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Biomedical subjects

D Laude

Publications and source records attributed to D Laude.

At least 37 records · Page 2Linked to original sources
PubMed1999

Effects of an auditory startle stimulus on blood pressure and heart rate in humans.

OBJECTIVE: To describe the effects of an auditory startle stimulus on blood pressure (BP) and heart rate (HR) in humans. DESIGN AND METHODS: Twenty-five volunteers, including nine untreated hypertensive subjects, were studied in the supine position. Polygraphic recordings were obtained for finger BP, R-R interval using ECG, respiratory movements using a thoracoabdominal belt and for electrooculomyogram using adhesive electrodes. Haemodynamic estimations were derived by modelling flow from the noninvasive BP signal. A background noise of 55 dB was administered through headphones and two acoustic startle stimuli (110 dB, 1-20 kHz, 0.15 s) were generated at 5-min intervals during the tele-expiratory phase. The sham stimulation (0 dB, event marker) was compared with the effects of the noise stimulus (one-way ANOVA with repeated measures followed by a protected t test for multiple comparisons). RESULTS: A biphasic cardiovascular profile was observed in response to noise stimulation. Blood pressure and HR increases were combined in the early response (0-10 s) observed after the immediate motor contraction (blink). The average systolic BP rise was 18.7+/-2.7 mmHg (peak at 5.1 s) and the average HR increase was 10.8+/-1.1 bpm (peak at 3.4 s) for the first stimulus. These effects were highly significant compared with the sham response (P < 0.01). The second stimulus elicited BP and HR rises of a lesser amplitude (P < 0.01). The delayed response (10-30 s) corresponded with a moderate BP decrease. The haemodynamic indexes suggest that the early rise in blood pressure reflects a rise in total peripheral resistance. CONCLUSION: This is the first description of the BP response to an acute loud noise in humans. The early (within 10 s) BP and HR rises may depend upon the autonomic component of the startle reflex. One application of this test could be the discrimination of the different classes of antihypertensive drugs according to their sites of action.

Acoustic Stimulation↗
PubMed1999

Short-term variability of blood pressure and heart rate in Guillain-Barré syndrome without respiratory failure.

The effect of Guillain-Barré syndrome (GBS) on the short-term variability of blood pressure and heart rate was evaluated in six patients presenting with a moderate form of the syndrome, i.e. unable to stand up unaided and without respiratory failure, at the height of the disease and during recovery. The patients were compared with six age-matched healthy volunteers. During the acute phase of the syndrome, GBS patients exhibited a significant heart rate elevation (+26 beats/min compared with healthy subjects), but the acceleratory response to atropine, or to 60 degrees head-up tilt, was maintained. Resting plasma noradrenaline levels were high in acute GBS, but the secretory response to tilt was preserved. Desensitization to noradrenaline was observed in acute GBS with a reduced pressor action of this alpha-adrenoceptor agonist. Blood pressure levels were normal and head-up tilt did not induce orthostatic hypotension in this moderate form of GBS. Power spectral analysis demonstrated marked alterations in cardiovascular variability. The overall heart period variability was markedly reduced with the reduction predominantly in the high-frequency (respiratory) range (-73%). The low-frequency component of heart period variability was also reduced (-54%). This cardiovascular profile of moderate GBS at the height of the disease could result from a demyelination of the reflex loop controlling respiratory oscillations in heart rate and from a desensitization of the arterial tree to an elevated plasma noradrenaline. Sympathetic nervous activation may contribute to the high resting heart rate in acute GBS.

Acute Disease↗
PubMed1999

Pulse rate variability is not a surrogate for heart rate variability.

To investigate the differences between heart rate (HR) variability and pulse rate (PR) variability, short-term variability of finger pulse wave and ECG signals were studied in 10 children with a fixed ventricular pacemaker rhythm (80 beats/min). Ten healthy children in sinus rhythm served as a reference population. Distal PR and HR were measured continuously using a Finapres device and an ECG respectively. Power spectra for HR and PR were calculated in both the supine and orthostatic positions. In paced subjects, PR spectra exhibited the characteristic respiratory peak, although the HR spectra were flat. Similarly, in healthy children the respiratory fluctuations were more pronounced when calculated from the finger pulse wave signal compared with the ECG signal. The overestimation of HR respiratory fluctuation resulting from distal PR measurement was more pronounced in the standing position; however, this postural effect was demonstrated only in healthy subjects. We observed mechanical respiratory modulation of distal PR independent of classical HR modulations. Our results suggest a mechanical respiratory influence via cardiac output and aortic transmural pressure changes on pulse wave velocity. We conclude that respiratory PR variability does not precisely reflect respiratory HR variability in standing healthy subjects and in patients with low HR variability. Consequently, HR modulation should be studied using the ECG signal rather than the distal pulse wave signal. However, when ECG recording is not available, the distal pulse wave is an acceptable alternative.

