scholarly journals Increased Efferent Cardiac Sympathetic Nerve Activity and Defective Intrinsic Heart Rate Regulation in Type 2 Diabetes

Diabetes ◽  
2015 ◽  
Vol 64 (8) ◽  
pp. 2944-2956 ◽  
Author(s):  
H.P. Aye Thaung ◽  
J. Chris Baldi ◽  
Heng-Yu Wang ◽  
Gillian Hughes ◽  
Rosalind F. Cook ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Heart Rate ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Cardiac Sympathetic Nerve ◽  
Nerve Activity ◽  
Rate Regulation ◽  
Heart Rate Regulation ◽  
Cardiac Sympathetic Nerve Activity

scholarly journals Adrenomedullin increases cardiac sympathetic nerve activity in normal conscious sheep

2005 ◽  
Vol 187 (2) ◽  
pp. 275-281 ◽  
Author(s):  
C J Charles ◽  
D L Jardine ◽  
M G Nicholls ◽  
A M Richards
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Vehicle Control ◽  
Cardiac Sympathetic Nerve ◽  
Burst Frequency ◽  
Nerve Activity ◽  
Cardiac Sympathetic Nerve Activity ◽  
Conscious Sheep

The sympathetic nervous system and adrenomedullin (AM) both participate in the regulation of cardiac and circulatory function but their interaction remains uncertain. We have examined the effects of AM on cardiac sympathetic nerve activity (CSNA) and hemodynamics and contrasted these effects with pressure-matched nitro-prusside (NP) administration in normal conscious sheep. Compared with vehicle control, arterial pressure fell similarly with AM (P=0.04) and NP (P<0.001). Heart rate rose in response to both AM (P<0.001) and NP (P=0.002) but the rise with AM was significantly greater than that induced by NP (P<0.001). Cardiac output increased in response to AM compared with both control and NP (both P<0.001). CSNA burst frequency (bursts/min) were increased in response to both AM (P<0.001) and NP (P=0.005) with the rise in burst frequency being greater with AM compared with NP (P<0.001). CSNA burst area/min was also raised by both AM (P=0.03) and NP (P=0.002) with a trend for burst area being greater with AM than NP (P=0.07). CSNA burst incidence (bursts/100 beats) showed no significant differences between any treatment day. In conclusion, we have demonstrated that AM is associated with a greater increase in CSNA and heart rate for a given change in arterial pressure than seen with the classic balanced vasodilator NP.

Stimulation of cardiac sympathetic nerve activity by central angiotensinergic mechanisms in conscious sheep

2004 ◽  
Vol 286 (6) ◽  
pp. R1051-R1056 ◽  
Author(s):  
Anna M. D. Watson ◽  
Rasim Mogulkoc ◽  
Robin M. McAllen ◽  
Clive N. May
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Hypertonic Saline ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Ang Ii ◽  
Cardiac Sympathetic Nerve ◽  
Nerve Activity ◽  
Cardiac Sympathetic Nerve Activity ◽  
Conscious Sheep

Central actions of angiotensin play an important role in cardiovascular control and have been implicated in the pathogenesis of hypertension and heart failure. One feature of centrally or peripherally administered angiotensin is that the bradycardia in response to an acute pressor effect is blunted. It is unknown whether after central angiotensin this is due partly to increased cardiac sympathetic nerve activity (CSNA). We recorded CSNA and arterial pressure in conscious sheep, at least 3 days after electrode implantation. The effects of intracerebroventricular infusions of ANG II (3 nmol/h for 30 min) and artificial cerebrospinal fluid (CSF) (1 ml/h) were determined. The response to intracerebroventricular hypertonic saline (0.6 M NaCl in CSF at 1 ml/h) was examined as there is evidence that hypertonic saline acts via angiotensinergic pathways. Intracerebroventricular angiotensin increased CSNA by 23 ± 7% ( P < 0.001) and mean arterial pressure (MAP) by 7.6 ± 1.2 mmHg ( P < 0.001) but did not significantly change heart rate ( n = 5). During intracerebroventricular ANG II the reflex relation between CSNA and diastolic blood pressure was significantly shifted to the right ( P < 0.01). Intracerebroventricular hypertonic saline increased CSNA (+9.4 ± 6.6%, P < 0.05) and MAP but did not alter heart rate. The responses to angiotensin and hypertonic saline were prevented by intracerebroventricular losartan (1 mg/h). In conclusion, in conscious sheep angiotensin acts within the brain to increase CSNA, despite increased MAP. The increase in CSNA may account partly for the lack of bradycardia in response to the increased arterial pressure. The responses to angiotensin and hypertonic saline were losartan sensitive, indicating they were mediated by angiotensin AT-1 receptors.

