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

The management of essential hypertension has increasingly focused on the use of diuretics, angiotensin-converting enzyme inhibitors, and angiotensin receptor blockers, which lower blood pressure (BP) through effects on blood volume and on the renin-angiotensin system. However, in many individuals these agents, whether given alone or in combination, fail to normalize BP. In such cases it is likely that hypertension is at least partly maintained by pathophysiologic mechanisms other than volume and the renin-angiotensin system, and therefore, that pharmacotherapy directed at other mechanisms is needed. One such form of hypertension is the often overlooked entity of neurogenic hypertension. The purpose of this article is to renew attention to this overlooked entity, to provide a very clinically oriented overview of its possible causes and manifestations, and to discuss the potentially important treatment implications of recognizing this form of hypertension. These implications underscore the need for further clinical and research attention concerning neurogenically mediated hypertension.
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PMID:Neurogenic essential hypertension revisited: the case for increased clinical and research attention. 1455 71

The authors present a case of medically refractory, neurogenic hypertension where the MR examination revealed an odontoid compression of the anterior medulla as a consequence of a basilar impression. Following transoral odontoidectomy and craniocervical fixation, the blood pressure in the 24-year-old woman returned to normal, and 1 year postoperatively she remains normotensive and off all medication. This reported case provides further support to the theory that there is a subgroup of patients who may have a vascular compression of the medulla with no neurological symptoms other than hypertension.
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PMID:[Odontoidectomy in the treatment of medically refractory, neurogenic hypertension]. 1463 95

Central nervous system mechanisms are involved in hypertension caused by chronic inhibition of nitric oxide (NO) synthesis. Chronic inhibition of NO synthesis might also activate the Rho/Rho-kinase pathway in the vasculature. We recently demonstrated that activation of the Rho/Rho-kinase pathway in the nucleus tractus solitarii (NTS) contributes to hypertensive mechanisms in spontaneously hypertensive rats. The aim of the present study was to determine whether activation of this pathway also contributes to neurogenic hypertensive mechanisms caused by chronic NO synthesis inhibition. The NO synthase inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME) was administered to Wistar-Kyoto rats in their drinking water (1 mg/mL) for 2 weeks. Bilateral microinjection of Y-27632, a specific Rho-kinase inhibitor, into the NTS elicited decreases in arterial pressure, heart rate, and renal sympathetic nerve activity in control rats and L-NAME-treated rats. The magnitude of the decrease, however, was significantly greater in L-NAME-treated than in control rats. In another group of rats, the specific Rho-kinase inhibitor, Y-27632, was administered intracisternally for 2 weeks with a mini-osmotic pump from the beginning of treatment with L-NAME. Y-27632 co-treatment significantly attenuated the increase in arterial pressure. Furthermore, the expression level of membranous RhoA and phosphorylation of the target proteins of Rho-kinase, the ERM (ezrin, radixin, moesin) family members, was significantly greater in L-NAME-treated rats than in control rats. These results indicate that activation of the Rho/Rho-kinase pathway in the NTS contributes to neurogenic hypertension caused by chronic NO synthase inhibition.
Hypertension 2004 Feb
PMID:Rho/Rho-kinase pathway in the brainstem contributes to hypertension caused by chronic nitric oxide synthase inhibition. 1473 30

Pherentasin, a highly active pressor substance producing a prolonged effect in the rat, has been obtained in a fairly pure form from the arterial blood of patients with hypertension. Its presence has been demonstrated by two biological methods. It was rarely found in normotensive blood. The blood of patients with renal or nephrogenic hypertension, either primary or secondary, consistently yielded this material. The blood of patients exhibiting neurogenic hypertension and the endocrine hypertensive syndrome had smaller amounts of it. Little or none was found in malignant hypertension. Perhaps pherentasin has a causal relation to the existence of arterial hypertension.
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PMID:Pressor substances in arterial hypertension. II. Demonstration of pherentasin, a vasoactive material procured from blood. 1478 36

