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Peter Friberg - One of the best experts on this subject based on the ideXlab platform.
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Role of the sympathetic nervous system in human Renovascular Hypertension
Current hypertension reports, 2000Co-Authors: Mats I. Johansson, Peter FribergAbstract:The findings in humans as to whether elevated sympathetic nerve activity contributes to Renovascular Hypertension have been less consistent compared with the results obtained in experimental models of Renovascular Hypertension. Collectively, there are several lines of evidence to support the view that sympathetic nerve activity is elevated in patients with Renovascular Hypertension. It is uncertain, however, whether this adrenergic overactivity is specific for Renovascular Hypertension per se, or the cause of severe Hypertension with target organ damage. Central or peripheral stimulation of sympathetic nerve activity by angiotensin II, or stimulation of central sympathetic outflow via afferent renal nerves of ischemic kidneys, are possible mechanisms to explain the elevated sympathetic nerve activity in Renovascular Hypertension. Therapy that diminishes the activity of the sympathetic nervous system and the renin-angiotensin system seems rational and could perhaps also improve the poor prognosis for these patients.
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increased sympathetic nerve activity in Renovascular Hypertension
Circulation, 1999Co-Authors: Mats I. Johansson, Mikael Elam, Bengt Rundqvist, Graeme Eisenhofer, Hans Herlitz, Gavin W Lambert, Peter FribergAbstract:Background—Increased sympathetic nerve activity may contribute to the progression of Renovascular Hypertension. Because previous results have been inconclusive, we investigated whether Renovascular hypertensives show increased total and regional sympathetic nerve activity. Methods and Results—Sixty-five patients underwent renal angiography and measurements of plasma renin activity and angiotensin II in conjunction with estimation of sympathetic nerve activity by means of radiotracer dilution and intraneural recordings of muscle sympathetic nerve activity (MSNA). Age-matched healthy subjects (n=15) were examined for comparison. Total body norepinephrine (NE) spillover, an index of overall sympathetic nerve activity, was increased by 100% and MSNA by 60% in the hypertensive patients compared with healthy subjects (P<0.01 for both). A subgroup of 24 patients with well-defined Renovascular Hypertension (cured or improved Hypertension after renal angioplasty) showed similar increases in total body NE spillover...
Mats I. Johansson - One of the best experts on this subject based on the ideXlab platform.
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Role of the sympathetic nervous system in human Renovascular Hypertension
Current hypertension reports, 2000Co-Authors: Mats I. Johansson, Peter FribergAbstract:The findings in humans as to whether elevated sympathetic nerve activity contributes to Renovascular Hypertension have been less consistent compared with the results obtained in experimental models of Renovascular Hypertension. Collectively, there are several lines of evidence to support the view that sympathetic nerve activity is elevated in patients with Renovascular Hypertension. It is uncertain, however, whether this adrenergic overactivity is specific for Renovascular Hypertension per se, or the cause of severe Hypertension with target organ damage. Central or peripheral stimulation of sympathetic nerve activity by angiotensin II, or stimulation of central sympathetic outflow via afferent renal nerves of ischemic kidneys, are possible mechanisms to explain the elevated sympathetic nerve activity in Renovascular Hypertension. Therapy that diminishes the activity of the sympathetic nervous system and the renin-angiotensin system seems rational and could perhaps also improve the poor prognosis for these patients.
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increased sympathetic nerve activity in Renovascular Hypertension
Circulation, 1999Co-Authors: Mats I. Johansson, Mikael Elam, Bengt Rundqvist, Graeme Eisenhofer, Hans Herlitz, Gavin W Lambert, Peter FribergAbstract:Background—Increased sympathetic nerve activity may contribute to the progression of Renovascular Hypertension. Because previous results have been inconclusive, we investigated whether Renovascular hypertensives show increased total and regional sympathetic nerve activity. Methods and Results—Sixty-five patients underwent renal angiography and measurements of plasma renin activity and angiotensin II in conjunction with estimation of sympathetic nerve activity by means of radiotracer dilution and intraneural recordings of muscle sympathetic nerve activity (MSNA). Age-matched healthy subjects (n=15) were examined for comparison. Total body norepinephrine (NE) spillover, an index of overall sympathetic nerve activity, was increased by 100% and MSNA by 60% in the hypertensive patients compared with healthy subjects (P<0.01 for both). A subgroup of 24 patients with well-defined Renovascular Hypertension (cured or improved Hypertension after renal angioplasty) showed similar increases in total body NE spillover...