Changes in AdSNA and arterial catecholamines to coronary occlusion in cats

1988 ◽  
Vol 255 (4) ◽  
pp. H704-H710 ◽  
Author(s):  
T. Honda ◽  
I. Ninomiya
Keyword(s):  
Heart Rate ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Coronary Occlusion ◽  
The Other ◽  
Cardiac Sympathetic Nerve ◽  
Nerve Activity ◽  
Control Value ◽  
Cardiac Sympathetic Nerve Activity ◽  
The Relationship

The relationship between adrenal (preganglionic) sympathetic nerve activity (AdSNA), cardiac sympathetic nerve activity (CSNA), and arterial catecholamines, i.e., epinephrine (Epi) and norepinephrine (NE), were analyzed during 200 s of occlusion of left anterior descending coronary artery in anesthetized cats. With coronary occlusion, AdSNA maximally increased to 168 +/- 20% (mean +/- SE) of the control value at 20 s and gradually decreased to 149 +/- 10% at 200 s. Mean CSNA (MCSNA), mean arterial pressure, and heart rate decreased significantly because of coronary occlusion. Arterial NE and Epi progressively increased from 0.54 +/- 0.05 and 0.29 +/- 0.03 ng/ml to 1.41 +/- 0.16 and 0.59 +/- 0.08 ng/ml at 3 min after the onset of occlusion, respectively. The correlation between AdSNA and arterial Epi (r = 0.71; P less than 0.01) and between AdSNA and arterial NE (r = 0.57; P less than 0.05) were significant, but the correlation between CSNA and arterial NE was not significant. On the other hand, in adrenalectomized cats, the increases in arterial Epi and NE did not appear during coronary occlusion. We concluded that, with coronary occlusion, AdSNA increased and, in turn, caused an increase in arterial Epi and NE.

Continual recordings of cardiac sympathetic nerve activity in conscious sheep

2002 ◽  
Vol 282 (1) ◽  
pp. H93-H99 ◽  
Author(s):  
David L. Jardine ◽  
Christopher J. Charles ◽  
Ian C. Melton ◽  
Clive N. May ◽  
Melanie D. Forrester ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Disease ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Low Frequency ◽  
Cardiac Sympathetic Nerve ◽  
Nerve Activity ◽  
Recording Time ◽  
Cardiac Sympathetic Nerve Activity ◽  
Conscious Sheep

Cardiac sympathetic nerve activity (CSNA) is of major importance in the etiology of heart disease but is impossible to measure directly in humans. Ovine and human cardiovascular systems are similar; therefore, we have developed a method for the daily recording of CSNA in conscious sheep. After thoracotomy, electrodes were glued into the left thoracic cardiac nerve and CSNA, blood pressure (BP), and heart rate were recorded daily. Satisfactory recordings ≥7 days of CSNA were obtained in 11 of 28 sheep (40%), mean recording time 10.6 days, range 7-47. During the first week, CSNA decreased gradually from 78 ± 8 at baseline to 60 ± 7 bursts/min on day 5( P = 0.02) or from 76 ± 9 to 57 ± 7 bursts/100 beats on day 7 ( P = 0.04). Similarly, BP decreased from 103 ± 4 to 94 ± 4 mmHg ( P = 0.03). Low-frequency heart rate variability decreased from 0.12 ± 0.02 to 0.06 ± 0.02 ms2on day 6 ( P = 0.004) but was not correlated to CSNA. In conclusion, CSNA that can be continually recorded in conscious sheep decreases during the first week postsurgery and, thereafter, stabilizes. This model should provide valuable insights in future investigations of cardiac disease.

