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Journal ArticleDOI

Acute Fulminating Neurogenic Hypertension Produced by Brainstem Lesions in the Rat

01 May 1973-Circulation Research (Lippincott Williams & Wilkins)-Vol. 32, Iss: 5, pp 584-593
TL;DR: The fulminating hypertension evoked by lesions of the nucleus tractus solitarii was due to the increased vasoconstriction caused by the augmented discharge of sympathetic nerves in response to central deafferentation of baroreceptor reflexes.
Abstract: Bilateral electrolytic lesions of the nucleus tractus solitarii in the rat at the level of the obex abolished baroreceptor reflexes and resulted in an immediate, marked elevation in systemic blood pressure without a change in heart rate. In unanesthetized rats the hypertension was associated with a marked increase in total peripheral resistance, a reduction in blood flow in the abdominal aorta, and an increase in central venous pressure. The cardiac output was reduced to 62% of control as a consequence of reduced stroke volume, which was reflected, in turn, by increased end-diastolic pressure. The hypertension was abolished and the end-diastolic pressure lowered by blockade of alpha receptors with phentolamine. The hypertension was not due to changes in blood gases or to release of agents from the kidneys or the adrenal glands; it was very sensitive to anesthetics and was abolished or aborted by midcollicular decerebration. Within hours after lesioning, the rats developed progressive congestive heart failure and died in shock, often in association with pulmonary edema. We concluded that the fulminating hypertension evoked by lesions of the nucleus tractus solitarii was due to the increased vasoconstriction caused by the augmented discharge of sympathetic nerves in response to central deafferentation of baroreceptor reflexes; the hypertension was mediated by alpha receptors and depended on the integrity of structures lying above the midbrain.
Citations
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Journal ArticleDOI
TL;DR: The autoradiographic material, and additional double-labeling experiments, were used to identify and to characterize projections that interconnect the A1, A2 and A6 regions, as well as possible projections from these cell groups to the spinal cord.

1,099 citations

Journal ArticleDOI
TL;DR: These functional, anatomical and neurochemical correlates of the alpha 2 binding site distribution establish a neurological basis for the complex pharmacological effects of centrally acting alpha 2 agonists.

711 citations

Book ChapterDOI
TL;DR: The chapter outlines the possible interrelationship between the modulatory biogenic amine-containing neurones and the baroreceptor reflex arc and discusses the possible site of these modulatory centers in the hypothalamus and in the brain stem.
Abstract: Publisher Summary In this chapter, the neuroanatomy of the baroreceptor reflex arc is reviewed and relevant new data are presented. The baroreceptor reflex arc consists of a multisynaptic neuronal chain. Primary neurones have perikarya in the nodose ganglion, and they connect the peripheral baroreceptor sites with the nucleus tractus solitarii (NTS) via fibres in the 9th and 10th cranial nerves. The first synapse in the baroreceptor reflex arc and also the origin of the secondary neurones are located in the caudal and partly in the commissural parts of the NTS. Neuroanatomical topography of the NTS and neighboring medullary nuclei in the rat is presented and detailed. The fibres of the secondary neurones terminate in various medullary nuclei and probably reach—directly or by multisynaptic pathways—the higher regions that may modulate the baroreceptor reflex arc. The chapter presents a discussion on the possible site of these modulatory centers in the hypothalamus and in the brain stem and of the loop of the descending fibres from these regions to the medullary and spinal baroreceptor neurones. The efferent preganglionic neurones of the baroreceptor reflex arc are located in the medulla oblongata and in the intermedio-lateral nucleus of the spinal cord. The chapter outlines the possible interrelationship between the modulatory biogenic amine-containing neurones and the baroreceptor reflex arc.

