Effect of human galanin on the response of circulating catecholamines to hypoglycemia in man

1995 ◽  
Vol 133 (6) ◽  
pp. 723-728 ◽  
Author(s):  
Ettore C degli Uberti ◽  
Maria R Ambrosio ◽  
Marta Bondanelli ◽  
Giorgio Transforini ◽  
Alberto Valentini ◽  
...  
Keyword(s):  
Heart Rate ◽  
Healthy Subjects ◽  
Sympathetic Nerve Activity ◽  
Heart Rate Response ◽  
Statistical Significance ◽  
Inhibitory Effect ◽  
Amino Acid Residues ◽  
Nerve Activity ◽  
Receptor Stimulation

degli Uberti EC, Ambrosio MR, Bondanelli M, Trasforini G, Valentini A, Rossi R, Margutti A, Campo M. Effect of human galanin on the response of circulating catecholamines to hypoglycemia in man. Eur J Endocrinol 1995;133:723–8. ISSN 0804–4643 Human galanin (hGAL) is a neuropeptide with 30 amino acid residues that has been found in the peripheral and central nervous system, where it often co-exists with catecholamines. In order to clarify the possible role of hGAL in the regulation of sympathoadrenomedullary function, the effect of a 60 min infusion of hGAL (80 pmol·kg−1 · min−1) on plasma epinephrine and norepinephrine responses to insulin-induced hypoglycemia in nine healthy subjects was investigated. Human GAL administration significantly reduced both the release of basal norepinephrine and the response to insulin-induced hypoglycemia, whereas it attenuated the epinephrine response by 26%, with the hGAL-induced decrease in epinephrine release failing to achieve statistical significance. Human GAL significantly increased the heart rate in resting conditions and clearly exaggerated the heart rate response to insulin-induced hypoglycemia, whereas it had no effect on the blood pressure. We conclude that GAL receptor stimulation exerts an inhibitory effect on basal and insulin-induced hypoglycemia-stimulated release of norepinephrine. These findings provide further evidence that GAL may modulate sympathetic nerve activity in man but that it does not play an important role in the regulation of adrenal medullary function. Ettore C degli Uberti, Chair of Endocrinology, University of Ferrara, Via Savonarola 9, I-44100 Ferrara, Italy

scholarly journals Acute sympathoexcitatory action of angiotensin II in conscious baroreceptor-denervated rats

2002 ◽  
Vol 283 (2) ◽  
pp. R451-R459 ◽  
Author(s):  
Ling Xu ◽  
Alan F. Sved
Keyword(s):  
Heart Rate ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Sympathetic Nerve Activity ◽  
Baroreceptor Reflex ◽  
Ang Ii ◽  
Nerve Activity ◽  
Induced Hypotension ◽  
Baroreceptor Reflexes

Angiotensin II (ANG II) has complex actions on the cardiovascular system. ANG II may act to increase sympathetic vasomotor outflow, but acutely the sympathoexcitatory actions of exogenous ANG II may be opposed by ANG II-induced increases in arterial pressure (AP), evoking baroreceptor-mediated decreases in sympathetic nerve activity (SNA). To examine this hypothesis, the effect of ANG II infusion on lumbar SNA was measured in unanesthetized chronic sinoaortic-denervated rats. Chronic sinoaortic-denervated rats had no reflex heart rate (HR) responses to pharmacologically evoked increases or decreases in AP. Similarly, in these denervated rats, nitroprusside-induced hypotension had no effect on lumbar SNA; however, phenylephrine-induced increases in AP were still associated with transient decreases in SNA. In control rats, infusion of ANG II (100 ng · kg−1 · min−1 iv) increased AP and decreased HR and SNA. In contrast, ANG II infusion increased lumbar SNA and HR in sinoaortic-denervated rats. In rats that underwent sinoaortic denervation surgery but still had residual baroreceptor reflex-evoked changes in HR, the effect of ANG II on HR and SNA was variable and correlated to the extent of baroreceptor reflex impairment. The present data suggest that pressor concentrations of ANG II in rats act rapidly to increase lumbar SNA and HR, although baroreceptor reflexes normally mask these effects of ANG II. Furthermore, these studies highlight the importance of fully characterizing sinoaortic-denervated rats used in experiments examining the role of baroreceptor reflexes.

