The Experts below are selected from a list of 73563 Experts worldwide ranked by ideXlab platform
Giacomo Deferrari - One of the best experts on this subject based on the ideXlab platform.
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serum uric acid and Target Organ damage in primary hypertension
Hypertension, 2005Co-Authors: Francesca Viazzi, Denise Parodi, Giovanna Leoncini, Angelica Parodi, Valeria Falqui, Elena Ratto, Simone Vettoretti, Gian Paolo Bezante, Massimo Del Sette, Giacomo DeferrariAbstract:The role of serum uric acid as an independent risk factor for cardiovascular and renal morbidity is controversial. A better understanding of its relationship with preclinical Organ damage may help clarify the mechanism(s) implicated in the development of early cardiovascular disease. We evaluated the association between uric acid and the presence and degree of Target Organ damage in 425 (265 males, 160 females) middle-aged, untreated patients with essential hypertension. Left ventricular mass index and carotid intima-media thickness were assessed by ultrasound scan. Albuminuria was measured as the albumin to creatinine ratio in 3 nonconsecutive first morning urine samples. Overall, patients with Target Organ damage had significantly higher levels of serum uric acid as compared with those without it (presence versus absence of left ventricular hypertrophy, P=0.04; carotid abnormalities, P<0.05; microalbuminuria, P<0.004; and at least 1 versus no Organ damage, P<0.03). In women, the occurrence and severity of each Target Organ damage we examined increased progressively from the lower to the upper serum uric acid tertiles (P<0.01). After adjustment for body mass index, age, creatinine clearance, and high-density lipoprotein cholesterol, each standard deviation increase in serum uric acid entailed a 75% higher risk of having cardiac hypertrophy and a 2-times greater risk of having carotid abnormalities. These results support the role of serum uric acid as an independent, modifiable marker of cardiovascular damage.
Masatsugu Horiuchi - One of the best experts on this subject based on the ideXlab platform.
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Inhibition of the renin–angiotensin system and Target Organ protection
Hypertension Research, 2009Co-Authors: Jun Iwanami, Masaki Mogi, Masaru Iwai, Masatsugu HoriuchiAbstract:The renin–angiotensin system (RAS) is involved in the pathological mechanisms of Target Organ damage, as well as in the induction of hypertension. RAS inhibition by angiotensin converting enzyme (ACE) inhibitors and angiotensin (Ang) II receptor blockers can prevent tissue damage by inhibition of Ang II type 1 receptor signaling. A beneficial effect of RAS inhibition on the heart, vasculature and kidney in cardiovascular disease has been reported. However, RAS inhibition can also prevent fibroproliferative diseases and damage of other tissues, such as brain, adipose tissue and muscle, because local RAS has an important role in tissue damage compared with circulating RAS. Moreover, other players, such as Ang II type 2 receptor signaling, aldosterone and ACE2 have been highlighted. Furthermore, there has also been a focus on the emerging concept of regulation of RAS, such as receptor-interacting proteins and receptor modifications, in the new discovery of therapeutic agents for tissue protection. The RAS has a pivotal role in various Target Organ damage, with complicated mechanisms; therefore, blockade of RAS may be therapeutically effective in preventing Organ damage, as well as in having an antihypertensive effect.
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Inhibition of the renin–angiotensin system and Target Organ protection
Hypertension Research, 2009Co-Authors: Jun Iwanami, Masaki Mogi, Masaru Iwai, Masatsugu HoriuchiAbstract:The renin–angiotensin system (RAS) is involved in the pathological mechanisms of Target Organ damage, as well as in the induction of hypertension. RAS inhibition by angiotensin converting enzyme (ACE) inhibitors and angiotensin (Ang) II receptor blockers can prevent tissue damage by inhibition of Ang II type 1 receptor signaling. A beneficial effect of RAS inhibition on the heart, vasculature and kidney in cardiovascular disease has been reported. However, RAS inhibition can also prevent fibroproliferative diseases and damage of other tissues, such as brain, adipose tissue and muscle, because local RAS has an important role in tissue damage compared with circulating RAS. Moreover, other players, such as Ang II type 2 receptor signaling, aldosterone and ACE2 have been highlighted. Furthermore, there has also been a focus on the emerging concept of regulation of RAS, such as receptor-interacting proteins and receptor modifications, in the new discovery of therapeutic agents for tissue protection. The RAS has a pivotal role in various Target Organ damage, with complicated mechanisms; therefore, blockade of RAS may be therapeutically effective in preventing Organ damage, as well as in having an antihypertensive effect.
Friedrich C. Luft - One of the best experts on this subject based on the ideXlab platform.
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Immune mechanisms in angiotensin II-induced Target-Organ damage.