Cássia T. Bergamaschi - One of the best experts on this subject based on the ideXlab platform.
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Mechanisms of renal sympathetic activation in Renovascular Hypertension
Experimental physiology, 2015Co-Authors: Ruy R. Campos, Elizabeth B. Oliveira-sales, Erika E. Nishi, Julian F. R. Paton, Cássia T. BergamaschiAbstract:New findings What is the topic of this review? This review addresses the underlying mechanisms involved in sympathoexcitation during Renovascular Hypertension, focusing on the importance of increased oxidative stress in the paraventricular nucleus and rostral ventrolateral medulla. What advances does it highlight? Whether renal or autonomic dysfunction is the major contributor to systemic Hypertension following a Renovascular insult is still a matter of debate. Here, we take an integrative approach by describing the crosstalk between the kidney and brain. We show how changes in the CNS, and in sympathetic premotor neurons in particular, are activated by ischaemic renal disease in an experimental model of Renovascular Hypertension. This review addresses the underlying mechanisms involved in the sympathoexcitation in Renovascular Hypertension. We focus on the importance of increased oxidative stress in the paraventricular nucleus of hypothalamus (PVN) and rostral ventrolateral medulla (RVLM) for the autonomic dysfunction associated with Renovascular Hypertension in the two-kidney, one-clip (2K-1C) model. We found in 2K-1C rats, 6 weeks after clipping, a significant increase in the mRNA and protein expression of the angiotensin II type 1 receptor within the RVLM and PVN. In addition, mRNA from NADPH oxidase subunits (p47phox and gp91phox) was greater in the RVLM and PVN of 2K-1C rats than in a sham-operated group. However, CuZn superoxide dismutase gene expression in these regions was not changed, suggesting that excessive production of reactive oxygen species overwhelms any endogenous antioxidant system in the RVLM and PVN in Renovascular Hypertension. In fact, acute administration of tempol or vitamin C (either i.v. or directly into the PVN or RVLM) caused a significant decrease in blood pressure and renal sympathetic nerve activity in 2K-1C rats, but not in control animals. Thus, we suggest that an increase in the activity of RVLM and PVN neurons triggered by angiotensin II and oxidative stress is a major mechanism involved in the maintenance of sympathoexcitation of the cardiovascular system in Renovascular Hypertension.
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Effects of mesenchymal stem cells in Renovascular Hypertension
Experimental physiology, 2015Co-Authors: Elizabeth B. Oliveira-sales, Vanessa Araujo Varela, Cássia T. Bergamaschi, Ruy R. Campos, Mirian A. BoimAbstract:New Findings What is the topic of this review? The major topic of this review addresses the effects of mesenchymal stem cell treatment in Renovascular Hypertension. What advances does it highlight? This therapy may be a promising strategy to treat Renovascular Hypertension and its renal consequences in the near future. Renovascular Hypertension induced by the two-kidney, one-clip technique is a renin–angiotensin system-dependent model that leads to renal vascular rarefaction, fibrosis and renal failure. Treatment of Renovascular Hypertension remains a challenge, and thus, new therapies are needed. In this report, we discuss the beneficial effects of mesenchymal stem cells on the reconstruction of the renal parenchyma of the stenotic kidney to improve vascular rarefaction and fibrosis. Mesenchymal stem cell therapy prevented the progressive increase in systolic arterial pressure, reduced sympathetic hyperactivity, improved renal morphology, induced neovascularization and reduced fibrosis in stenotic kidneys. Although this therapy may be a promising strategy to treat Renovascular Hypertension and its renal consequences, further studies are necessary to improve the efficiency of mesenchymal stem cells.
Laura P. Svetkey - One of the best experts on this subject based on the ideXlab platform.
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Diagnosis and management of Renovascular Hypertension.
Cardiology in review, 2000Co-Authors: Preston S. Klassen, Laura P. SvetkeyAbstract:Renovascular Hypertension caused by renal artery stenosis accounts for a small portion of overall Hypertension but remains important as the most common potentially curable form of high blood pressure. Diagnosis depends on developing an index of suspicion for Renovascular Hypertension based on the history and physical exam, as well as judicious use of noninvasive and invasive testing. Determining which noninvasive diagnostic test to use remains a persistent dilemma. Treatment options include renal artery angioplasty, arterial stenting, surgery, and medical therapy. The goals of therapy are reduction of blood pressure and protection of renal function. This review discusses the pathophysiology and epidemiology of Renovascular Hypertension, various noninvasive tests used in diagnosis, and results offered by different treatment modalities. A diagnostic and therapeutic algorithm is offered based on a review of the literature and the experience at our institution.
