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Brain renin-angiotensin system (RAS) could regulate oxidative stress in the paraventricular nucleus (PVN) in the development of hypertension. This study was designed to explore the precise mechanisms of RAS acting on reactive oxygen species (ROS) in salt-induced hypertension. Male Wistar rats were administered with a high-salt diet (HS, 8.0% NaCl) for 8 weeks to induced hypertension. Those rats were received PVN infusion of AT1R antagonist losartan (LOS, 10 μg/h) or microinjection of small interfering RNAs for protein kinase C γ (PKCγ siRNA) once a day for 2 weeks. High salt intake resulted in higher levels of AT1R, PKCγ, Rac1 activity, superoxide and malondialdehyde (MDA) activity, but lower levels of copper/zinc superoxide dismutase (Cu/Zn-SOD), superoxide dismutase (SOD) and glutathione (GSH) in PVN than control animals. PVN infusion of LOS not only attenuated the PVN levels of AT1R, PKCγ, Rac1 activity, superoxide and decreased the arterial pressure, but also increased the PVN antioxidant capacity in hypertension. PVN microinjection of PKCγ siRNA had the same effect on LOS above responses to hypertension but no effect on PVN level of AT1R. These results, for the first time, identified that the precise signaling pathway of RAS regulating ROS in PVN is via AT1R/PKCγ/Rac1 in salt-induced hypertension.
Significant innovations have defined the approach to the proximal thoracic aorta. Aortic proteolysis predisposes to dissection and aneurysm. Losartan may prevent aortic root dilation in Marfan syndrome. The Loeys-Dietz syndrome mandates early aortic intervention. Because genetic aortopathies have a multicenter registry, further aortic molecular advances are likely. Acute intramural hematoma (IMH) may be due to aortic dissection with unrecognized microintimal tears. Type-A IMH is often a surgical emergency, whereas type-B IMH often requires medical management. Because preoperative ischemia predicts mortality in type-A dissection, it is logical to classify this disease by ischemic presentation. Because advanced age worsens the outcome in type-A dissection, transcatheter interventions should be urgently developed for this high-risk subgroup. Aortic arch repairs shorter than 45 minutes in duration are safely performed under deep hypothermic circulatory arrest with/without perfusion adjuncts. Bilateral antegrade cerebral perfusion (ACP) offers the best neuroprotection for complex repairs longer than 45 minutes. Axillary artery cannulation improves outcomes in proximal thoracic aortic procedures. Contralateral hemispheric ischemia is possible with unilateral ACP because cross-cerebral perfusion may be inadequate. Arch repair with ACP and moderate HCA is safe and effective and represents a research opportunity for pharmacologic ischemic preconditioning. Antegrade thoracic aortic stenting for DeBakey 1 dissection thromboses the distal false lumen to improve long-term aortic outcomes. Endovascular arch repair is feasible and may soon be done off-pump. These described innovations have collectively ushered in a paradigm shift in diseases affecting the ascending aorta and aortic arch.
TLR4 may lead to inflammatory reaction in hypertensive renal injury. Fos or/and Los can decrease the expressions of TLR4 and correlate inflammatory factors, which may be part of the renal protective mechanism.
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We communicated the central effect of angiotensin III (ANG III), a potent signal for extracellular dehydration, on single neurons in the caudal hypoglossal nucleus of Sprague-Dawley rats anesthetized with pentobarbital sodium. A significant number (121 of 168) of caudal hypoglossal neurons responded to intracerebroventricular application of ANG III (80 or 160 pmol), with either an increase (n = 83) or decrease (n = 38) in their spontaneous discharge. These effects of ANG III were significantly reversed by intracerebroventricular application of the nonpeptide angiotensin AT1 receptor antagonist losartan (40 nmol), but not by the AT2 antagonist, PD-123319. The hypoglossal neuronal responses to repeated administration of ANG III (80 pmol), delivered at an interval < or = 18 min, exhibited acute tachyphylaxis. Intracerebroventricular administration of the cholinergic dipsogen, carbachol (50 ng), or the osmotic stimulant, hypertonic saline (0.5 M), also elicited responses in ANG III-responsive hypoglossal neurons. These results suggest that neurons in the caudal hypoglossal nucleus may serve as the final common pathway for extracellular and, possibly, intracellular thirst in the rat. Furthermore, it is likely that the action of ANG III is mediated by the AT1 subtype of angiotensin receptors.