Role of median preoptic area in vasopressin-mediated bradycardia

1988 ◽  
Vol 254 (6) ◽  
pp. H1172-H1178 ◽  
Author(s):  
K. P. Patel ◽  
P. G. Schmid
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Sympathetic Nerve Activity ◽  
Preoptic Area ◽  
Local Administration ◽  
Base Line ◽  
Preoptic Nucleus ◽  
Nerve Activity ◽  
Median Preoptic Nucleus

To determine whether neural traffic through the median preoptic nucleus (MnPO) is involved in arginine vasopressin (AVP)-mediated bradycardia and sympathoinhibition, we recorded reflex decreases in heart rate (HR) and lumbar sympathetic nerve activity, in response to increases in arterial pressure induced either by intravenous phenylephrine (PE) or AVP before, during, and after local administration of lidocaine (200 nl, 2%) in the MnPO of chloralose-anesthetized rabbits. Base-line blood pressure and HR did not change in response to administration of lidocaine into the MnPO. Blockade of neural traffic (by lidocaine) in the MnPO produced an attenuation of AVP-mediated bradycardia but not the baroreflex-mediated bradycardia caused by PE. Lidocaine in the MnPO did not alter the sympathoinhibition produced with AVP. These results indicate that part of the bradycardia produced by AVP is mediated via forebrain structures such as the MnPO and is selective for bradycardia. Additionally, this response was mimicked by administration of yohimbine, an alpha 2-antagonist, into the MnPO, which suggests that noradrenergic mechanisms are involved in the baroreflex-mediated facilitation of bradycardia by AVP at the level of the MnPO.

Low-dose B-type natriuretic peptide raises cardiac sympathetic nerve activity in sheep

2014 ◽  
Vol 307 (2) ◽  
pp. R206-R211 ◽  
Author(s):  
Christopher J. Charles ◽  
David L. Jardine ◽  
Miriam T. Rademaker ◽  
A. Mark Richards
Keyword(s):  
Heart Rate ◽  
Natriuretic Peptide ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Low Dose ◽  
Statistical Significance ◽  
Burst Frequency ◽  
Nerve Activity ◽  
Cardiac Sympathetic Nerve Activity ◽  
Conscious Sheep

The reported effects of atrial natriuretic peptide (ANP) on sympathetic nerve activity (SNA) are variable, dependent on concomitant hemodynamic actions, and likely to be regionally differentiated. There are few reports of the effect of B-type natriuretic peptide (BNP) on SNA and none have measured cardiac SNA (CSNA) by direct microneurography. We measured the effects of low-dose ANP and BNP (2.4 pmol·kg−1·min−1 infused for 120 min) on CSNA and hemodynamics in conscious sheep ( n = 8). While there was a trend for mean arterial pressure and cardiac output to fall with both ANP and BNP, changes were not significant compared with vehicle control. However, BNP did significantly reduce systolic arterial (97 ± 4.2 vs. 107 ± 6.8 mmHg during control; P = 0.043) and pulse pressures (0.047) and increase heart rate (110 ± 6.7 vs. 96 ± 7.3 beats/min; P = 0.044). Trends for these hemodynamic parameters to change with ANP did not achieve statistical significance. ANP also had no significant effect on any CSNA parameters measured. In contrast, BNP induced a rise in both CSNA burst frequency (∼20 bursts/min higher than control, P = 0.011) and burst area (∼40% higher than control, P = 0.013). BNP-induced rises in burst incidence (bursts/100 beats), and burst area per 100 beats, however, were not significant. In conclusion, BNP infused at low doses that only had subtle effects on hemodynamics increased CSNA burst frequency and burst are per minute. This increase in CSNA may in large part be secondary to an increase in heart rate as CSNA burst incidence and burst area per 100 beats were not significantly increased. This study provides no evidence for inhibition of CSNA by natriuretic peptides.

