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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sinoaortic denervation SAD in dog induces a permanent rise in blood pressure and heart rate leading to an experimental model of arterial hypertension. This model is associated with a marked increase in plasma catecholamine levels during the two first months. The present study investigates the changes in some renal vasoactive systems (renin activity, aldosterone and kallikrein) and cortical renal beta adrenoceptors during the development of this experimental neurogenic hypertension in dogs. SAD dogs exhibited a biphasic change in plasma renin activity and catecholamines: 1 month after SAD, plasma noradrenaline rose and renin activity decreased. These parameters return to normal values 18 months after SAD whereas blood pressure remained elevated. In contrast, plasma aldosterone levels decreased and urinary sodium increased. Urinary kallikrein was enhanced 1 month after SAD and showed a marked decrease 18 months later when compared with pre-SAD values. Cortical renal beta adrenoceptors (evaluated by 125I-cyanopindolol) exhibited a permanent decrease (Bmax) whatever the duration of arterial hypertension. These results show that SAD-induced hypertension in dog is associated with changes in renal vasoactive system involving urinary excretion of kallikrein and cortical renal beta adrenoceptors. These alterations could be involved in the maintenance of arterial hypertension in this experimental model.
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PMID:[Renal adrenergic beta receptors and experimental neurogenic hypertension]. 165 44

Neuronal organisation of hypothalamo-bulbar mechanisms of regulation of vascular tonus was studied in anesthetised and immobilised cats. The descending influence of posterior, tuberal and anterior structures of the hypothalamus on the activity of antidromically identified sympatho-activating reticulospinal neurons of the ventrolateral region of medulla oblongata is realised by mono-, oligo- and polysynaptic mechanisms. Chronic neurogenic hypertension was induced in rats by overloading the higher nervous activity. Arterial hypertension did not develop in chemically desympathized cats. Central and peripheral neurohumoral mechanisms of vascular tonus regulation are discussed.
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PMID:[The physiological mechanisms of the neurohumoral regulation of vascular tonus]. 168 35

There is ample evidence that the sympathetic nervous system is important in the etiology of essential hypertension. Plasma catecholamines such as norepinephrine and epinephrine are the most common indexes of sympathetic function used in studies of essential hypertension. Plasma norepinephrine is higher in young essential hypertensive patients than in normotensive subjects. Other methods to examine sympathetic activity, such as blood pressure response to sympatholytic agents, measurement of regional sympathetic activity, vascular reactivity to sympathetic agonists, power spectral analysis, and microneurography, have all provided further evidence for enhanced sympathetic activity in essential hypertension, especially in younger subjects. Certain groups that make up a substantial part of the essential hypertensive population, such as obese subjects, have heightened sympathetic activity that could contribute to hypertension. Plasma norepinephrine levels are significantly higher in obese compared with nonobese subjects, and the remarkable fall in blood pressure with weight loss in obese subjects is correlated with reductions in plasma norepinephrine. Antihypertensive agents have variable effects on sympathetic activity; some agents (diuretics and direct vasodilators) have elevating effects, some agents (centrally acting agents and alpha-antagonists) have lowering effects, and others (converting enzyme inhibitors, calcium blockers, and beta-blockers) have mixed effects. Tailoring therapy toward agents that reduce sympathetic activity for specific groups perceived as having neurogenic hypertension, such as obese subjects, is a goal yet to be attained.
Hypertension 1992 Jan
PMID:Obesity, the sympathetic nervous system, and essential hypertension. 173 Apr 57

A large body of evidence indicates that the central nervous system plays an essential role in the pathogenesis of hypertension. However, in many cases the specific brain regions involved and the mechanisms by which these regions promote hypertension are not known. In recent years, research in this and other laboratories has attempted to determine the mechanisms by which neural and humoral signals arising in response to pathological conditions (often occurring in the periphery) interact with the central nervous system to produce hypertension. In this article, we illustrate the coupling of peripheral and central factors in the pathogenesis of hypertension by examining the central actions of angiotensin II and mineralocorticoids in the expression of renal hypertension and mineralocorticoid-salt hypertension, respectively. We also review recent data from this laboratory illustrating the involvement of medullary vasomotor centers in the development of neurogenic hypertension after sinoaortic deafferentation and in the maintenance of hypertension in the spontaneously hypertensive rat.
Hypertension 1991 Nov
PMID:Central nervous system and the pathogenesis of hypertension. Sites and mechanisms. 193 89