Adolescent↗
PubMed1998

Contribution of the autonomic nervous system to blood pressure and heart rate variability changes in early experimental hyperthyroidism.

A great deal of uncertainty persists regarding the exact nature of the interaction between autonomic nervous system activity and thyroid hormones in the control of heart rate and blood pressure. We now report on thyrotoxicosis produced by daily intraperitoneal (i.p.) injection of L-thyroxine (0.5 mg/kg body wt. in 1 ml of 5 mM NaOH for 5 days). Control rats received i.p. daily injections of the thyroxine solvent. In order to estimate the degree of autonomic activation in hyperthyroidism, specific blockers were administered intravenously: atropine (0.5 mg/kg), prazosin (1 mg/kg), atenolol (1 mg/kg) or the combination of atenolol and atropine. A jet of air was administered in other animals to induce sympathoactivation. Eight animals were studied in each group. The dose and duration of L-thyroxine treatment was sufficient to induce a significant degree of hyperthyroidism with accompanying tachycardia, systolic blood pressure elevation, increased pulse pressure, cardiac hypertrophy, weight loss, tachypnea and hyperthermia. In addition, the intrinsic heart period observed after double blockade (atenolol + atropine) was markedly decreased after treatment with L-thyroxine (121.5+/-3.6 ms vs. 141.2+/-3.7 ms, P < 0.01). Of the autonomic indices, vagal tone (difference between heart period obtained after atenolol and intrinsic heart period) was negatively linearly related to intrinsic heart period (r = 0.71, P < 0.05). Atenolol modified neither the heart period nor blood pressure variability in rats with hyperthyroidism and in these rats the jet of air did not significantly affect the heart period level. The thyrotoxicosis was associated with a reduction of the 0.4 Hz component of blood pressure variability (analyses on 102.4 s segments, modulus 1.10+/-0.07 vs. 1.41+/-0.06 mm Hg, P < 0.01) and prazosin was without effect on this 0.4 Hz component in these animals. These data show a functional diminution of the vascular and cardiac sympathetic tone in early experimental hyperthyroidism. The marked rise in the intrinsic heart rate could be the main determinant of tachycardia. The blood pressure elevation may reflexly induce vagal activation and sympathetic (vascular and cardiac) inhibition.

Adrenergic alpha-Antagonists↗
PubMed1998

Autonomic contribution to the blood pressure and heart rate variability changes in early experimental hyperthyroidism.

OBJECTIVE: To study the interaction between autonomic nervous activity and thyroid hormones in the control of heart rate (HR) and blood pressure (BP). DESIGN AND METHODS: Thyrotoxicosis was produced by injections of L-thyroxine (0.5 mg/kg/day for five days). Blockers were atropine (0.5 mg/kg), atenolol (1 mg/kg) or prazosin (1 mg/kg). Eight animals were studied in each group. Spectral analyses was performed using continuous BP time series obtained in conscious rats. RESULTS: Thyroxine treatment was sufficient to induce a significant degree of tachycardia (423+/-6 vs 353+/-4 bpm, P < 0.001, unpaired Student's t test), systolic BP elevation (142+/-3 vs 127+/-2 mmHg, P < 0.001) and cardiac hypertrophy (1.165+/-0.017 vs 1.006+/-0.012 g, P < 0.001). The intrinsic HR was markedly increased after treatment with thyroxine (497+/-16 vs 373+/-10 bpm, P < 0.05). Vagal tone was positively linearly related to intrinsic HR (r = 0.84, P< 0.01). Atenolol neither modified HR nor BP variability in rats with hyperthyroidism. The thyrotoxicosis was associated with a reduction of the 0.4 Hz component of BP variability (modulus 1.10+/-0.07 vs 1.41+/-0.06 mmHg, P < 0.01). Prazosin was without effect on this 0.4 Hz component in hyperthyroid animals. CONCLUSIONS: These data show a functional diminution of the vascular and cardiac sympathetic tone in early experimental hyperthyroidism. The marked rise in the intrinsic HR could be the main determinant of tachycardia. The BP elevation may reflexly induce vagal activation and sympathetic (vascular and cardiac) inhibition.

