scholarly journals Role of the nucleus ambiguus in the regulation of heart rate and arterial pressure.

Hypertension ◽  
1988 ◽  
Vol 11 (6_pt_2) ◽  
pp. 602-607 ◽  
Author(s):  
B H Machado ◽  
M J Brody
2018 ◽  
Vol 596 (8) ◽  
pp. 1373-1384 ◽  
Author(s):  
Thomas J. Hureau ◽  
Joshua C. Weavil ◽  
Taylor S. Thurston ◽  
Ryan M. Broxterman ◽  
Ashley D. Nelson ◽  
...  

2002 ◽  
Vol 283 (2) ◽  
pp. R451-R459 ◽  
Author(s):  
Ling Xu ◽  
Alan F. Sved

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.


1983 ◽  
Vol 244 (1) ◽  
pp. R74-R77 ◽  
Author(s):  
J. Schwartz ◽  
I. A. Reid

The role of vasopressin in the regulation of blood pressure during water deprivation was assessed in conscious dogs with two antagonists of the vasoconstrictor activity of vasopressin. In water-replete dogs, vasopressin blockade caused no significant changes in mean arterial pressure, heart rate, plasma renin activity (PRA), or plasma corticosteroid concentration. In the same dogs following 48-h water deprivation, vasopressin blockade increased heart rate from 85 +/- 6 to 134 +/- 15 beats/min (P less than 0.0001), increased cardiac output from 2.0 +/- 0.1 to 3.1 +/- 0.1 1/min (P less than 0.005), and decreased total peripheral resistance from 46.6 +/- 3.1 to 26.9 +/- 3.1 U (P less than 0.001). Plasma renin activity increased from 12.4 +/- 2.2 to 25.9 +/- 3.4 ng ANG I X ml-1 X 3 h-1 (P less than 0.0001) and plasma corticosteroid concentration increased from 3.2 +/- 0.7 to 4.9 +/- 1.2 micrograms/dl (P less than 0.05). Mean arterial pressure did not change significantly. When the same dogs were again deprived of water and pretreated with the beta-adrenoceptor antagonist propranolol, the heart rate and PRA responses to the antagonists were attenuated and mean arterial pressure decreased from 103 +/- 2 to 91 +/- 3 mmHg (P less than 0.001). These data demonstrate that vasopressin plays an important role in blood pressure regulation during water deprivation in conscious dogs.


2010 ◽  
Vol 461 (1) ◽  
pp. 23-28 ◽  
Author(s):  
João Paulo J. Sabino ◽  
Gabriela Bombarda ◽  
Carlos Alberto A. da Silva ◽  
Rubens Fazan ◽  
Maria Cristina O. Salgado ◽  
...  

1978 ◽  
Vol 235 (5) ◽  
pp. R286-R293
Author(s):  
J. Ciriello ◽  
F. R. Calaresu

The role of the external cuneate nucleus (ECN) in the control of heart rate was systematically investigated in 26 chloralosed and 2 decerebrated, paralyzed, and artifically ventilated cats. Electrical stimulation of histologically verified sites in the ventral ECN and dorsal spinal trigeminal tract elicited a marked decrease in heart rate, with threshold currents of 5-25 muA and an optimal frequency of 20 Hz when using a 0.2 ms pulse; this response was shown to be due to vagal excitation. In seven experiments intravenous pentobarbital sodium decreased the magnitude of the bradycardia elicited by stimulation of the ECN, of the nucleus ambiguus (AMB), and of the cervical vagus significantly less than the response from the nucleus of the tractus solitarius. In eight additional experiments in cats with lesions of the AMB made 11-27 days earlier stimulation of the ECN elicited a bradycardia of the same magnitude as that observed in intact animals, although the bradycardia elicited by stimulation of the ipsilateral cervical vagus was significantly reduced by the lesion. Similarly, lesions of the ECN in four cats significantly attenuated the bradycardia elicited by stimulation of the ipsilateral cervical vagus. These results suggest that the ECN is a site of origin of cardioinhibitory axons in the cat.


Endocrinology ◽  
2008 ◽  
Vol 149 (7) ◽  
pp. 3576-3580 ◽  
Author(s):  
Hiroyoshi Sei ◽  
Katsutaka Oishi ◽  
Sachiko Chikahisa ◽  
Kazuyoshi Kitaoka ◽  
Eiji Takeda ◽  
...  

Arterial pressure (AP), heart rate (HR), and cardiovascular diseases, including ischemic heart attack and cerebrovascular accident, show diurnal variation. Evidence that circadian-related genes contribute to cardiovascular control has been accumulated. In this study, we measured the AP and HR of Clock mutant mice on the Jcl/ICR background to determine the role of the Clock gene in cardiovascular function. Mice with mutated Clock genes had a dampened diurnal rhythm of AP and HR, compared with wild-type control mice, and this difference disappeared after adrenalectomy. The diurnal acrophase in both mean arterial pressure and HR was delayed significantly in Clock mutant mice, compared with wild-type mice, and this difference remained after adrenalectomy. Clock mutant mice had a lower concentration of plasma aldosterone, compared with wild-type mice. Our data suggest that the adrenal gland is involved in the diurnal amplitude, but not the acrophase, of AP and HR, and that the function of the Clock gene may be related to the nondipping type of AP elevation.


Neuroreport ◽  
2000 ◽  
Vol 11 (3) ◽  
pp. 481-485 ◽  
Author(s):  
Piero Ruggeri ◽  
Antonio Battaglia ◽  
Rosa Ermirio ◽  
Elena Grossini ◽  
Claudio Molinari ◽  
...  

1978 ◽  
Vol 45 (4) ◽  
pp. 574-580 ◽  
Author(s):  
F. Bonde-Petersen ◽  
L. B. Rowell ◽  
R. G. Murray ◽  
G. G. Blomqvist ◽  
R. White ◽  
...  

Ten men repeatedly performed leg exercise (100–150 W) for 7 min with 30-min recovery periods interspersed. Both legs were made ischemic by total occlusion (OCCL), first for 3 min immediately after exercise and second for 30 s before exercise ended and 3 min into recovery. In addition legs were occluded for 3 min at rest (seated). OCCL at rest increased mean arterial pressure (MAP) by 9 Torr but did not affect cardiac output (CO) or heart rate (HR). OCCL at the end of exercise significantly raised MAP and HR above control values during 3-min recovery but CO was unaffected. OCCL 30 s before the end of exercise further increased MAP and HR significantly during recovery; MAP, CO, and HR were significantly increased above control values (CO by 2.1 1-min-1) during the 3rd min of recovery. We conclude that a strong reflex from ischemic legs maintains normal or elevated CO during leg OCCL. Thus CO was too high relative to total vascular conductance so that MAP was elevated.


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