386 citations

Journal ArticleDOI
TL;DR: It seems clear that central monoaminergic systems participate in the regulation of normal blood pressure and that their function is altered in experimental hypertension, but it is not yet clear which changes are of primary causal importance and which are secondary in nature.
Abstract: • Central catecholaminergic nerves have an integral place in the central connections of the autonomic nervous system, and they play an important role in the regulation of arterial blood pressure (1-19). Some evidence suggests that central serotonergic nerves also participate in the control of blood pressure (19-24). Studies in various models of experimental hypertension have demonstrated changes in the metabolism and the activity of these central monoaminergic nerves (3, 9, 13, 24). In addition, selective ablation of central catecholaminergic or serotonergic nerves with a variety of chemical compounds profoundly modifies the development of high blood pressure in a number of experimental models (7, 8, 10, 11, 17, 23, 24). It seems clear that central monoaminergic systems participate in the regulation of normal blood pressure and that their function is altered in experimental hypertension. However, the exact significance of these changes in experimental hypertension has not been established. Moreover, it is not yet clear which changes are of primary causal importance and which are secondary in nature. The development of histochemical fluorescence methods for cellular localization of biogenic amines has facilitated the mapping of specific catecholaminergic and serotonergic tracts in the central nervous system (CNS) (25-27). During the last decade it was widely held that only two catecholamines were important neurotransmitters in the CNS—dopamine in the basal ganglia and limbic systems and norepinephrine more diffusely. There is now good evidence from new immunohistochemical methods (28) and sensitive biochemical assays (29) that epinephrine is also a central neurotransmitter. Since many of the studies on brain amines and blood pressure regulation have not differentiated between dopamine, norepinephrine, and epi-

340 citations


Cites background from "Acute Fulminating Neurogenic Hypert..."

  • ...Doba and Reis (16) have also shown that midcollicular decerebration abolishes NTS hypertension, suggesting that the elevated blood pressure depends on the activity of descending suprabulbar pathways....

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  • ...The role of brain amines has been examined in two forms of experimental neurogenic hypertension, the first being produced by bilateral section of the carotid sinus and aortic nerves (9, 10, 23, 24) and the second by central deafferentation following bilateral lesions of the NTS (16, 17)....

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  • ...The inhibitory fibers probably do not terminate on the primary baroreceptor synapse in the NTS, since lesions of the NTS do not cause a bradycardia (16), but on a secondary synapse beyond the NTS (Fig....

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References
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Journal ArticleDOI

438 citations

Journal ArticleDOI
TL;DR: Evidence was found that extensive pressor and depressor regions within the reticular formation of the medulla which yield maximal or near maximal responses to low intensity stimulation are revealed, which served to confirm the contention of Scott that the discrete points on the floor of the fourth ventricle are of little function lasignificance.
Abstract: IN 1870 it was demonstrated that the maintenance of normal cardiovascular function is dependent upon the integrity of structures which are located in the rostra1 portion of the medulla oblongata of the brain stem. (For studies of Dittmar and of Owsjannikow, see 2.) It was later suggested by Porter (18) that this bulbar system might be subdivided into a “vasoreflex” center and a “vasotonic” center. In an attempt to localize these bulbar centers with greater accuracy, Ranson and Billingsley (20) explored the floor of the fourth ventricle with stimulating electrodes searching for vasomotor reactions. They identified relatively discrete points which yield significant responses to low intensity stimulation:a pressor point in the fovea inferior at the apex of the ala cinerea and a depressor point in the area postrema just lateral to the obex. They also found somewhat variable pressor responses in the region of the facial colliculus which they attributed to Porter’s %asotonic” center. Chen, Lim, Wang, and Yi confirmed the presence of the pressor and depressor points and contended that the pressor point represents a center concerned with the excitation of the entire sympathetic system (6) while the depressor point is concerned with the inhibition of the sympathetic system (10). On the other hand, the concept that these points on the floor of the fourth ventricle represent integrative centers for pressor and depressor functions has been challenged by Scott (21). He found that destruction of these regions by cautery did not interfere with normal pressor and depressor functions except in so far as there was damage to afferent vasomotor pathways. These divergent points of view were resolved by exploring the deeper structures of the medulla, a procedure which was made possible by the introduction of the HorsleyClarke stereotaxic instrument. Orienting fine needle electrodes with the aid of this instrument, Wang and Ranson (22) explored the entire substance of the brain stem from the pons to the decussation of the pyramids. A similar though less extensive exploration has been carried out by Monnier (12). This method revealed extensive pressor and depressor regions within the reticular formation of the medulla which yield maximal or near maximal responses to low intensity stimulation. This evidence served to confirm the contention of Scott that the discrete points on the floor of the fourth ventricle are of little function lasignificance, since they are merely points where the deeper lying centers come close enough to the surface to be stimulated by superficial electrodes.

388 citations

Journal ArticleDOI

316 citations


"Acute Fulminating Neurogenic Hypert..." refers background in this paper

  • ...the paramedian reticular nucleus (11-16), should...

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  • ...Our findings suggest that baroreceptors, after terminating in the medulla (11-17) engage in longloop cardiovascular reflexes with higher brain areas....

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  • ...First, the critical site in the brainstem which had to be damaged bilaterally to produce this syndrome was the middle third of the NTS located at the obex, the so-called intermediate zone of the nucleus (11)....

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