P4388Acute detrimental effects of e-cigarette and tobacco cigarette smoking on blood pressure and sympathetic nerve activity in healthy subjects

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
K Dimitriadis ◽  
C Tsioufis ◽  
K Kontantinou ◽  
I Liatakis ◽  
E Andrikou ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Nervous System ◽  
Cigarette Smoking ◽  
Sympathetic Nerve ◽  
Healthy Subjects ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Tobacco Cigarette ◽  
Sympathetic Nervous

Abstract Background/Introduction Tobacco cigarette smoking is related with atherosclerosis progression, blood pressure increase and changes in sympathetic nerve activity. However, there are scarce data on the impact of e-cigarettes that have been proposed as less harmful alternatives on the cardiovascular system and sympathetic drive. Purpose This study aimed to assess the acute effects of tobacco cigarettes, e-cigarettes and sham smoking on blood pressure and sympathetic nervous system in healthy subjects. Methods We studied 10 normotensive male habitual smokers (mean age 33 years, body mass index: 24.1 kg/m2, office blood pressure=117/72 mmHg) free of cardiovascular disease. The study design was randomized and placebo controlled with 3 experimental sessions (sham smoking, tobacco cigarette smoking, and e-cigarette smoking) in random order, each session on a separate day. Subjects smoked 2 tobacco cigarettes containing 1.1 mg nicotine or simulate smoking (sham smoking) with the 2 cigarettes separated by 5 minutes, while 45 minutes after finishing the second cigarette, subjects smoked a third cigarette or sham cigarette. Additionally, participants smoked e-cigarettes for a period of 5 and 30 minutes. In all occasions, sympathetic drive was assessed by muscle sympathetic nerve activity (MSNA) (baroreflex-dependent) and skin sympathetic nerve activity (SSNA) (baroreflex-independent) based on established methodology (microneurography). Results After the first, second and third tobacco cigarette smoking there was markedly and significantly increase in mean arterial pressure (by 11.2±1.4%, 12.3±1.3% and 13.1±1.4%, respectively, p<0.05 for all) and heart rate (by 25.1±3.7%, 26.3±2.7% and 25.9±3.7%, respectively, p<0.05 for all). Similarly e-cigarette smoking at 5 and 30 minutes was accompanied by augmentation of mean arterial pressure (by 10.9±1.2% and 12.8±1.4%, respectively, p<0.05 for both) and heart rate (by 22.5±3.3% and 23.9±3.8%, respectively, p<0.05 for both). Regarding the effect on sympathetic nervous system, the first, second and third tobacco cigarette smoking was accompanied by lower MSNA (by 28.1±4.4%, 29.6±5.3% and 30.1±5.2%, respectively, p<0.05 for all), whereas SSNA was increased (by 98.2±19.4%, 100.2±22.7% and 101.5±21.6%, respectively, p<0.05 for all). Additionally, e-cigarette smoking at 5 and 30 minutes caused a decrease in MSNA (by 26.9±3.6%, and 28.3±5.1%, respectively, p<0.05 for both), and an augmentation in SSNA (by 97.9±20.1% and 100.9±20.6%, respectively, p<0.05 for both). Sham smoking was devoid of any effects on blood pressure, MSNA and SSNA. Conclusions E-cigarette smoking acutely increases blood pressure and has a detrimental effect on sympathetic nerve activity regulation similar to tobacco smoking in healthy subjects. Our findings underscore the negative impact of e-cigarettes on cardiovascular and autonomic nervous system and could aid further recommendation in their use.

scholarly journals Sympathetic nerve activity changes following acute exposures to electronic and tobacco cigarette smoking in humans