Animals↗
PubMed1998

Acute effects of bisoprolol on respiratory sinus arrhythmia.

Respiratory sinus arrhythmia (RSA) is often quantified by computing the spectra of heart period (HP) or of its reciprocal heart rate (HR) at the respiratory frequency. This study was undertaken to describe the effect of an acute beta-blockade achieved with bisoprolol on RSA, obtained during a calibrated breathing (breathing frequency 0.25 Hz, tidal volume VT 500 or 700 mL) in 15 normal volunteers, using a double-blind, placebo-controlled, cross-over method. The two heart signals were computed and the RSA values were compared to the individual estimates of vagal tone obtained using an additional atropine injection. The difference between the HP (or HR) value obtained after beta-blockade and the HP (or HR) value observed following the double blockade (bisoprolol plus atropine) was taken as an index of cardiac vagal tone. Bisoprolol administration resulted in a significant reduction in HR reaching 60.3 +/- 1.4 bpm at VT of 500 mL (compared to 70.5 +/- 1.8 bpm with placebo, P < 0.001). Changes in HP were also significant with an increase in HP reaching 1004.5 +/- 22.2 msec at this controlled VT (compared to 860.3 +/- 21.5 msec with placebo, P < 0.001). Similar changes were observed at a VT of 700 mL. The relationship between RSA in bpm and vagal tone was not significant for HR while a significant positive relationship was observed between RSA in msec and vagal tone for the two respiratory patterns (r = 0.65 for a tidal volume of 500 mL, P < 0.01, and r = 0.62 for 700 mL, P < 0.05). This demonstrates that the detection of the variability effect highly depends upon the unit. The parallelism between vagal tone and RSA supports the view that the HF component of HRV in msec quantifies the vagal tone. The increased RSA during beta-blockade could well reflect this vagotonic effect of this class of drugs.

Acute-Phase Reaction↗
PubMed1998

Heart rate control of blood pressure variability in children: a study in subjects with fixed ventricular pacemaker rhythm.

1. To investigate the influence of heart rate variability on blood pressure variability, short-term variability in heart rate and blood pressure was studied in 10 children with fixed ventricular pacemaker rhythm (80 beats/min). Ten healthy children, in sinus rhythm, served as a reference population. 2. Arterial blood pressure and heart rate were measured continuously using a finger arterial device and an ECG respectively. Power spectra for heart rate and blood pressure (systolic and diastolic) were calculated in both supine and orthostatic positions. In addition, acute changes in blood pressure and heart rate during active standing were studied. 3. Healthy children exhibited considerable heart rate variability, which was slightly more pronounced in the supine position, while children with a fixed ventricular rate had no heart rate variability in either position. 4. Despite the differences in heart rate variability, mean systolic blood pressure and its variability profiles were poorly affected by the suppression of heart rate variability. The lack of autonomic control on the sinus node was associated with a reduction in magnitude of the changes in systolic blood pressure variability induced by orthostatic posture. 5. The suppression of heart rate fluctuations induced a noticeable decrease in diastolic blood pressure fluctuations, which was most conspicuous in the children with fixed cardiac rhythm when in the supine position. This may be explained by the lack of diastolic blood pressure fluctuations, physiologically due to heart rate fluctuations through the run-off effect: the longer the cardiac cycle, the greater the diastolic pressure decay. These results may challenge the classical theory of baroreflex-mediated diastolic blood pressure control described in adult patients. 6. During active standing, the early drop in systolic blood pressure was greater in subjects with fixed ventricular rhythm. A rise in heart rate of 36 beats/min was observed in the healthy subjects in response to active standing. 7. We conclude that in normal children, heart rate fluctuations increase the blood pressure variability rather than buffering it. However, during acute orthostatic stress, the abrupt baroreflex-mediated heart rate rise may partly compensate for the reduction in blood pressure.

Adolescent↗
PubMed1997

[Short-term variability of blood pressure].