Annals of Medicine, 2012Co-Authors: Friedrich C. Luft, Ralf Dechend, Dominik N. MüllerAbstract:Inflammation and activation of immunity are central features in the pathogenesis of atherosclerosis, ischemic myocardial injury, and hypertension-induced Target-Organ damage. The renin-angiotensin-aldosterone system can initiate not only innate but also acquired immunity. The latter process includes formation of activating antibodies directed at the angiotensin (Ang) II receptor. Ang II not only regulates vascular tone and sodium balance, but also activates immune cells and promotes cell infiltration into Target Organs. Studies showed that macrophages and various T cell subtypes play a pivotal role in Target-Organ damage and even in the regulation of blood pressure and responses to Ang II. Experimental and clinical evidence shows that adaptive transfer of immune cells, rendering mice deficient for a certain subset of immune cells, or immunosuppressive treatment affects blood pressure and ameliorates Target-Organ damage. Neural mechanisms interact with and regulate these processes. Understanding the mechanisms could direct us to novel therapies.
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Immune-related effects in hypertension and Target-Organ damage.
Current opinion in nephrology and hypertension, 2011Co-Authors: Dominik N. Müller, Heda Kvakan, Friedrich C. LuftAbstract:Purpose of review Several studies published in the past three decades have suggested that inflammation and activation of immunity are central features in the pathogenesis of atherosclerosis, ischemic myocardial injury, and also in hypertension-induced Target Organ damage. A better understanding of this field could help us to explain the increased cardiovascular risk in patients with chronic inflammation. Recent findings Recent studies have demonstrated that macrophages and various T-cell subtypes play a pivotal role in the regulation of blood pressure and Target Organ damage. Hypertensive stimuli such as the effector molecule of the renin-angiotensin system, angiotensin II, not only regulate vascular tone and sodium balance, but also activate immune cells and promote cell infiltration into Target Organs. Experimental and clinical evidence show that adaptive transfer of immune cells, rendering mice deficient for a certain subset of immune cells, or immunosuppressive treatment affects blood pressure and ameliorates Target Organ damage. Summary The aim of this review is to summarize and discuss some of the more recent insights as to how immune cells might affect the regulation of blood pressure and the pathogenesis of hypertension-induced Target Organ damage.
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Immunology in Hypertension, Preeclampsia, and Target-Organ Damage
Hypertension (Dallas Tex. : 1979), 2009Co-Authors: Stefan Verlohren, Dominik N. Müller, Friedrich C. Luft, Ralf DechendAbstract:Hypertension generally brings to mind hemodynamic mechanisms, increased peripheral vascular resistance, the laws of Ohm or Hagen-Poisseule, and perhaps Target-Organ damage mediated through acceleration of atherosclerosis, vasculitis, or other concomitant processes. However, innate and acquired adaptive cellular or even antibody-mediated immunity plays an active role in the pathogenesis of hypertension (Figure 1). In primarily angiotensin (Ang) II-dependent animal models for end-Organ damage, an intense inflammatory component, namely, inflammation, that was principally steered by the innate-immunity regulator nuclear factor κB (NF-κB) was observed. Immunosuppression with dexamethasone, the tumor necrosis factor (TNF)-α soluble receptor, etanercept, and mycophenolate decreased albuminuria, NF-κB activation, and infiltration of all of the immunocompetent cells in the animals but had little or no effect on blood pressure.1 Using mechanisms to block NF-κB either pharmacologically or subsequently locally in endothelial cells with Cre/lox transgenic mice harboring an endothelial cell-restricted NF-κB superrepressor Iκ-B-α-ΔN (Tie-1-ΔN mice), it became evident that innate immune mechanisms were certainly important in Target-Organ damage.2 Since then, numerous observations have been made regarding immune mechanisms that influence hypertension development and its resultant Target-Organ damage.3–6 These findings may offer important new insights into our understanding of mechanisms and could influence treatment. Figure 1. Immunity schematic: all of the various components can be activated by Ang II. Some components also influence the blood pressure-raising responses of Ang II. Guzik et al7 showed recently that mice lacking T and B cells (RAG-1−/− mice) have blunted hypertension and do not develop Target-Organ damage after Ang II or desoxycorticosterone acetate-salt treatment. Adoptive transfer of T but not B cells restored these abnormalities. Adoptive transfer of T cells lacking the G protein-coupled receptor Ang II type 1 (AT1) blunted Ang II-dependent hypertension. Ang II increased T-cell markers of activation and tissue homing in wild-type mice but not in …
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direct renin inhibition with aliskiren in hypertension and Target Organ damage
Clinical Journal of The American Society of Nephrology, 2006Co-Authors: Dominik N. Müller, Friedrich C. LuftAbstract:The Joint National Committee and the World Health Organization are in agreement that hypertension in most patients who are treated is controlled inadequately and that rates of cardiovascular morbidity remain high. Additional pharmacologic treatments could ameliorate this situation. The renin-angiotensin-aldosterone system has been a highly successful pharmacologic Target, as the system is strongly implicated in the development of hypertension-related Target Organ damage. However, compensatory increases in plasma renin levels that lead to adjustments in angiotensin production and conversion present limitations for existing renin-angiotensin-aldosterone system inhibitors. A once-daily, orally effective, small-molecule renin inhibitor, aliskiren, is now available to address angiotensin production directly at its rate-limiting step. Studies in humans attest to an effective BP-lowering effect, a side effect profile no different from AT1 receptor blockers, and the option of combination therapies. A novel animal model of high human renin hypertension in the rat attest to Target Organ protection. Because angiotensin receptor blockade, angiotensin-converting enzyme inhibition, calcium channel blockade, and diuretic therapy all lead to sharp increases in plasma renin activity, aliskiren offers a novel circumvention.
