scholarly journals Azelnidipine inhibits the sympathetic nerve activity and improves baroreflex control of heart rate via anti‐oxidant effect in the rostral ventrolateral medulla

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Satomi Konno ◽  
Yoshitaka Hirooka ◽  
Takuya Kishi ◽  
Yasuaki Koga ◽  
Shuuichiro Araki ◽  
...  
Keyword(s):  
Heart Rate ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Anti Oxidant ◽  
Oxidant Effect

Galanin microinjection into rostral ventrolateral medulla of the rat is hypotensive and attenuates sympathetic chemoreflex

2009 ◽  
Vol 296 (4) ◽  
pp. R1019-R1026 ◽  
Author(s):  
Stephen B. G. Abbott ◽  
Paul M. Pilowsky
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Cardiovascular Response ◽  
Cardiovascular Responses ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Nerve Activity ◽  
Somatosympathetic Reflex

Galanin is present in neurons in the brain that are important in the control of arterial pressure, and intracisternal administration of galanin evokes hypotension, but the site of action is unknown. In urethane-anesthetized, vagotomized mechanically ventilated Sprague-Dawley rats ( n = 34), we investigated the effects of microinjecting galanin (1 mM, 50 nl, 50 pmol) into the rostral ventrolateral medulla on resting splanchnic sympathetic nerve activity, arterial pressure, heart rate, and phrenic nerve activity. Second, we determined the effect of microinjecting galanin into the rostral ventrolateral medulla on the cardiovascular response to stimulation of central and peripheral chemoreceptors, arterial baroreceptors, and the somatosympathetic reflex. Galanin caused a prolonged reduction in resting splanchnic sympathetic nerve activity (−37.0 ± 7.2% of baseline), mean arterial pressure (−17.0 ± 3.5 mmHg), and heart rate (−25.0 ± 9.1 beats/min). Galanin increased the sympathoinhibitory response to aortic depressor nerve stimulation by 51.8%, had no effect on the somatosympathetic reflex, and markedly attenuated the effect of hypercapnia and hypoxia on arterial pressure (by 65% and 92.4% of control, respectively). These results suggest a role for galanin neurotransmission in the integration of the cardiovascular responses to hypoxia, hypercapnia, and the sympathetic baroreflex in the rostral ventrolateral medulla. The data suggest that galanin may be an important peptide in the homeostatic regulation of chemosensory reflexes.

scholarly journals Hypertension in Patients with Neurovascular Compression Is Associated with Increased Central Sympathetic Outflow

2002 ◽  
Vol 13 (1) ◽  
pp. 35-41
Author(s):  
Hans P. Schobel ◽  
Helga Frank ◽  
Ramin Naraghi ◽  
Helmut Geiger ◽  
Elmar Titz ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Cold Pressor Test ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Neurovascular Compression ◽  
Sympathetic Outflow ◽  
Nerve Activity ◽  
Central Sympathetic Outflow

ABSTRACT. Recent data suggest a causal relationship between essential hypertension and neurovascular compression (NVC) at the rostral ventrolateral medulla. An increase of central sympathetic outflow might be an underlying pathomechanism. The sympathetic nerve activity to muscle was recorded in 21 patients with hypertension with NVC (NVC+ group) and in 12 patients with hypertension without NVC (NVC− group). Heart rate variability, respiratory activity, BP, and central venous pressure at rest and during unloading of cardiopulmonary baroreceptors with lower-body negative pressure and during a cold pressor test were also measured. Resting sympathetic nerve activity to muscle was twice as high in the NVC+ group compared with the NVC− group (34 ± 22 versus 18 ± 6 bursts/min; P < 0.05). Resting heart rate (P = 0.06) and low- to high-frequency power ratio values (P = NS) (as indicators of cardiac sympathovagal balance) tended to be augmented as well in the NVC+ group. The sympathetic nerve activity to muscle response to the cold pressor test was increased in the NVC+ group versus the NVC− group (+15 ± 11 versus 6 ± 12 bursts/min; P = 0.05), but hemodynamic and sympathetic nerve responses to lower-body negative pressure did not differ between the two groups. It is concluded that NVC of the rostral ventrolateral medulla in patients with essential hypertension is accompanied by increased central sympathetic outflow. Therefore, these data support the hypothesis described in the literature: in a subgroup of patients, essential hypertension might be causally related to NVC of the rostral ventrolateral medulla, at least in part, via an increase in central sympathetic outflow.

scholarly journals Insulin in the Brain Increases Gain of Baroreflex Control of Heart Rate and Lumbar Sympathetic Nerve Activity

Hypertension ◽  
2008 ◽  
Vol 51 (2) ◽  
pp. 514-520 ◽  
Author(s):  
Mollie P. Pricher ◽  
Korrina L. Freeman ◽  
Virginia L. Brooks
Keyword(s):  
Heart Rate ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
The Brain

Effects of NO on baroreflex control of heart rate and renal nerve activity in conscious rabbits

1996 ◽  
Vol 270 (6) ◽  
pp. R1361-R1370 ◽  
Author(s):  
J. L. Liu ◽  
H. Murakami ◽  
I. H. Zucker
Keyword(s):  
Heart Rate ◽  
Sympathetic Nerve ◽  
Baroreflex Sensitivity ◽  
Sympathetic Nerve Activity ◽  
Control Level ◽  
Relative Role ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Baroreflex Control ◽  
Synthase Inhibitor

Recent data suggest that nitric oxide (NO) plays a role in the modulation of sympathetic nerve activity and baroreflex sensitivity. Most of these studies have been carried out in anesthetized preparations, and little if any comparison has been made on the relative role of NO on the baroreflex control of heart rate and sympathetic nerve activity. In the present studies, the effect of the NO synthase inhibitor NG-nitro-L-arginine (L-NNA) on the baroreflex control of heart rate (HR) and renal sympathetic nerve activity (RSNA) were investigated in conscious, instrumented rabbits. Intravenous bolus injections of 13 mg/kg of L-NNA decreased baseline HR (from 205.0 +/- 6.0 to 145.5 +/- 8.2 beats/min; P < 0.05) without significant changes in mean arterial pressure (MAP) and RSNA. L-NNA significantly reduced the lower plateau of the HR-MAP curves and increased the sensitivities of baroreflex control of HR and RSNA. L-Arginine (600 mg/kg i.v.) but not D-arginine reversed the above effects. The effects of L-NNA on baseline HR were not completely blocked by metoprolol (2 mg/kg) or by atropine (0.2 mg/kg). After pretreatment with metoprolol, baroreflex sensitivity was reduced and L-NNA increased baroreflex sensitivity back to the control level. After pretreatment with atropine, L-NNA still reduced the lower plateau but did not significantly affect baroreflex sensitivity. L-NNA increased the HR responses but not the RSNA response to electrical stimulation of the aortic nerve in chloralose-anesthetized, sinoaortic-denervated (SAD) rabbits. L-NNA had no effect on the HR response to right vagal stimulation. In both conscious intact and SAD rabbits, L-NNA did not increase baseline RSNA. These results suggest that endogenous NO decreases baroreflex control of HR and RSNA. Both sympathetic and parasympathetic components play a role in the effects of NO on the baroreflex control of HR. The effects of NO in the central nervous system play a more important role in the baroreflex control of HR than of RSNA.

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