Systemic Arterial Pressure Variations Induced by the Stimulation of Bradykinin-Sensitive Vascular Receptors

Author(s):  
G. Tallarida ◽  
R. Cassone ◽  
A. Semprini ◽  
M. Condorelli
1985 ◽  
Vol 63 (9) ◽  
pp. 1122-1132 ◽  
Author(s):  
J. A. Armour ◽  
W. C. Randall

Electrical stimulation of a canine vagosympathetic complex or a cardiopulmonary nerve can elicit a variety of negative chronotropic and inotropic cardiac responses, with or without alterations in systemic arterial pressure. In the period immediately following cessation of such a stimulation "rebound" tachycardia, increased inotropism above control values in one or more regions of the heart, and (or) elevation in systemic arterial pressure can occur. These "rebound" phenomena are abolished by propranolol or ipsilateral chronic sympathectomy. It is proposed that "vagal" poststimulation "rebound" of the canine cardiovascular system is primarily the result of activation of sympathetic neural elements present in the vagosympathetic complexes or cardiopulmonary nerves.


1959 ◽  
Vol 196 (5) ◽  
pp. 1053-1056 ◽  
Author(s):  
Edward Herzig ◽  
Walter S. Root

Pressures in the femoral artery and in the marrow of the femur of adult cats anesthetized with Nembutal were measured, using 16 gauge needles and Stratham strain gauge transducers. Records were obtained by means of a Sanborn twin viso, model 60. Bone marrow pressures varied between 24 and 114 mm Hg in different animals. Occlusion of the arterial supply caused a fall in marrow pressure. Stimulation of the cut peripheral end of either vagus reduced both systemic and marrow pressures. Stimulation of the cut peripheral end of the splanchnic nerve, or intravenous injection of epinephrine or norepinephrine, increased systemic arterial pressure and decreased marrow pressure. Stimulation of the peripheral end of the abdominal sympathetic trunk reduced marrow pressure. The increase in systemic arterial pressure produced by occlusion of both carotid arteries is associated with an increase in marrow pressure. Marrow pressures are decreased after a large hemorrhage or when amyl nitrite is inhaled. Unilateral denervation of the blood vessels supplying the femur of a decerebrate cat produces a higher marrow pressure as compared with that present in the contralateral innervated femur.


1999 ◽  
Vol 276 (1) ◽  
pp. H242-H247 ◽  
Author(s):  
John Ciriello ◽  
Stefanie Roder

GABAergic inputs have been demonstrated in the central nucleus of the amygdala (ACe). However, the contribution of these inhibitory inputs to the cardiovascular responses elicited from the ACe is not known. Experiments were done in chloralose-anesthetized, paralyzed, and artificially ventilated male Wistar rats to investigate the effects of microinjections of GABA, the selective GABAA-receptor antagonist bicuculline, or the GABAB-receptor antagonist phaclofen, in the ACe on the mean arterial pressure (MAP) and heart rate (HR) responses elicited byl-glutamate (Glu) stimulation of the ACe. Microinjections of Glu in the ACe elicited decreases in MAP (−13.7 ± 1.6 mmHg) and HR (−5.3 ± 1.9 beats/min). The MAP and HR responses elicited by Glu stimulation of the ACe were significantly reduced (89%) by the prior microinjection of GABA in the same ACe site. In addition, at some sites in the ACe at which microinjection of Glu did not elicit depressor responses, Glu injections in the presence of phaclofen elicited decreases in MAP (−9.5 ± 1.0 mmHg) and variable changes in HR. On the other hand, the magnitude of the depressor responses elicited during stimulation of the ACe site in the presence of bicuculline was significantly attenuated (60%), whereas phaclofen had no effect on the magnitude of the depressor responses elicited by Glu stimulation of the ACe. These data suggest that GABAergic mechanisms in the ACe alter the excitability of ACe neurons involved in mediating changes in systemic arterial pressure and HR.


Owing to the large amount of conflicting data regarding the activity of the pulmonary vasomotor nerves, modern reviewers of the literature generally conclude that vasomotor influences play no important part in the regulation of the pulmonary blood flow. Previous work on the subject falls sharply into two groups, experiments on the whole animal and those on isolated perfused lungs. It must be confessed that a careful survey of the work on the whole animal purporting to demonstrate the functional activity of these nerves reveals with few exceptions the absence of a sufficient proof owing to the difficulties of obtaining well controlled experimental conditions, and this no doubt accounts for the scepticism prevalent at the present time. Among the doubt accounts for the scepticism prevalent at the present time. Among the exceptions are the classical experiments of Bradford and Dean (1889, a , 1889, b , 1894) on the dog, curarised and atropinised. These investigators showed that stimulation of the peripheral ends of the cut thoracic nerves from D2-D7 would sometimes cause a pulmonary arterial pressure rise without either cardiac acceleration or a systemic arterial pressure rise, and in general their results were confirmed by Francois-Franck (1895, a , 1895, b ) and Plumier (1904, a ). Excitaion of the vagus in these experiments produced no effect on the pulmonary arterial pressure, probably because, as suggested by Luck-hardt and Carlson (1921), atropine was injected to eliminate the effect of vagus stimulation on the heart. Further, they presented evidence of reflex of pulmonary vasoconstriction caused by excitation of the upper thoracic posterior roots, and Francois-Franck (1896) was able to demonstrate the same effect by stimulation of the central ends of the splachnic or anterior crural nerves. Bradford and Dean ( loc . Cit .) and Weber (1910) also observed that a reflex change in the pulmonary arterial pressures occurred after central stimulation of the divided vagus nerve, and Schafer (1920) reported a reflex pulmonary arterial pressure fall after stimulation of the depressor nerve. The investigations of Bradford and Dean and of Wood (1902, 1910, 1911) on the relations of the pulmonary and aortic pressure during asphyxia were adduced as evidence in favour of the presence of a vasoconstriction nerve supply to the lungs, but the production of an adrenalinæmia in these experiments was not considered.


2020 ◽  
Vol 43 (10) ◽  
pp. 1057-1067 ◽  
Author(s):  
Gean Domingos-Souza ◽  
Fernanda Machado Santos-Almeida ◽  
César Arruda Meschiari ◽  
Nathanne S. Ferreira ◽  
Camila A. Pereira ◽  
...  

2004 ◽  
Vol 355 (1-2) ◽  
pp. 73-76 ◽  
Author(s):  
Chi-Li Gong ◽  
Yung-Tsung Chiu ◽  
Nai-Nu Lin ◽  
Shinn-Zong Lin ◽  
Fu-Chou Cheng ◽  
...  

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