Francesca Viazzi - One of the best experts on this subject based on the ideXlab platform.
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serum uric acid and Target Organ damage in primary hypertension
Hypertension, 2005Co-Authors: Francesca Viazzi, Denise Parodi, Giovanna Leoncini, Angelica Parodi, Valeria Falqui, Elena Ratto, Simone Vettoretti, Gian Paolo Bezante, Massimo Del Sette, Giacomo DeferrariAbstract:The role of serum uric acid as an independent risk factor for cardiovascular and renal morbidity is controversial. A better understanding of its relationship with preclinical Organ damage may help clarify the mechanism(s) implicated in the development of early cardiovascular disease. We evaluated the association between uric acid and the presence and degree of Target Organ damage in 425 (265 males, 160 females) middle-aged, untreated patients with essential hypertension. Left ventricular mass index and carotid intima-media thickness were assessed by ultrasound scan. Albuminuria was measured as the albumin to creatinine ratio in 3 nonconsecutive first morning urine samples. Overall, patients with Target Organ damage had significantly higher levels of serum uric acid as compared with those without it (presence versus absence of left ventricular hypertrophy, P=0.04; carotid abnormalities, P<0.05; microalbuminuria, P<0.004; and at least 1 versus no Organ damage, P<0.03). In women, the occurrence and severity of each Target Organ damage we examined increased progressively from the lower to the upper serum uric acid tertiles (P<0.01). After adjustment for body mass index, age, creatinine clearance, and high-density lipoprotein cholesterol, each standard deviation increase in serum uric acid entailed a 75% higher risk of having cardiac hypertrophy and a 2-times greater risk of having carotid abnormalities. These results support the role of serum uric acid as an independent, modifiable marker of cardiovascular damage.
Jun Iwanami - One of the best experts on this subject based on the ideXlab platform.
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Inhibition of the renin–angiotensin system and Target Organ protection
Hypertension Research, 2009Co-Authors: Jun Iwanami, Masaki Mogi, Masaru Iwai, Masatsugu HoriuchiAbstract:The renin–angiotensin system (RAS) is involved in the pathological mechanisms of Target Organ damage, as well as in the induction of hypertension. RAS inhibition by angiotensin converting enzyme (ACE) inhibitors and angiotensin (Ang) II receptor blockers can prevent tissue damage by inhibition of Ang II type 1 receptor signaling. A beneficial effect of RAS inhibition on the heart, vasculature and kidney in cardiovascular disease has been reported. However, RAS inhibition can also prevent fibroproliferative diseases and damage of other tissues, such as brain, adipose tissue and muscle, because local RAS has an important role in tissue damage compared with circulating RAS. Moreover, other players, such as Ang II type 2 receptor signaling, aldosterone and ACE2 have been highlighted. Furthermore, there has also been a focus on the emerging concept of regulation of RAS, such as receptor-interacting proteins and receptor modifications, in the new discovery of therapeutic agents for tissue protection. The RAS has a pivotal role in various Target Organ damage, with complicated mechanisms; therefore, blockade of RAS may be therapeutically effective in preventing Organ damage, as well as in having an antihypertensive effect.
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Inhibition of the renin–angiotensin system and Target Organ protection
Hypertension Research, 2009Co-Authors: Jun Iwanami, Masaki Mogi, Masaru Iwai, Masatsugu HoriuchiAbstract:The renin–angiotensin system (RAS) is involved in the pathological mechanisms of Target Organ damage, as well as in the induction of hypertension. RAS inhibition by angiotensin converting enzyme (ACE) inhibitors and angiotensin (Ang) II receptor blockers can prevent tissue damage by inhibition of Ang II type 1 receptor signaling. A beneficial effect of RAS inhibition on the heart, vasculature and kidney in cardiovascular disease has been reported. However, RAS inhibition can also prevent fibroproliferative diseases and damage of other tissues, such as brain, adipose tissue and muscle, because local RAS has an important role in tissue damage compared with circulating RAS. Moreover, other players, such as Ang II type 2 receptor signaling, aldosterone and ACE2 have been highlighted. Furthermore, there has also been a focus on the emerging concept of regulation of RAS, such as receptor-interacting proteins and receptor modifications, in the new discovery of therapeutic agents for tissue protection. The RAS has a pivotal role in various Target Organ damage, with complicated mechanisms; therefore, blockade of RAS may be therapeutically effective in preventing Organ damage, as well as in having an antihypertensive effect.