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To assess the effects of pharmacological interruption of the renin-angiotensin system on the fibrinolysis, tissue plasminogen activator antigen (t-PA), plasminogen activator inhibitor-1 antigens (PAI-1) and neurohormones, such as plasma renin activity, norepinephrine, angiotensin II (AII) and IV (AIV) concentrations, were measured in 60 hypertensives. Among them, 48 patients were divided into two groups (25 with 10-20 mg quinapril and 23 with 50-100 mg losartan) who received the drug for 6 months. AII had a weak positive correlation with free PAI-I (n = 60, r = 0.26, p < 0.05) whereas AIV had a strong positive correlation with free PAI-I (n = 60, r = 0.57, p < 0.0001). In both treatment groups, blood pressures were significantly reduced to similar levels after drug treatment. While plasma renin activity increased significantly in both groups after drug treatment, only the losartan group showed significant increases in AII and AIV concentrations. In the quinapril group, there was a significant change in t-PA (p < 0.001) without changes in PAI-1. In the losartan group, free PAI-I and total PAI-I (p < 0.05 for free PAI-I and p < 0.04 for total PAI-I) were significantly increased without a change in t-PA. Thus, quinapril enhanced fibrinolysis but losartan attenuated it. These unique effects of each drug on the fibrinolytic system appear to be associated with changes in AII and AIV concentrations.
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Reverse transcriptase-polymerase chain reaction was performed to determine the expression of angiotensinogen, renin, angiotensin-converting enzyme and angiotensin receptor subtype 1 mRNA. The presence of AngII in ureteral tissue was determined by immunohistochemistry. Human and pig ureteral smooth muscle strips were suspended in tissue baths to determine the effect of the AngII receptor antagonist losartan on the frequency and amplitude of spontaneous ureteral contractions. Electrical field stimulation was performed before and after exposure to losartan.
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These results support the importance of cross-talk among different cell types in the regulation of vascular or renal function. ET-1, and particularly ECE-1, might constitute a target in this regulation. In addition, locally synthesized AII could be one of the mediators involved in the down-regulation of ECE-1.
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The left ventricular midwall shortening-circumferential end-systolic stress relationship in 45 normotensive Wistar rats was used to calculate the ratio of observed to predicted left ventricular midwall fractional shortening. At the endpoint, afterload-independent midwall shortening was higher in Dahl S rats on losartan or tap water, and in Dahl R rats on losartan than in weight-matched normotensive Wistar rats (all P<0.05). Afterload-independent midwall shortening was related to the left ventricular chamber dimension in a learning series of 109 rats (64 Goldblatt and 45 normotensive rats on a normal sodium diet; r = 0.73) and was adjusted in Dahl rats to a constant left ventricular internal diameter (6.9 mm) by the learning regression equation. The adjusted afterload-independent midwall shortening was still higher in Dahl S rats on losartan than in controls (P<0.02). Left ventricular internal diameter-adjusted afterload-independent midwall shortening was inversely related to the left ventricular mass in both Dahl S and Dahl R groups (r = -0.40 and -0.72, both P<0.04).
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Appreciation of the role of aldosterone in cardiovascular and renal disease has increased in the last 50 years. The use of spironolactone was limited by adverse sexual effects, including gynaecomastia. Eplerenone is a newer aldosterone antagonist that is much more selective, with minimal affinity for progesterone and androgenic receptors; therefore, there are very few reports of adverse sexual effects. A review of published trials shows that eplerenone reduces blood pressure (BP) in a dose-dependent manner, from 50 to 200 mg/day, and to a similar degree as enalapril. It has an additive effect when given to patients inadequately controlled on an angiotensin-converting enzyme inhibitor or an angiotensin-receptor blocker. Eplerenone performs better than losartan in African-American patients and lowers BP regardless of initial plasma renin activity. The risk of hyperkalaemia is low, similar to that of enalapril, and < 1% of patients have had to be withdrawn from studies because of elevated serum potassium levels. Eplerenone is an effective, well-tolerated antihypertensive agent that may be used alone or in conjunction with other agents; apart from the risk of hyperkalaemia, adverse effects are similar to placebo.
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Despite progress in the detection and treatment of hypertension the percentage of patients with controlled hypertension has failed to increase. The problem of poor blood pressure control is even more serious in elderly hypertensives than in the rest of the population. The antihypertensive drugs of the AIIRA (non-peptide angiotension II receptor antagonist) class are drugs whose use and experience are increasing and whose properties make them particularly useful in the elderly. We tried to assess the efficacy of treatment with losartan, the first AIIRA drug in a cohort of elderly patients with essential hypertension and to assess the percentage of patients achieving optimum BP control and to evaluate its safety, tolerability and metabolic effects. The intervention proved to be highly effective, achieving the anticipated blood pressure levels in the elderly in 77% of subjects after a 16-week follow-up, with very good tolerability. Renal function remained unchanged, as did the subjects' lipid profile.
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An ARB combined with an ACE inhibitor may benefit heart failure patients who are receiving all other recommended therapies. Further trials are needed to evaluate long-term safety effectiveness, quality of life, and survival before the combination can be recommended for routine use.
Radiation-induced optic nerve damage was reduced by ramipril, a prodrug angiotensin-converting enzyme inhibitor (ACEI). This study was to determine the optimum dose and administration time of ramipril for mitigating radiation-induced optic neuropathy.