To assess the ability of biofeedback (BFB) in controlling hypertension a study was made of 40 hypertensive patients selected by means of the cardiovascular response to an arithmetic test. The patients were divided into four treatment groups: 10 patients were treated with diuretic therapy (D-T), 10 with beta-blocker therapy (Bb-T), 10 with BFB treatment, while 10 had no treatment at all (N-T). The BFB treatment consisted of 36 sittings where patients were requested to control muscular contraction, peripheric temperature and heart rate (HR) by means of a correlated acoustic signal. The results for blood pressure and HR reductions were compared during a 12-month follow-up period. The results for systolic blood pressure, diastolic blood pressure and HR indicate the efficacy of BFB for selected patients and suggest the possibility of using BFB treatment in the first stages of suspected neurogenic hypertension.
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PMID:Efficacy of biofeedback treatment compared with drug therapy in hypertensive patients. 205 51

Pathophysiological effects of the autonomic nervous system are clearly seen in young patients with a high cardiac output and borderline hypertension. As the hypertension progresses, there is a change from the hyperkinetic circulation in borderline hypertension to the increased vascular resistance seen in established hypertension. This hemodynamic transition is caused by decreased beta-adrenergic responsiveness and decreased end-diastolic distension of the heart combined with an increased alpha-adrenergic responsiveness of the resistance vessels. In parallel, the sympathetic tone decreases in the course of hypertension. This transition in sympathetic tone can be explained by the hypothesis of the 'blood pressure seeking properties of the brain'. The central nervous system 'seeks' to maintain a higher pressure. When vascular overresponsiveness sets in, less sympathetic drive is needed to maintain a neurogenic hypertension. Sympathetic overactivity in borderline hypertension is associated with overweight subjects, insulin resistance and dyslipidemia. This suggests a new area of research to investigate the basis of metabolic abnormalities in hypertension.
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PMID:Changing role of the autonomic nervous system in human hypertension. 209 97

Passive or neurogenic hypertension was produced by ligation of the aorta or microinjection of glutamate diethyl ester (GDEE) into the intermediate one-third of the nucleus tractus solitarius (NTS), respectively, in 44 anesthetized, artificially ventilated rats. After bilateral sympathectomy, the blood flow (microsphere method) was increased in the cerebral cortex, thalamus, and mesencephalon in a pressure-dependent manner in the face of neurogenic hypertension, as compared with the flow during passive hypertension. We speculate that some neurogenic mechanism tends to impair cerebrovascular autoregulation when afferents arising from cardiovascular receptors were blocked by GDEE within the NTS.
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PMID:An increase in regional brain blood flow during hypertension induced by chemical inhibition of the nucleus tractus solitarius in rats. 225 67

Patients with borderline hypertension frequently have a hyperkinetic circulation that is neurogenic and can be normalized with autonomic blockade of the heart. The abnormality is of central nervous system origin and due to increased sympathetic stimulation and decreased vagal inhibition of the heart. A subset of patients characterized by high plasma renin and norepinephrine values clearly has a neurogenic hypertension since their blood pressure becomes normal after cardiac blockade and vascular alpha-adrenergic blockade. Since many patients with borderline hypertension have a high cardiac output, and the majority of patients with more advanced hypertension have increased vascular resistance, two questions arise. Is the "hyperkinetic state" a special condition unrelated to established hypertension or is there, in the course of hypertension, a transition from "high output" to "high resistance" state? The literature strongly suggests that patients with hyperkinetic borderline hypertension later proceed to develop the established high resistance form of hypertension. The most likely mechanism for this transition is a change in cardiac and vascular responsiveness due to prolonged excess sympathetic stimulation combined with structural pressure-induced changes in these organs. This analysis of the events in the course of hypertension is of necessity based on an arbitrary definition of the hyperkinetic state usually set at a cardiac index at least two standard deviations above the normal mean. A bivariate analysis of our data (268 normotensive and 186 patients with borderline hypertension) suggests that there indeed are two different populations in this data set. Based on this commingling analysis, the occurrence of a hyperkinetic state was five-fold as frequent in patients with borderline hypertension than in the normotensive population.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sympathetic hyperactivity in early stages of hypertension: the Ann Arbor data set. 246 97

