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 13,001 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The objective of the present study was to find out whether brain vasopressin (AVP) and angiotensin II (Ang II) are involved in pressor response to intracerebroventricular (ICV) infusion of interleukin-1 beta (IL-1beta). The experiments were performed on conscious, 12- to 14-week-old Sprague-Dawley rats. Mean arterial blood pressure (MAP) and heart rate (HR) were recorded continuously under baseline conditions and during ICV infusion periods. In the first part of the study, the rats were ICV-infused with one of the following: 0.9% NaCl saline (5 microl/h-control), IL-1beta (100 ng/h), angiotensin AT1 receptor antagonist (losartan 10 microg/h), IL-1beta together with losartan, V1 receptors antagonist (V1ANT), d(CH2)5[Tyr(Me)2,Ala-NH2(9)]AVP, 400 ng/h) or IL-1beta together with V1ANT. Saline infusion did not influence MAP, while administration of IL-1beta elicited a significant but transient increase in MAP. The pressor response to IL-1beta was abolished by losartan but not by V1ANT. On the other hand, combined administration of IL-1beta and V1ANT resulted in increase in HR, which was absent during infusion of IL-1beta alone. In the second part of the study after ICV pretreatment with IL-1beta or 0.9% NaCl (control), the rats received ICV infusion of one of the following: 0.9% NaCl saline, subpressor dose of Ang II (5 ng/15 s) or subpressor dose of AVP (5 ng/15 s). Subpressor doses of Ang II and AVP did not influence MAP and HR in saline-pretreated rats. The same dose of Ang II but not AVP applied in IL-1beta-pretreated rats resulted in a significant increase in MAP. The study provides evidence that IL-1beta through its action in the brain increases sensitivity to central pressor action of Ang II. Additionally, we found that AVP and in particular V1 receptors do not play important role in the central pressor action of IL-1beta, however, they may influence its effect on HR regulation.
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PMID:Centrally administered interleukin-1 beta sensitizes to the central pressor action of angiotensin II. 1676 25

The most important task of classification of hypertension in pregnancy is to establish whether hypertension predates pregnancy (so-called pre-existing hypertension) or whether this is pregnancy-induced hypertension (so-called gestational hypertension). Pre-existing hypertension is diagnosed either before pregnancy or within 20 weeks of gestation. Gestational hypertension is characterized by poor perfusion of several organs, and the elevated blood pressure (BP) represents usually only one of the characteristic features. Non-pharmacological treatment of hypertension should be considered in pregnant females with systolic BP 140-150 mm Hg or diastolic BP 90-99 mm Hg. Salt restriction or weight reduction is not recommended. Systolic BP > or = 170 or diastolic BP > or = 110 mm Hg in a pregnant woman should be regarded as an emergency requiring hospitalization. Drug treatment with intravenous labetalol, or oral methyldopa or nifedipine should be considered. The thresholds at which to initiate antihypertensive therapy is systolic BP of 140 mm Hg or diastolic BP of 90 mm Hg in women with gestational hypertension without proteinuria or in those with pre-existing hypertension before 28 weeks' gestation. Drug treatment is to be initiated at the same threshold levels in females with gestational hypertension and proteinuria or those presenting with symptoms at any time during the pregnancy, those with pre-existing hypertension in the presence of associated conditions or organ damage and, also, those with pre-existing hypertension and superimposed gestational hypertension. In other cases, it is recommended to institute antihypertensive medication at systolic BP of 150 mm Hg or diastolic BP of 95 mm Hg. For non-severe hypertension, methyldopa, labetalol, calcium-channel blockers should be considered the drugs of choice. ACE inhibitors and angiotensin II antagonists (AT1-blockers) are contraindicated in pregnancy.
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PMID:[Hypertension in pregnancy]. 1963 40