Previous investigations have demonstrated that capsaicin-sensitive sensory nerves are involved in the development of hypertension in some rat models of hypertension. To determine the role played by calcitonin gene-related peptide (CGRP; the predominant neurotransmitter in capsaicin-sensitive sensory nerves) in a rat model of neurogenic hypertension, in which hypertension was induced by injecting 50 microl of 10% phenol in the lower pole of the left kidney, systolic blood pressure (SBP) was monitored by the tail-cuff method throughout the experiment. Fifteen days after injection of phenol, mean arterial pressure (MAP), concentrations of CGRP in the plasma, the expression of CGRP mRNA in dorsal root ganglia (DRG) and CGRP content in laminae I and II of the spinal cord were measured. SBP was significantly increased 5 days after the intrarenal injection of phenol (164+/-7 mm Hg, p<0.01). At the end of experiment, blood pressure (BP) was significantly elevated in the phenol-injected rats compared with the controls (SBP: 187+/-6 vs. 122+/-4 mm Hg, p<0.01; MAP: 157.56+/-3.02 vs. 103.80+/-2.04 mm Hg, p<0.01). Treatment with capsaicin, which selectively depletes neurotransmitters from the capsaicin-sensitive nerves, failed to enhance the development of hypertensive responses to the intrarenal injection of phenol. Intravenous administration of CGRP(8-37), the specific CGRP receptor antagonist, also failed to increase the already elevated MAP. The expression of CGRP mRNA (both alpha- and beta-CGRP isoforms), the content of CGRP in laminae I and II of the dorsal horn of the spinal cord and the concentration of CGRP in the plasma was decreased in the rats treated with phenol. These results suggest that CGRP does not play a counterregulatory role in the phenol-induced hypertensive rats, and support the hypothesis that reduction of CGRP (alpha and beta isoforms) could contribute to a blood pressure elevation in this setting.
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PMID:Role of calcitonin gene-related peptide in the phenol-induced neurogenic hypertension in rats. 1512 Apr 75

A balance between production and elimination of reactive oxygen species such as superoxide anion (O2*-) and hydrogen peroxide (H2O2) tightly regulates the homeostasis of cellular oxidative stress, which contributes to a variety of cardiovascular diseases, including hypertension. The present study assessed the hypothesis that O2*- or H2O2 levels augmented by the reduced molecular synthesis or enzyme activity of superoxide dismutase (SOD), catalase (CAT), or glutathione peroxidase (GPx) in the rostral ventrolateral medulla (RVLM), where sympathetic premotor neurons that generate tonic vasomotor tone are located, contribute to the pathogenesis of hypertension. We found that copper/zinc SOD (SOD1), manganese SOD (SOD2), or CAT, but not GPx, mRNA or protein expression and enzyme activity in the RVLM of spontaneously hypertensive rats (SHR) were significantly lower than those in normotensive Wistar-Kyoto (WKY) rats, along with a significantly higher level of O2*- or H2O2. A causative relationship between these biochemical correlates of oxidative stress and neurogenic hypertension was established when gene transfer by microinjection of adenovirus encoding SOD1, SOD2, or CAT into the bilateral RVLM promoted a long-lasting reduction in arterial pressure in SHR, but not WKY rats, accompanied by an enhanced SOD1, SOD2, or CAT protein expression or enzyme activity and reduced O2*- or H2O2 level in the RVLM. These results together suggest that downregulation of gene expression and enzyme activity of the antioxidant SOD1, SOD2, or CAT may underlie the augmented levels of O2*- and H2O2 in the RVLM, leading to oxidative stress and hypertension in SHR.
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PMID:Reduction in molecular synthesis or enzyme activity of superoxide dismutases and catalase contributes to oxidative stress and neurogenic hypertension in spontaneously hypertensive rats. 1671 3