Cardiac sympathetic nerve activity and heart rate during coronary occlusion in awake cats

1986 ◽  
Vol 251 (3) ◽  
pp. H528-H537 ◽  
Author(s):  
I. Ninomiya ◽  
K. Matsukawa ◽  
T. Honda ◽  
N. Nishiura ◽  
M. Shirai
Keyword(s):  
Heart Rate ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Early Stage ◽  
Coronary Artery Occlusion ◽  
Conscious State ◽  
Initial Increase ◽  
Cardiac Sympathetic Nerve ◽  
Nerve Activity ◽  
Cardiac Sympathetic Nerve Activity

Responses in efferent cardiac sympathetic nerve activity (CSNA) and heart rate (HR) to a 100-s anterior descending coronary artery occlusion were measured in cats under awake, atropinized, anesthetized, or anesthetized and atropinized states. In the conscious state, at 20 and 90 s of occlusion, CSNA increased by 23% and then decreased by 7%, respectively, whereas HR decreased by 5 and 17%, respectively. With atropinization and/or anesthesia, the initial increase in CSNA was inhibited and the later decrease in CSNA was enhanced, whereas the bradycardia was diminished. HR changed in proportion to CSNA responses with high correlations, i.e., r = +0.89, +0.90, +0.96, and +0.91 for the four states, respectively. In the conscious state, the CSNA-HR relation line shifted toward bradycardia, but this shift was blocked by atropinization and anesthesia. This finding suggested that, in the conscious state, cardiac vagal nerve activity (CVNA) increased immediately and did not decrease during occlusion. At the early stage of occlusion, HR response (bradycardia or tachycardia) was determined by the relative contribution of enhanced CSNA and CVNA. At the later stage of occlusion, bradycardia was induced by a combination of decreased CSNA and enhanced CVNA. In anesthesia and/or atropinization it was induced mainly by the decreased CSNA.

scholarly journals Arterial baroreflex control of sympathetic nerve activity and heart rate in patients with type 2 diabetes

2016 ◽  
Vol 311 (5) ◽  
pp. H1170-H1179 ◽  
Author(s):  
Seth W. Holwerda ◽  
Lauro C. Vianna ◽  
Robert M. Restaino ◽  
Kunal Chaudhary ◽  
Colin N. Young ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Type 2 Diabetes ◽  
Heart Rate ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Group Differences ◽  
Arterial Baroreflex ◽  
Nerve Activity ◽  
Baroreflex Control

Despite greater blood pressure reactivity to acute cardiovascular stressors and a higher prevalence of hypertension in type 2 diabetes (T2D) patients, limited information is available regarding arterial baroreflex (ABR) control in T2D. We hypothesized that ABR control of muscle sympathetic nerve activity (MSNA) and heart rate (HR) are attenuated in T2D patients. Seventeen T2D patients (50 ± 2 yr; 31 ± 1 kg/m2), 9 weight-matched controls (WM-CON, 46 ± 2 yr; 32 ± 2 kg/m2) and 10 lean controls (Lean-CON, 49 ± 3 yr; 23 ± 1 kg/m2), underwent bolus infusions of sodium nitroprusside (100 μg) followed 60 s later by phenylephrine (150 μg) and weighted linear regression performed. No group differences in overall sympathetic baroreflex gain were observed (T2D: −2.5 ± 0.3 vs. WM-CON: −2.6 ± 0.2 vs. Lean-CON: −2.7 ± 0.4 arbitrary units·beat·mmHg−1, P > 0.05) or in sympathetic baroreflex gain when derived separately during blood pressure (BP) falls (nitroprusside) and BP rises (phenylephrine). In contrast, overall cardiac baroreflex gain was reduced in T2D patients compared with Lean-CON (T2D: 8.2 ± 1.5 vs. Lean-CON: 15.6 ± 2.9 ms·mmHg−1, P < 0.05) and also tended to be reduced in WM-CON (9.3 ± 1.9 ms·mmHg−1) compared with Lean-CON ( P = 0.059). Likewise, during BP rises, cardiac baroreflex gain was reduced in T2D patients and weight-matched controls compared with lean controls ( P < 0.05), whereas no group differences were found during BP falls ( P > 0.05). Sympathetic and cardiac ABR gains were comparable between normotensive and hypertensive T2D patients ( P > 0.05). These findings suggest preserved ABR control of MSNA in T2D patients compared with both obese and lean age-matched counterparts, with a selective impairment in ABR HR control in T2D that may be related to obesity.

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