Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

---

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

SURROGATE END-POINTS FOR PROGNOSIS OF HYPERTENSION: The identification of surrogate measures of cardiovascular risk in patients with hypertension may allow clinicians to better estimate a patient's long-term prognosis and monitor the effects of antihypertensive therapy in reducing risk and thereby reducing the cardiovascular complications of hypertension. PROGNOSTIC LIMITATIONS OF OFFICE BLOOD PRESSURE: Previous studies have shown that office blood pressure may predict the incidence of fatal and nonfatal cardiovascular complications of hypertension. However, evidence also suggests that the predictive value of office blood pressure is limited and that it does not provide accurate estimates of the changes in the cardiovascular risk profile that can occur with antihypertensive treatment. PROGNOSTIC VALUE OF 24-H AMBULATORY BLOOD PRESSURE: Cross-sectional studies have shown that 24-h average blood pressure values are more closely correlated with hypertensive target-organ damage [e.g. left ventricular hypertrophy (LVH), retinopathy, increased serum creatinine, albuminuria, and microalbuminuria] than are office blood pressure values. Although longitudinal evidence of the clinical relevance of 24-h ambulatory blood pressure monitoring is limited, preliminary data from a recently completed trial, the Study on Ambulatory Pressure and Lisinopril Evaluation (SAMPLE), have clearly shown the superiority of 24-h blood pressure monitoring over office readings in predicting the regression of LVH in hypertensive patients following treatment to reduce blood pressure.
...
PMID:Can good surrogate end-points predict the prognosis of hypertensive patients? 986 98

Previous studies showed a renoprotective effect of l-arginine in experimental uremia. Whether this was caused by an increased nitric oxide (NO) release or depended on l-arginine per se is not clear. Here, we evaluated whether chronic administration of an NO donor, molsidomine, controlled systemic blood pressure and renal disease progression and prolonged survival in rats with renal mass reduction (RMR). Rats with RMR received the following daily in the drinking water: group 1 (n = 21), no specific therapy (vehicle); group 2 (n = 12), molsidomine, 120 mg/L; group 3 (n = 9), lisinopril, 25 mg/L; and group 4 (n = 12), reserpine, 5 mg/L, hydralazine, 80 mg/L, and hydrochlorothiazide, 25 mg/L, from day 21 after surgery, when rats had hypertension and proteinuria, until the death of the vehicle-treated rats. Molsidomine normalized systemic hypertension, only partially reduced proteinuria and serum creatinine levels, but significantly prolonged animal survival, particularly in the early stage of the disease. Lisinopril at a similar systemic blood pressure was even better than molsidomine in limiting proteinuria, preserving renal function, and prolonging survival, but triple therapy, despite being effective on blood pressure, offered no renoprotection or prolonged survival. Endothelin-1 (ET-1) levels, formed in excessive amounts by the kidneys of these animals, were reduced by molsidomine and lisinopril, but not by triple therapy. The prolongation of survival by NO donor could be attributed to its effect of reducing ET levels, which in turn may limit the smooth muscle cell proliferation and matrix accumulation responsible for organ and, especially, myocardial fibrosis in uremia.
...
PMID:Renoprotection by nitric oxide donor and lisinopril in the remnant kidney model. 1019 19

Inhibitors of angiotensin converting enzyme (ACE inhibitors) have been introduced more than fifteen years ago into the treatment of hypertension, congestive heart failure, myocardial infarction and diabetic nephropathy. The therapeutic success is related to their action in reduction of plasma and tissue angiotensin II concentrations and potentiation of endogenous kinins. They are able to improve myocardium metabolic status, prevent cardiac hypertrophy, limit myocardial infarct size, and thus prevent heart failure. Since 1987 ACE inhibitors are introduced in the clinical practice in our clinic. We introduced the therapy with lisinopril (Lopril), in 70% of patients among 2855 patients that were admitted in Coronary Care Unit in 1997 and 1998. Lisinopril was introduced as soon as the patient was admitted, together with fibrinolitic, Heparin and Aspirin therapy. Since that time we noticed decrease in postinfarction heart failure in comparison to previous years. We recommend permanent therapy with a small doses of ACE inhibitors in patients with heart infarction.
...
PMID:[Converting enzyme inhibitors in acute myocardial infarct and heart failure]. 1035 28