The regulation of blood pressure (BP) is traditionally described in terms of homeostasis, and indicates that BP although being continuously perturbed by external stimulations always displays the tendency to come back toward a reference set point. Experimental and clinical studies indicate that these fluctuations occurring around the average present a source of complementary information on the mechanism of cardiovascular control. Recently a wide variety of algorithm and models have been proposed to study the cardiovascular system through new technics of continuous non invasive BP or heart rate (HR) measurements. They give new insites for the evaluation of hypertensive patients and relevance to the understanding of the role of the disorder of the tonic regulation of BP, rather than its short-term variability or reactivity. However, if available data unequivocally indicate that the analysis of variability is a useful tool, the interpretation of those data in clinical trials is not always optimal because there is lot of interaction between BP, HR and other biological signals, and furthermore the use of laboratory data introduces problems to predict what happens on daily life ambulatory conditions.

Autonomic Nervous System↗
PubMed1995

Spectral analysis of systolic blood pressure and heart rate after heart transplantation in children.

1. The aim of the study was to examine the short-term variability in blood pressure and heart rate in 19 children who had received heart transplants and in eight normal control children. 2. Blood pressure was determined by a finger arterial pressure device. We examined the power spectra for heart rate and systolic blood pressure in the supine and tilted positions. In addition, we studied the acute changes in blood pressure and heart rate during active standing. 3. In the transplanted children we could distinguish two groups (groups A and B) in whom heart rate variability differed, although in both it was greatly reduced compared with controls (group C). In group A there were no significant fluctuations in the mid-frequency range for heart rate. The gain of the relationship between systolic blood pressure and heart rate was very low and there were virtually no heart rate changes associated with passive tilting. 4. By contrast, in group B transplant patients the heart rate variability, as assessed by standard deviation, was about half that of normal controls. The power spectra attenuation was greater in the high-frequency than in the mid-frequency bands. On passive tilting the latter became enhanced, but not the high-frequency variability. On active standing the tachycardic response was about half that of controls. The findings suggest some reinnervation involving cardiac sympathetic fibres to a greater degree than the fast-responding vagal fibres. 5. In both groups A and B the drop in systolic blood pressure observed early in active standing was about 4-6 times as great as in controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMed1995

Spectral analysis of systolic blood pressure and heart rate oscillations related to respiration.

1. Non-invasive assessment of short-term systolic blood pressure (SBP) and heart rate (HR) variability was obtained with the plethysmographic finger blood pressure measurement device. Respiration was measured with a respiratory inductive plethysmograph, which was calibrated prior to each study. 2. The effects of breathing pattern on the respiratory (high frequency, HF) component of the SBP or HR spectrum were analysed by Fourier transform. 3. Our quantification of the changes in the HF (respiratory) peak of the HR or SBP spectrum with changes in tidal volume (VT) and breathing frequency (BF) indicates that the modulus of this component may be predicted for any combination of depth and frequency of breathing. 4. The modulus of this HF component for the HR or SBP spectrum was linearly related to the respiratory sinus arrhythmia (RSA) or to the SBP oscillation related to respiration.

Adult↗
PubMed1995

Effect of autonomic blockade on heart rate and blood pressure in sleep apnea syndrome.

To determine the impact of the autonomic nervous system on hemodynamic responses to sleep apnea we studied 7 male patients (48 +/- 6 years, BMI = 29.7 +/- 2.9 kg/m2) with an apnea index = 33 + 11/h. In two hypertensives, therapy was withdrawn 2 weeks before the study. During a full night polysomnography EEG, EOG, EMG, respiration, oximetry, heart rate (HR) and blood pressure (BP) (Finapres 23OOE) were recorded. Placebo and 3 short-acting autonomic blockers were randomly i.v. administered: antimuscarinic (atropine 1 mg, A), beta 1 blocker (esmolol 40 mg, E), alpha blocker (nicergoline 2.5 mg, N). A total of 367 obstructive apneas in NREM sleep were studied. With atropine, HR was increased at the beginning of apnea (P1)(74.5 +/- 2 bpm vs 65.4 +/- 2 bpm with placebo) and at the end apnea (P3) (76.6 +/- 1.9 bpm vs 67.1 +/- 1.76 bpm). At the resumption of breathing (RB), HR still increased (83.5 +/- 1.5 bpm vs 80.1 +/- bpm). Nicergoline had no significant effect on HR but significantly decreased SBP (117.8 +/- 1.4 mmHg vs 127 +/- 1.6 with placebo, p < 0.001). Nevertheless, the rise in BP from P3 to RB remained significant (p < 0.001). Esmolol significantly decreased HR at P1 (68.1 +/- 1.9 bpm vs 73.9 +/- 1.9 bpm) and at RB (75.9 +/- 1.9 vs 81.6 +/- 1.8). With A, the rise in HR at end-apnea (P3) suggests a vagal hyperactivity during this phase which is blunted at resumption when HR is unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1995

Cardiovascular reactivity to a new mental stress test: the maze test.

