, baseline mean arterial pressure was significantly higher (P= 0.02) in DSAP-treated rats (108 ± 2 and 107 ± 2 mmHg on days 21 and 25, respectively, n= 9) compared with saline-treated rats (103 ± 2 and 102 ± 2 mmHg on days 21 and 25 respectively, n= 9). Sixty minutes of restraint stress significantly raised mean arterial pressure in all rats, but the magnitude of the increase was significantly greater in DSAP- compared with saline-treated rats from minutes 15–55 of the stress period, with no significant difference between day 1 and day 5 (P < 0.01, Fig. 4A). The total integrated increase in mean arterial pressure during stress was 800 ± 128 and 655 ± 116 mmHg (min) on days 21 and 25, respectively, for saline-treated rats and 1115 ± 116 and 1035 ± 113 mmHg (min) for DSAP-treated rats. DSAP treatment had an overall effect to enhance the arterial pressure response to stress (P < 0.01) with no significant effect of time (Day 1 compared with Day 5, P= 0.35) and no significant interaction between DSAP treatment and time (P= 0.78). Recovery from stress was assessed during the 30 min period immediately following the period of restraint. Blood pressure during the recovery period was significantly greater in DSAP- compared with saline-treated rats (P= 0.048, Fig. 4A). The total integrated increase in mean arterial pressure during the recovery period was 293 ± 48 and 361 ± 51 mmHg (min) on days 21 and 25 respectively for saline-treated rats and 419 ± 65 and 476 ± 68 mmHg (min) for DSAP-treated rats. The blood pressure increase during the recovery period was significantly greater on day 25 compared with day 21 for the first 10 min of the recovery period in both saline- and DSAP-treated rats. Changes in mean arterial pressure (MAP; A) and heart rate (HR) in beats per minute (bpm; B) in response to 60 min of restraint stress and 30 min of recovery from stress on the first day (Day 21, left) and last day (Day 25, right) of repeated stress in saline-treated (continuous lines and squares) and DSAP-treated (dashed lines and open circles) rats DSAP-mediated lesioning of NTS catecholaminergic neurons significantly enhanced the arterial pressure responses to stress and stress recovery (*P < 0.05). There were no effects of DSAP on the heart rate response to stress (B). The blood pressure and heart rate responses during the first 10 min of the recovery period were greater on day 25 compared with day 21 (†P < 0.05). Baseline heart rate during the 30 min prior to stress was similar in DSAP-treated rats (356 ± 11 and 337 ± 9 beats min−1 on days 21 and 25, respectively) compared with saline-treated rats (358 ± 7 and 336 ± 5 beats min−1 on days 21 and 25, respectively), but fell significantly between the first and fifth days of repeated restraint (P= 0.02). There were no effects of DSAP on the heart rate increase during either the stress (P= 0.09; Fig. 4B) or recovery period (P= 0.83). The heart rate response during the first 10 min of the recovery period was greater on day 25 compared with day 21. Spontaneous baroreflex sensitivity and spectral analysis of heart rate and blood pressure variability were assessed during the 30 min baseline period prior to the first and fifth stresses. There were no effects of either DSAP or stress on resting spontaneous baroreflex sensitivity (Fig. 5A). DSAP also failed to influence the power of the very low and low frequency components of blood pressure variability, but repeated stress reduced power in both frequency components regardless of treatment (Fig. 5B and C). DSAP had no significant effect on the low frequency component of heart rate variability, but it increased the power of the high frequency range prior to the first stress (P= 0.04). Repeated stress decreased the power of low and high frequency components in both the saline and DSAP groups (Fig. 5D and E). The ratio of low to high frequency power for heart rate variability was not affected significantly either by DSAP or stress (Fig. 5F). Spontaneous baroreceptor reflex (BRR) sensitivity determined by the sequence method (A), spectral analysis of blood pressure variability (BPV: B: very low frequency component, VLF; C:" @default.
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• W1498348401 title "Nucleus of the solitary tract catecholaminergic neurons modulate the cardiovascular response to psychological stress in rats" @default.
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