Fixed-dose combination antihypertensive therapy has received interest since the publication of the JNC-VI report. Relatively few head-to-head comparative studies between fixed-dose combinations and first-line monotherapies for hypertension have been published. The objective of this study was to conduct a meta-analysis of various first-line monotherapies and the fixed-dose combination of amlodipine/benazepril. The results of the meta-analysis were used to compare the efficacy and safety of the first-line monotherapies with amlodipine/benazepril. The meta-analysis included 82 studies that included 110 treatment groups (cohorts). The study compared nine different monotherapies and one combination therapy (amlodipine/benazepril). Of the 82 studies, 22 were placebo-controlled and 60 were active treatment controlled. The mean absolute decrease in supine diastolic blood pressure (BP) ranged from 9.7 to 13.3 mm Hg with verapamil showing the greatest effect and captopril the least (13.3 +/- 3.0 mm Hg; 9.7 +/- 2.9 mm Hg, respectively). When studies were weighted by sample size, atenolol, verapamil, lisinopril and amlodipine/benazepril showed the greatest BP effect. When studies were weighted by variance, amlodipine/benazepril and atenolol showed the greatest BP effect. The percentage of patients controlled on therapy ranged from 54% to 79%. Lisinopril and amlodipine/benazepril showed the greatest percent controlled. The overall incidence of adverse effects ranged from 12.1% to 41.8% with lisinopril having the lowest and nifedipine having the highest incidence. The overall incidence of adverse effects resulting in drug discontinuance ranged from 1.3% to 10.7%, with amlodipine/benazepril having the lowest and nifedipine having the highest incidence. The results of the meta-analysis indicate that amlodipine/benazepril produces above average reductions in BP with a lower than average incidence of overall side effects and the lowest incidence of adverse effects resulting in drug discontinuance. The fixed-dose combination of amlodipine/benazepril achieves its goal of effective BP lowering with a minimum of significant side effects.
...
PMID:Fixed-dose combination vs monotherapy in hypertension: a meta-analysis evaluation. 1044 13

Hypertension affects 58 million Americans. Dentists frequently encounter patients who are using one or more antihypertensive medications. This study evaluates the incidence of active duty soldiers dispensed antihypertensive medications at a large military installation. Lisinopril was the most frequently prescribed antihypertensive medication during a 2-month period in 1997 and was followed by hydrochlorothiazide, amlodipine, propranolol, felodipine, verapamil, atenolol, diltiazem, terazosin, clonidine, nifedipine, and metoprolol. These 12 drugs accounted for 93.46% of all antihypertensive medications dispensed. In this study, the percentage of active duty soldiers dispensed any antihypertensive medication was 1.51% (30 different medications were dispensed); 0.16% of all soldiers younger than age 30 and 1.25% of all soldiers older than age 30 were prescribed 1 of the 12 most commonly prescribed antihypertensive agents. Considering the same top-12 antihypertensive agents, the percentage of male soldiers younger than 30 who received a prescription was 0.24% and the percentage of male soldiers older than 30 who received a prescription was 4.3%. The percentage for males older than 40 receiving 1 of the 12 medications listed above was 12.05%. Similarly, the percentages for females were 0.27% for younger than 30, 1.87% for older than 30, and 3.51% for older than 40. Active duty males older than age 30 were more than twice as likely to be prescribed an antihypertensive agent than females in the same age group. Male active duty soldiers older than age 40 were more than 50 times more likely to be prescribed an antihypertensive agent than active duty males younger than 30.
...
PMID:The incidence of active duty dental patients taking antihypertensive medications. 1054 31

1. To determine whether the antihypertensive response in deoxycorticosterone acetate (DOCA) salt-treated rats was mediated by kinins on the luminal side of renal tubules or in the circulation, selective urinary kininase inhibitors were administered to normal Brown Norway Kitasato (BN-Ki) rats and kininogen-deficient Brown Norway Katholiek (BN-Ka) rats. 2. Kinins were degraded by neutral endopeptidase (NEP) and carboxypeptidase Y-like kininase (CPY) in urine, but were inactivated mainly by angiotensin-converting enzyme (ACE) in the plasma. 3. Ebelactone B inhibited CPY, while poststatin inhibited CPY and NEP. 4. Daily administration of poststatin (5 mg/kg per day, s.c.) for 3 days reduced blood pressure (BP) in DOCA salt-treated BN-Ki rats, but not in BN-Ka rats. 5. Ebelactone B (5 mg/kg per day, s.c.) also reduced BP in BN-Ki rats, which was accompanied by increased urinary sodium excretion, but had no effect on BP in BN-Ka rats. 6. Lisinopril (5 mg/kg per day, s.c.) had no effect on BP in either rat strain. 7. Arterial kinin levels in BN-Ki rats increased significantly (2.2-4.6 pg/mL) with captopril (10 mg/kg, s.c.). However, arterial kinin levels that induced hypotension following the infusion of bradykinin (1000 ng/kg per min, i.v.) were 110-fold higher than endogenous arterial kinin levels attained following captopril. 8. These results suggest that inhibition of kinin degradation on the luminal side of the renal tubules may effectively attenuate hypertension.
...
PMID:Inhibition of kinin degradation on the luminal side of renal tubules reduces high blood pressure in deoxycorticosterone acetate salt-treated rats. 1069 33

