Role of the Sympathetic Nervous System in the Cardiovascular Effects of Cocaine

Gillis, R. A.; Lc, Bachenheimer; Kl, Dretchen; Hk, Erzouki; Ym, Hernandez; Rk, Jain; Mk, Jain; Fe, Kuhn; Quest, John A.; Gl, Schaer

doi:10.1037/e496272006-008

Cited by 22 publications

(27 citation statements)

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“…19 Although catecholamine release might have been a potential mechanism in the present study, we can rule out this phenomenon because sympathetic innervation of the carotid was sectioned in these experiments.…”

Section: Discussion Liameter Inmentioning

confidence: 99%

Carotid sinus baroreceptor sensitivity in experimental heart failure.

Wang¹,

Chen²,

Zucker³

1990

Circulation

136

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Single-unit carotid sinus baroreceptor activity was recorded in normal and heart-failure (pacing-induced) dogs. The sensitivity of these units was compared between the two groups of dogs. After development of clinical heart failure, the animals were anesthetized, and the left carotid sinus was vascularly isolated and perfused with oxygenated Krebs-Henseleit solution. Single-unit baroreceptor discharge was recorded from the carotid sinus nerve in response to stepwise increases in carotid sinus pressure (CSP). In addition, the carotid sinus diameter was measured with sonomicrometer crystals. In this way, both CSP-discharge and CSP-diameter curves were constructed for both normal and heart-failure dogs. Analysis of these curves demonstrated that the heart-failure group exhibited a significant decrease in peak discharge (48.1±3.0 vs. 22.2±+ 2.2 spikes/sec; p<0.001) and a significant elevation in threshold pressure compared with the normal animals (91.0 +5.0 vs. 119.1±+4.4 mm Hg; p<0.001). The peak slope of the CSP-discharge curve was also significantly lower in the heart-failure group (0.63 ±0.06 vs. 0.40 ±0.09 spikes/sec/mm Hg; p <0.05). In the heart-failure group, perfusion of the carotid sinus with ouabain (0.01 ,ug/ml) caused a significant decrease in threshold pressure and a significant increase in peak discharge frequency, as well as an increase in slope of the CSP-discharge curve. There were no changes in CSP-diameter relations in response to ouabain. This dose of ouabain had no effect on pressure-discharge relations or carotid sinus diameters in normal dogs. Perfusion of the isolated carotid sinus with a Krebs-Henseleit solution with 50% of the normal potassium ion concentration had no effect on peak discharge or slope, but this perfusion protocol significantly reduced threshold pressure in heart-failure dogs. Low potassium ion concentration had no effect in the normal dogs. From these data, we conclude that there is attenuation of the carotid sinus baroreceptor discharge sensitivity in this model of low-output heart failure. The data are consistent with the view that there is an augmentation of Na+,K+-ATPase activity in the carotid sinus baroreceptor. (Circulation 1990;81:1959-1966 T he reflex control of the circulation is clearly abnormal in heart failure.1-8 The arterial baroreflex is abnormal in both low-and high-output heart failure in humans3'4 and in animals.5-8 The mechanisms for this reflex abnormality are not completely understood. Derangements in any part of the reflex arc could be responsible for the depression in baroreflex sensitivity that has been observed in heart failure.Clearly, data indicate that the efferent components of the baroreflex control of heart rate are abnormal,2'4 and it has also been shown that both catecholamine synthesis and responsiveness are depressed in heart failure. both systemic norepinephrine clearance and spillover are abnormal in heart failure.1" Evidence from this laboratory also suggests that both carotid and aortic baroreceptor discharge sensitivities are depres...

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Section: Discussion Liameter Inmentioning

confidence: 99%

Carotid sinus baroreceptor sensitivity in experimental heart failure.

Wang¹,

Chen²,

Zucker³

1990

Circulation

136

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“…These results suggest that the effects of ouabain and the OLC in the RVLM are at least partly mediated by M 2 muscarinic mechanisms. Cardiac glycosides including ouabain enhance the release of acetylcholine from parasympathetic nerve endings (42). In the brain, ouabain was reported to induce the release of acetylcholine from cortical synaptosomes in vitro (20)(21)(22).…”

Section: Discussionmentioning

confidence: 99%

Role of ouabain-like compound in the rostral ventrolateral medulla in rats.

Teruya¹,

Yamazato²,

Muratani³

et al. 1997

J. Clin. Invest.

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To determine whether ouabain-like compound (OLC) exerts modulatory influences on the activity of vasomotor neurons in the rostral ventrolateral medulla (RVLM), we examined the effects of microinjecting ouabain, digoxin-specific antibody Fab fragments, and mAb against ouabain on the rat RVLM. Microinjection of ouabain into the unilateral RVLM of anesthetized normotensive rats elicited dose-dependent increases in mean arterial pressure (MAP) and renal sympathetic nerve activity (

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“…All of these influences lead to a reduction in afterload and so are beneficial in heart failure. 5 showed a significant increase in left ventricular ejection fraction and the German and Austrian Xamoterol Study Group8 found that digoxin produced significant improvement in the symptoms and signs of heart failure together with a reduction in the cardiothoracic ratio. These are not simply short term effects.…”

Section: Introductionmentioning

confidence: 99%