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Renovascular Hypertension in Blacks
American journal of hypertension, 1996Co-Authors: Osemwegie Emovon, Saadoon Kadir, Paul E. Klotman, N. Reed Dunnick, Laura P. SvetkeyAbstract:To define the clinical characteristics of Renovascular Hypertension (RVH) and determine the clinical usefulness of captopril stimulated peripheral renin and postcaptopril renography in blacks at risk for RVH, 79 clinically selected hypertensive blacks were evaluated. Unstimulated (U-PRA), captopril stimulated (S-PRA) peripheral renin, and postcaptopril renography (PC-RENO) were obtained. All subjects underwent conventional renal arteriography. Renal artery stenosis (RAS) was present in 14 of 79 (18%) patients. Renovascular Hypertension (RVH) was found in 7 of 79 (9%) patients. S-PRA had a sensitivity and specificity of 38% and 86% respectively to detect RAS; and a sensitivity and a specificity of 17% and 85% respectively to detect RVH. PC-RENO had a sensitivity and a specificity of 64% and 58% respectively to detect RAS; and a sensitivity and a specificity of 67% and 58% respectively to detect RVH. This study suggests that RAS occurs in 18% of clinically selected hypertensive blacks. RVH was present in 9% of this population. Captopril stimulated peripheral renin and postcaptopril renography are not useful as screening tools for the diagnosis of Renovascular disease in blacks. Blacks at high risk should be evaluated with angiography.
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Similar prevalence of Renovascular Hypertension in selected blacks and whites.
Hypertension (Dallas Tex. : 1979), 1991Co-Authors: Laura P. Svetkey, N R Dunnick, Saadoon Kadir, Stephen R. Smith, C B Dunham, Michael B. Lambert, Paul E. KlotmanAbstract:Renovascular Hypertension is a potentially curable form of high blood pressure that is thought to be extremely rare among blacks. We demonstrate, however, that in a clinically selected population, the prevalence of Renovascular Hypertension is similar in blacks and whites. We prospectively evaluated 167 hypertensive subjects who had one or more clinical features known to be associated with Renovascular Hypertension. All subjects had captopril-stimulated peripheral renin measurements and conventional renal arteriography. All significant renal artery stenoses (greater than 50% luminal narrowing) were treated with percutaneous transluminal angioplasty or surgery. Renovascular Hypertension was diagnosed if there was a blood pressure response to interventional therapy, according to the criteria established by the Cooperative Study of Renovascular Hypertension. Of the total group evaluated, 24% (39 of 167) had renal artery stenosis and 14% (23 of 167) had Renovascular Hypertension. Renal artery stenosis or occlusion was found in 27% (26 of 97) of whites and 19% (13 of 67) of blacks (p = 0.27). Renovascular Hypertension was diagnosed in 18% (17 of 97) of whites and 9% (6 of 67) of blacks evaluated (p = 0.25). Renovascular Hypertension was associated with severe or refractory Hypertension and with smoking, but there were no racial differences in these associations. Blacks with Renovascular Hypertension tended to have low captopril-stimulated peripheral renin activity. We conclude that blacks with clinical features suggestive of Renovascular Hypertension should be evaluated with angiography. Captopril-stimulated plasma renin may not be useful in detecting blacks with Renovascular Hypertension, but this and other potential screening tests require further evaluation.
Mark Mitsnefes - One of the best experts on this subject based on the ideXlab platform.
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neonatal Renovascular Hypertension due to prenatal traumatic retroperitoneal hematoma
Pediatric Nephrology, 2005Co-Authors: Adley P Dixo, Prasad Devaraja, Mark MitsnefesAbstract:This report describes severe Hypertension in a 7-week-old male infant found to have Renovascular disease from an organized hematoma due to prenatal trauma. As such, this case illustrates a novel acquired, congenital mechanism of Renovascular Hypertension. The importance of considering prenatal as well as postnatal etiologies of acquired Renovascular Hypertension in neonates is emphasized. Likewise, attention must be drawn to the classic presentation of congestive heart failure in a child with severe Hypertension.