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
K Dimitriadis ◽  
K Narkiewicz ◽  
I Leontsinis ◽  
D Konstantinidis ◽  
C Mihas ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cigarette Smoking ◽  
Sympathetic Nerve ◽  
Healthy Subjects ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Tobacco Cigarette ◽  
Significant Difference ◽  
The Impact

Abstract Background/Introduction Tobacco cigarette (TC) smoking acutely increases blood pressure and sympathetic nerve activity, whereas there are scarce data on the impact of electronic cigarette (EC). Purpose The aim of the study was to assess the acute effects of TC, EC and sham smoking on blood pressure, heart rate and sympathetic nervous system in healthy subjects. Methods We studied 12 normotensive male habitual smokers (mean age 33 years) free of cardiovascular disease. The study design was randomized and placebo controlled with 3 experimental sessions (sham smoking, tobacco cigarette smoking, and e-cigarette smoking) in random order, each session on a separate day. Subjects smoked 2 tobacco cigarettes containing 1.1 mg nicotine or simulate smoking (sham smoking) with the 2 cigarettes separated by 5 minutes. Additionally, participants smoked e-cigarettes for a period of 5 and 30 minutes. In all occasions, sympathetic drive was assessed by muscle sympathetic nerve activity (MSNA) (baroreflex-dependent) and skin sympathetic nerve activity (SSNA) (baroreflex-independent) based on established methodology (microneurography). Results After the first and second TC smoking, there was significant increase in mean arterial pressure (MAP) (by 6 and 8 mmHg, respectively, overall p&lt;0.001) and heart rate (by 8 and 12 beats/minute, respectively, overall p&lt;0.001) compared to baseline. Similarly, EC smoking at 5 and 30 minutes compared to baseline was accompanied by augmentation of MAP (by 6 and 10 mmHg, respectively, overall p&lt;0.001) and heart rate (by 5 and 9 beats/minute, respectively, overall p&lt;0.001). Sham smoking was accompanied by a reduction in MAP after the first and second cigarette compared to baseline (by 2 and 4 mmHg, respectively, p=0.001), whereas there was no significant difference in heart rate (p=NS). The first and second TC smoking was characterized by lower muscle MSNA (by 6 and 6 bursts/minute, respectively, overall p&lt;0.001) compared to baseline, whereas SSNA was increased (by 9 and 10 bursts/minute respectively, overall p&lt;0.001). Additionally, EC smoking at 5 and 30 minutes caused a decrease in MSNA (by 8 and 8 bursts/minute, respectively, overall p&lt;0.00) and an augmentation in SSNA (by 7 and 9 bursts per minute, respectively, overall p&lt;0.001) compared to baseline. Sham smoking had no significant effect on MSNA and SSNA (p=NS for both). Conclusions Sympathetic, pressor and heart rate unfavorable responses to EC smoking are similar to those elicited by TC in healthy subjects. Our findings provide novel insights into the negative impact of EC on cardiovascular system and support opinions recommending great caution concerning EC use. FUNDunding Acknowledgement Type of funding sources: None.

Dynamics of muscle sympathetic nerve activity in advanced heart failure patients

1996 ◽  
Vol 271 (5) ◽  
pp. H1962-H1969
Author(s):  
A. H. Nguyen ◽  
A. Garfinkel ◽  
D. O. Walter ◽  
M. A. Hamilton ◽  
G. C. Fonarow ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Frequency Modulation ◽  
Healthy Subjects ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Low Frequency ◽  
Nerve Activity ◽  
Heart Failure Patients ◽  
Patients With Heart Failure