Hypertension caused by arterial compression of the rostral ventrolateral medulla is well described. Much less information is available on the association between neurogenic hypertension and posterior fossa brain tumors. To date, multiple reports have supported the impression that a small subpopulation of patients with posterior fossa tumors can present with arterial hypertension, and many of those patients achieved significant improvement of their hypertension after tumor resection and medullary decompression. To review the relationship between posterior fossa brain tumors and hypertension, we detail the history, basic science, and clinical reports along with an illustrative case regarding this topic.
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PMID:Posterior fossa brain tumors and arterial hypertension. 1692 59

New evidence that has emerged during the past several years clearly demonstrates that reactive oxygen species (ROS) in the brain play a crucial role in blood pressure regulation by serving as signaling molecules within neurons of cardiovascular control regions. In the forebrain, midbrain, and hindbrain, a key role for oxidant stress in the pathogenesis of angiotensin II-dependent and various other models of neurogenic hypertension has also been uncovered. As in the peripheral vasculature, NAD(P)H oxidase appears to be a major enzymatic source of brain ROS, and various homologues of the catalytic subunit of this enzyme appear to be differentially localized to cardiovascular-regulating nuclei in the brain. Recent studies have begun to elucidate the downstream effects of ROS in neurons, and it is now clear that ROS may interact with a number of well-described intracellular signaling pathways involved in neuronal activation. These exciting new discoveries have furthered our understanding of the pathogenesis of neurogenic hypertension and may ultimately lead to the development of new treatments. In this review, we discuss recent evidence in support of a role for brain ROS in the pathogenesis of hypertension and summarize current studies aimed at uncovering the complex mechanisms by which brain ROS regulate blood pressure in both health and cardiovascular disease.
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PMID:Reactive oxygen species in the neuropathogenesis of hypertension. 1714 22

Circulating angiotensin II (Ang II) combined with high salt intake increases sympathetic nerve activity (SNA) in some forms of hypertension. Ang II-induced increases in SNA are modest, delayed, and specific to certain vascular beds. The brain targets for circulating Ang II are neurons in the area postrema (AP), subfornical organ (SFO), and possibly other circumventricular organs. Ang II signaling is integrated with sodium-sensitive neurons in the SFO and/or organum vasculosum of the lamina terminalis (OVLT) and drives sympathetic premotor neurons in the rostral ventrolateral medulla (RVLM) via the paraventricular nucleus (PVN). It is likely that, over time, new patterns of gene expression emerge within neurons of the SFO-PVN-RVLM pathway that transform their signaling properties. This transformation is critical in maintaining increased SNA. Identification of a novel gene supporting this process may provide new targets for treatment of neurogenic hypertension.
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PMID:Circulating angiotensin II and dietary salt: converging signals for neurogenic hypertension. 1751 30

Considering the importance of the renin-angiotensin system (RAS) for the central control of blood pressure and that nicotine increases the probability of development of hypertension associated to genetic predisposition, our aims are (1) to determine RAS in cultured neurons and glia from the brainstem and hypothalamus of spontaneously hypertensive (SHR) and Wistar Kyoto (WKY) rats; (2) to analyze the possibility of nicotine to interact with brain RAS; and (3) to hypothesize any contribution of nicotine and RAS to the development of neurogenic hypertension. This study demonstrated physiological differences in RAS between cultured neuronal and glial cells from the brainstem and hypothalamus of SHR and WKY neonate rats. Our study also featured evidences of direct modulation of the RAS by nicotine in neurons and glia of brainstem and hypothalamus, which seems to be differential between the two rat strains. Such modulation gives us a clue about the mechanisms possibly involved in the genesis of neurogenic hypertension in vivo, for example, increase in angiotensin II type 1 receptor binding and decrease in angiotensin-converting enzyme 2. In conclusion, we demonstrated that neuronal and glial RAS from the brainstem and hypothalamus of SHR differ from WKY rats and nicotine differentially modulates the brain RAS in SHR and WKY.
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PMID:Nicotine modulates the renin-angiotensin system of cultured neurons and glial cells from cardiovascular brain areas of Wistar Kyoto and spontaneously hypertensive rats. 1795 38


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