The clinical value of the combination of amlodipine and eplerenone is unclear. This study was undertaken to test whether eplerenone potentiates the protective effects of amlodipine against hypertensive cardiovascular injury. Salt-loaded Dahl salt-sensitive hypertensive rats (DS rats) were given (1) vehicle, (2) an antihypertensive dose of amlodipine, (3) a non-antihypertensive dose of eplerenone or (4) combined amlodipine and eplerenone for 6 weeks, and the effects on cardiovascular injuries were compared. There was no significant difference among the four groups regarding plasma aldosterone, urine volume or urinary electrolytes. A subpressor dose of eplerenone markedly ameliorated vascular endothelial dysfunction, cardiac inflammation and fibrosis in DS rats to a similar degree as an antihypertensive dose of amlodipine. Addition of eplerenone to amlodipine, without affecting blood pressure, enhanced the improvement by amlodipine of vascular endothelial function, cardiac inflammation, fibrosis and diastolic dysfunction in DS rats. Additive beneficial effects of eplerenone were attributed to additive potentiation of eNOS and Akt phosphorylation and additive reduction of oxidative stress. Eplerenone significantly attenuated cardiovascular NADPH oxidase activity by reducing gp91(phox) upregulation and attenuated the upregulation of cardiovascular AT1 receptor, but amlodipine failed to affect them. Thus, the normalization by eplerenone of gp91(phox) and AT1 receptor upregulation seems to be at least partially responsible for the additive benefits of eplerenone in the prevention of hypertensive cardiovascular injury. The combination of amlodipine and eplerenone may be a promising therapeutic strategy for cardiovascular disease in salt-sensitive hypertension.
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PMID:Eplerenone potentiates protective effects of amlodipine against cardiovascular injury in salt-sensitive hypertensive rats. 2161 6

This study was undertaken to elucidate a novel mechanism underlying angiotensin II-induced cardiac injury, focusing on the role of oxidative stress and myocardial capillary density. Salt-loaded Dahl salt-sensitive hypertensive rats (DS rats), a useful model for hypertensive cardiac remodeling or heart failure, were orally given irbesartan (an AT1 receptor blocker), tempol (a superoxide dismutase mimetic) or hydralazine (a vasodilator). Irbesartan significantly ameliorated left ventricular ischemia and prevented the development of cardiac hypertrophy and fibrosis in DS rats. The benefits were associated with the attenuation of oxidative stress, normalization of myocardial capillary density and inhibition of capillary endothelial apoptosis. Moreover, DS rats with significant cardiac hypertrophy and fibrosis displayed decreased myocardial vascular endothelial growth factor (VEGF) expression and increased cardiac apoptosis signal-regulating kinase 1 (ASK1) activation. Treatment with irbesartan significantly reversed these phenotypes. Tempol treatment of DS rats mimicked all the above-mentioned effects of irbesartan, indicating the critical role of oxidative stress in cardiac injury. We also investigated the role of VEGF and ASK1 in oxidative stress-induced endothelial apoptosis by using cultured endothelial cells from wild-type and ASK1-deficient mice. Oxidative stress-induced ASK1 activation led to endothelial apoptosis, and VEGF treatment prevented oxidative stress-induced endothelial apoptosis by inhibiting ASK1 activation. We obtained the first evidence that oxidative stress-induced cardiac VEGF repression and ASK1 activation caused the enhancement of endothelial apoptosis and contributed to a decrease in myocardial capillary density. These effects resulted in angiotensin II-induced progression of cardiac injury.
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PMID:Novel mechanism of angiotensin II-induced cardiac injury in hypertensive rats: the critical role of ASK1 and VEGF. 2208 32

Salt sensitive hypertension is known to be a contributing factor for the progression of kidney disease. This study was undertaken to investigate the role of excessive dietary salt on renal function and to evaluate the effect of valsartan and amlodipin given as a combination therapy on blood pressure and parameters specific to the renal function in salt loaded SHR rats. 48 male SHR rats at age of 20 weeks and body weight ranging between 270-350 g were used. SHR rats were divided into 3 groups: control group of rats -SHRC (n = 16) given tab water ad libitum and two salt treated groups in which tab water was replaced with a solution of NaCl (1%) from age of 8 weeks given ad libitum: SHRVAL+AMLO group (n = 16) where investigated drugs were administered at a dose of 10 mg/kg/ b.w. (valsartan) and 5 mg/kg/ b.w. (amlodipin) by gavage and SHR NaCl group (n = 16) that received saline in the same volume and the same time intervals as the SHRVAL+AMLO group. For a period of 12 weeks we have investigated the effect of the VAL+AMLO drug combination on systolic blood pressure (SBP), body weight and renal function tests. Salt loading with 1% solution in the SHR NaCl group has lead to significant increase of blood pressure, proteinuria and decrease in creatinine clearance. Combined treatment with AT1 receptor blocker and calcium antagonist has managed to control blood pressure and ameliorated renal damage.
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PMID:Protective effects of AT1-receptor blocker and CA antagonist combination on renal function in salt loaded spontaneously hypertensive rats. 2607 78


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