The response to the maze test was studied in 31 subjects on no medication, including seven subjects with mild essential hypertension. Beat-by-beat finger blood pressure (BP) was measured with a Finapres device. Pulse interval from which heart rate (HR) was derived was obtained from the BP signal. A period of 5 min baseline was used to define resting levels of systolic BP and HR using 20-s averaged values for the calculation of the 95% confidence limit of the two variables. The average test duration was 10 min. During this period a series of video-displayed mazes had to be solved with easy mazes preceding difficult ones. No subject had been exposed to the test before. The maximal BP elevation associated with the test was 27 mmHg. The HR response averaged 11 beats/min. Significant elevations were observed for half the test duration. No significant relationship between these two responses was observed and some subjects exhibited isolated systolic BP or HR responses. When indices obtained during this active mental stress were compared to resting values, positive correlations were observed. When the resting standard deviation (SD) of systolic BP was higher the systolic response was greater. A similar relationship was observed for HR. In addition, when the systolic BP level at rest was higher, the systolic BP reactivity index was greater. However, systolic BP or HR at baseline were not predictive of the systolic BP or HR responses. This study demonstrates the applicability of a new test to assess cardiovascular reactivity.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

[Spectrum analysis of heart rate and arterial systolic pressure after heart transplantation in children].

The aim was to examine the short-term variability of blood pressure (BP) and heart rate (HR) in 19 children who had received heart transplants and in 8 normal control children. BP was determined by a finger arterial pressure device. We examined the power spectra for HR and systolic blood pressure (SBP) in the supine and standing posture. In the transplanted children we could distinguish two groups (groups A and B) in whom HR variability differed, though in both it was greatly reduced compared to controls (group C). In group A there were no significant fluctuations in the mid frequency (MF) range for HF. Gain of the relationship between SBP and HR was very low and there were virtually no HR changes associated with passive tilting. By contrast, in group B transplant patients the HR variability, as assessed by standard deviation was about half that of normal controls. The power spectra attenuation was greater in the high frequency (HF) than in the MF bands. On standing the latter became enhanced, but not the HF variability. The findings suggest some reinnervation involving cardiac sympathetic fibres to a greater degree than the fast-responding vagal fibres. Time since operation was a critical factor for reinnervation since all subjects from group B were transplanted more than 44 months prior to the recording. We conclude that in a proportion of children who have received heart transplantation there is a delayed reinnervation of the heart, which probably involves sympathetic effectors rather than the vagus.

Age Factors↗
PubMed1994

[Reproducibility of short-term variability indicators of blood pressure].

The aim of this study was to estimate the degree of reproducibility of blood pressure (BP) variability profile between 2 clinic visits. We recruited 15 untreated subjects (6 hypertensives, 9 normotensives) from the outpatient clinic. This group had undergone at least one BP measurement by the same investigator (A.G.). The subjects underwent 5-min BP monitoring (Finapres) during standing and after a rest in a supine position, at 10 AM and at 23 degrees C in a quiet room. Measurements were repeated after 7 days. A fast Fourier transform algorithm was used for analysis. There was no order effect with no difference between visits 1 and 2. Coefficients of variation (CV) for systolic BP, diastolic BP and heart rate were 9, 6 and 12%. High CVs of 20% were observed for the overall variability (total power) and the low frequency (LF, Mayer wave) component of BP. However the normalized LF (LF/total area) exhibited a acceptable CV of 15%. In conclusion the BP variability profile differences observed between visits might reflect intrasubject effect. This should be considered for assessing BP variability profile and for drug trial design.

Adult↗
PubMed1993

Effects of the cold pressor test on short-term fluctuations of finger arterial blood pressure and heart rate in normal subjects.