Muscle sympathetic nerve activity (MSNA) is increased in patients with heart failure compared with healthy subjects. We applied spectral and correlation techniques to determine if qualitative as well as quantitative differences in MSNA differentiate heart failure patients from healthy subjects. We recorded MSNA, heart rate, and respiration in 11 heart failure patients and 10 healthy humans. Our results are as follows. 1) Statistically significant low-frequency modulation of MSNA at 0.029 +/- 0.002 Hz (mean +/- SE; range 0.026-0.038 Hz) was found in 10 of 11 heart failure patients but in only 2 of 10 healthy controls (differences between groups, P < 0.01; chi 2 test). 2) Heart rate and respiration also demonstrated significant low-frequency modulation in a similar range. 3) Spectral and correlation techniques revealed that low-frequency modulation of MSNA was highly correlated with low-frequency modulation of respiration in heart failure patients, but not in healthy subjects. In contrast, low-frequency modulation of MSNA did not correlate well with low-frequency modulation of heart rate. In summary, low-frequency modulation of respiration is coupled to low-frequency modulation of MSNA in heart failure patients, but not in normal subjects. We speculate that this low-frequency modulation of respiration may represent subclinical Cheyne-Stokes breathing, which has marked qualitative effects on MSNA in patients with heart failure.

scholarly journals Acute and chronic sympathomimetic effects of e-cigarette and tobacco cigarette smoking: role of nicotine and non-nicotine constituents

2020 ◽  
Vol 319 (2) ◽  
pp. H262-H270 ◽  
Author(s):  
Sara Arastoo ◽  
Kacey P. Haptonstall ◽  
Yasmine Choroomi ◽  
Roya Moheimani ◽  
Kevin Nguyen ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Cigarette Smoking ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Vascular Effects ◽  
Nerve Activity ◽  
Tobacco Cigarette

Chronic electronic cigarette (EC) users and tobacco cigarette (TC) smokers exhibit a similar level of sympathetic nerve activity as estimated by heart rate variability. Acute increases in blood pressure (BP) and heart rate in EC users are attribute to nicotine, not non-nicotine, constituents in EC aerosol. Acute TC smoking increased BP significantly more than acute EC use, despite similar increases in plasma nicotine, suggestive of additional adverse vascular effects attributable to combusted, non-nicotine constituents in TC smoke.

High-fat feeding alters the cardiovascular role of the hypothalamic paraventricular nucleus

2010 ◽  
Vol 298 (3) ◽  
pp. R799-R807 ◽  
Author(s):  
Feng Chen ◽  
Joo Lee Cham ◽  
Emilio Badoer
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Paraventricular Nucleus ◽  
Sympathetic Nerve ◽  
High Fat Diet ◽  
Sympathetic Nerve Activity ◽  
Hypothalamic Paraventricular Nucleus ◽  
High Fat ◽  
Nerve Activity

Increased sympathetic nerve activity is associated with obesity-related hypertension, but the underlying central neural mechanisms are not clear. We examined the role of the hypothalamic paraventricular nucleus (PVN) in the regulation of sympathetic nerve activity in rats fed a normal chow diet (controls) and rats fed a high-fat diet (36% fat) over 12 wk. The effects on blood pressure, heart rate, and lumbar sympathetic nerve activity (LSNA) induced by microinjection of the GABAA receptor agonist muscimol or the antagonist bicuculline were monitored in anesthetized rats. Body weight of rats fed the high-fat diet was not significantly different from controls, but a significant 80% increase in epididymal fat mass, significantly elevated fasting blood glucose, and significantly impaired glucose tolerance were observed in rats fed the high-fat diet. Resting blood pressure and heart rate were not significantly different between rats fed the high-fat diet and controls. Muscimol microinjected into the PVN elicited a greater reduction of blood pressure and LSNA in rats fed the high-fat diet than controls: −14 ± 6 vs. −7 ± 2 mmHg and −35 ± 6 vs. −10 ± 9% ( P < 0.05). Microinjection of bicuculline into the PVN increased blood pressure and LSNA, but the responses were similar in rats fed the high-fat diet and controls. In conclusion, the role of the paraventricular nucleus in cardiovascular regulation can be altered by a diet high in fat, even when hypertension and obesity are absent.

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