Evidence for increased sympathetic drive, as assessed both by measurements of plasma norepinephrine and by studies of tritiated norepinephrine kinetics, is most frequently obtained in young hypertensive patients. During the initial phases of hypertension, the increased sympathetic drive may persistently elevate arterial pressure through effects on the heart, the blood vessels, and the kidneys. In some patients, signs of a hyperkinetic circulation--including elevated heart rate and, less often, high cardiac output--predominate. In others, elevated vascular resistance, reflecting increased alpha-adrenergic tone, is the principal hemodynamic aberration. Even in patients with high cardiac output, a relative increase of vascular alpha-adrenergic tone accounts for their higher blood pressure. Increased sympathetic drive to the kidneys diminishes the efficiency of pressure diuresis, which is designed to restore normal arterial pressure. Although increased plasma norepinephrine levels are not consistently observed among older hypertensive patients compared with age-matched controls, neurogenic hypertension is not only a temporary event. In fact, tachycardia, which is neutrogenically mediated, doubles the risk of sustained hypertension later in life. The precise sequence of events in the transition from a principally neurogenic hypertension early in life to a predominantly nonneurogenic hypertension later in life is not known, although it likely includes decreased beta-receptor sensitivity with consequently reduced tachycardia and beta-mediated vasodilation. Functional diminution in endothelium-dependent vasodilation may augment sensitivity to vasoconstrictors such as norepinephrine and serotonin. Moreover, structural vascular changes nonspecifically enhance vascular reactivity to all vasoactive compounds and may provide a more permanent basis for altered pressure diuresis. Thus, hypertension initiated predominantly by neurogenic mechanisms could be sustained later without excessive sympathetic drive.
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PMID:Neurogenic mechanisms initiating essential hypertension. 268 92

The effect of afferent renal nerve transection (tARN) on the metabolic activity of forebrain structures the activity of which was altered after aortic depressor nerve transection (tADN) was studied using the hexokinase (HK) histochemical method in the rat. In tADN-sham (s) ARN rats, increases in HK activity were observed in the medial septum (MS), median preoptic nucleus (MnPO), subfornical organ, supraoptic nucleus, nucleus circularis (Nc), magnocellular, and dorsal and medial (mpPVH) parvocellular components of paraventricular nucleus, the anterior, lateral, and dorsomedial (DMH) hypothalamus, and in the central and medial nuclei of the amygdala. In addition, a decrease in HK activity was seen in the dorsal arcuate nucleus (dArc). Similarly, increases in HK activity were seen in sADN-tARN rats in all the above structures except MS, Nc, and DMH, where no changes were observed, and dArc, where an increase in HK activity was noted. The bed nucleus of the stria terminalis, lateral preoptic nucleus (POA), and ventral (v) Arc also showed elevated HK activity. In contrast, the increased HK activity after either tADN or tARN alone was returned to levels not different from sADN-sARN rats in all structures in the tADN-tARN rats, except MnPO, mpPVH, and dArc, where the level of HK activity was only attenuated, and MS, POA, and vArc, where it remained elevated. These data suggest that similar forebrain structure are associated with the hypertension after tADN and are involved in the integration of ARN information and that these sites of interaction are involved in the maintenance and the reversal of the neurogenic hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal denervation alters forebrain hexokinase activity in neurogenic hypertensive rats. 270 81


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