The effect of the cold pressor test on autonomic cardiovascular control was studied non-invasively by means of spectrum analysis of periodic heart rate and blood pressure fluctuations in ten normal subjects. Fast Fourier Transform algorithm based on a 256-point time series (sampling rate 2 Hz, i.e. 2-min and 8-s) was used to estimate the amplitude spectra of heart rate and blood pressure rhythmicity at the low frequency (70-140 mHz) and respiration related frequency (230-270 mHz) band. Respiration rate was controlled at 250 mHz. Auto- and cross-spectral techniques were used to determine the complex relationship between systolic blood pressure and heart rate fluctuations in the frequency domain. The spectral pattern of systolic and diastolic blood pressure showed a marked increment of the absolute and relative (100 multiplied with absolute value/total area under the curve of the amplitude spectrum from 15-500 mHz) low frequency component: control vs. cold pressor test--systolic blood pressure--absolute values (in [mmHg/Hz1/2]): 634.4 +/- 48.9 vs. 827.4 +/- 69.9*; relative values (in [%]): 26 +/- 2 vs. 32 +/- 2*; diastolic blood pressure--absolute values: 433.2 +/- 42.3 vs. 537.2 +/- 45.8*; relative values: 35 +/- 3 vs. 40 +/- 2*, (average +/- SEM, *P < 0.05). The cold pressor test induced no change in average heart rate; the absolute low frequency component in heart rate spectra increased clearly during the test: low frequency component (in [bpm/Hz1/2]): 586.9 +/- 89.9 vs. 712.0 +/- 91.4*, while the relative low frequency component did not change: 29 +/- 3 vs. 30 +/- 3.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Effect of breathing pattern on blood pressure and heart rate oscillations in humans.

1. The relationships of respiratory sinus arrhythmia (RSA) and respiratory changes in systolic blood pressure (SBP) to tidal volume (VT) and breathing frequency (BF), were quantified during voluntary control of VT and BF in healthy subjects. 2. Respiration was measured non-invasively with a respiratory inductive plethysmograph, which was calibrated prior to each study while breathing through a pneumotachygraph. Finger arterial blood pressure was measured non-invasively by the Finapres. 3. Heart rate (HR) increased during inspiration, with a nearly fixed time delay for most VT and BF approximating 0.9 s. The magnitude of RSA increased with increases in VT and with decreases in BF. SBP decreased during inspiration, with a time delay which increased as BF decreased, resulting in a phase delay approximating 160 degrees. The magnitude of the inspiratory fall in SBP increased with increases in VT. Increased amplitudes of RSA and SBP variation occurred at the lowest BF, consistent with the possibility of interactions between respiratory-related influences and those due to 'slow waves' of vasomotor tone. 4. The present results are consistent with the conclusion that respiratory effects on SBP are caused by a mechanism other that simply changes in HR.

Adult↗
PubMed1993

Are 5-HT1A autoreceptors involved in the inhibitory effect of ipsapirone on cold-elicited thyrotropin secretion?

Administration of the serotonin (5-HT)1A receptor agonist ipsapirone has been shown to decrease cold-elicited thyrotropin (TSH) secretion. We have analyzed (1) the influence of 5-HT1A receptors and ipsapirone metabolism into 1-(2-pyrimidinyl)-piperazine (1-PP, an alpha 2-adrenoceptor antagonist) on the effect of ipsapirone on TSH release, and (2) the interaction between the corticosterone-releasing effect of ipsapirone and its inhibitory influence on TSH release. Pretreatment with proadifen (50 mg/kg, 5 h before ipsapirone), i.e. an inhibitor of ipsapirone metabolism into 1-PP, did not affect ipsapirone-induced inhibition of cold-elicited TSH secretion. Pretreatment (15 min before ipsapirone) with the 5-HT1/5-HT2 receptor antagonist metergoline 2 mg/kg) or with the 5-HT1A receptor blocker (-)-pindolol (5 mg/kg) increased baseline and cold-elicited TSH release but the inhibitory influence of ipsapirone on cold-elicited TSH release was alleviated by (-)-pindolol pretreatment only. Cold exposure increased corticosterone release, an effect which was insensitive to (-)-pindolol pretreatment. Lastly, pretreatment with the 5-HT synthesis inhibitor p-chlorophenylalanine prevented the immediate inhibitory effect of the selective 5-HT1A receptor agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) upon cold-induced TSH release, but it amplified the late release of TSH in cold-exposed 8-OH-DPAT-injected rats. These results suggest that presynaptic 5-HT1A receptors mediate ipsapirone-induced inhibition of cold-elicited TSH release, an effect which may be partially opposed by postsynaptic 5-HT1A receptor stimulation.

8-Hydroxy-2-(di-n-propylamino)tetralin↗