Angiotensin-converting enzyme (ACE) inhibitors reduce systemic and coronary vasoconstriction by modulating sympathetic neuroeffector function and by decreasing sympathetic activation. Here, blood pressure, and tissue concentrations of noradrenaline and neuropeptide Y (NPY) were studied in normotensive and spontaneously hypertensive rats (SHR) after 2 weeks treatment with lisinopril (0.3 mg/day; osmotic mini-pump). MAP was reduced in both normotensive rats and SHR after lisinopril by 32 mm Hg and 66 mm Hg respectively (P < 0.001 compared to corresponding control rats). NPY levels were significantly higher in extracts of atria, kidney, spleen and adrenal of normotensive rats compared to SHR. Lisinopril treatment increased NPY levels in atria and skeletal muscle extracts of SHR by 15% and 70% respectively (P < 0.05). Lisinopril also significantly increased noradrenaline content of the atria by 16% in SHR (P < 0. 05). The decrease in MAP and increase in tissue levels of sympathetic neurotransmitters provide further evidence that inhibition of ACE decreases sympathetic neurotransmission leading to accumulation of stored neurotransmitters. Journal of Human Hypertension (2000) 14, 381-384
...
PMID:Effect of lisinopril on tissue levels of neuropeptide Y in normotensive and spontaneously hypertensive rats. 1087 99

The pharmacology of angiotensin-converting-enzyme (ACE) inhibitors and their role in the renin-angiotensin system (RAS) are described, and pharmacokinetic properties and common adverse events are presented. ACE inhibitors play a vital role in the RAS by regulating the potent vasoconstrictor angiotensin II. All ACE inhibitors share the same basic structure; however, they can be separated on the basis of their functional (binding) group: carboxyl, sulfhydryl, or phosphinyl. These functional groups are, in part, responsible for differences in the pharmacokinetic and safety profiles of these agents. Captopril and lisinopril are the only ACE inhibitors that are not prodrugs requiring activation through hepatic biotransformation. Differences among the ACE inhibitors in lipophilicity are described; fosinopril has the greatest lipophilicity and lisinopril the least. ACE is found in numerous tissues, and there is increasing evidence of differences among ACE inhibitors in their ability to inhibit tissue ACE. Most ACE inhibitors are eliminated mainly by the kidneys and to a lesser extent through the liver. Lisinopril is the only ACE inhibitor that does not require hepatic metabolism. In the selection of an ACE inhibitor for once-daily use to treat hypertension, differences in trough-peak ratios are clinically relevant. Fosinopril, ramipril, and trandolapril have minimum trough-peak ratios of 50% or greater. ACE inhibitors are generally well tolerated, with hypotension, cough, and hyperkalemia being the most frequently reported adverse effects for the entire class. Drug interactions across the ACE inhibitor class as well as agent-specific interactions are described. Factors to be considered in the selection of an ACE inhibitor include differences in potency, affinity for ACE, pharmacokinetics, and toxicity that are related to structural properties of the drug; whether the trough-peak ratio enables use of a once-daily dose; and potential adverse effects related to a drug's functional (binding) group.
...
PMID:Overview of the angiotensin-converting-enzyme inhibitors. 1103 16

We have previously reported that the renal kallikrein-kinin system suppressed the development of deoxycorticosterone acetate (DOCA)-salt hypertension. Kinins were degraded in the kidney mainly by carboxypeptidase Y (CPY)-like kininase. Blockade of renal kinin degradation may reduce hypertension in the developmental stage. We constructed an antisense oligonucleotide against rat CPY homologue (5'-CAT-CTC-TGC-TTC-CTT-GTG-TC-3', AS) and its randomized control oligonucleotide (5'-TCC-TTC-CTG-CTT-GAG-TTC-CT-3', RC), and prepared an HVJ-liposome complex that prolongs and increases the effectiveness of the antisense oligonucleotide. Antisense oligonucleotide was transfected (25 nmole rat(-1), in terms of nucleotide) into the kidney from the renal artery. Blood pressure was measured through a catheter inserted into the abdominal aorta. Mean blood pressure (MBP) in DOCA-salt treated (for 2 weeks) Sprague Dawley strain rats was 130+/-3 mmHg (n=11), and was reduced significantly (P<0.05) more by AS transfection (122+/-4 mmHg, n=6) than by RC treatment (137+/-6 mmHg, n=5) 4 days after the transfection. This reduction in MBP was accompanied by increased urinary sodium excretion (AS, 8.4+/-1.5 mmole day(-1); RC, 4.6+/-0.5 mmole day(-1), P<0.05) and a reduction in urinary CPY-like kininase activity. Ebelactone B (5 mg kg(-1), twice a day, p.o.), an inhibitor for urinary CPY-like kininase, also reduced MBP and induced natriuresis to the same degree as AS. Lisinopril, an inhibitor for angiotensin converting enzyme (ACE) failed to reduce the elevated MBP. These results suggest that CPY-like kininase may have more contribution than ACE to degrade kinin in the kidney, and that knockdown of CPY-like kininase in the kidney may partly prevent rat DOCA-salt hypertension.
...
PMID:In vivo transfer of antisense oligonucleotide against urinary kininase blunts deoxycorticosterone acetate-salt hypertension in rats. 1103 Jul 33

Both angiotensin II and vascular endothelial growth factor are angiogenic agents that have recently been implicated in the pathogenesis of proliferative diabetic retinopathy. In this study, retinal neovascularization was examined in a model of retinopathy of prematurity with the use of neonatal transgenic (mRen-2)27 rats, which overexpress renin in tissues, and Sprague-Dawley rats. Blockers of the renin-angiotensin system were administered during the neovascularization period. The ACE inhibitor lisinopril and the angiotensin type 1 receptor antagonist losartan both increased retinal renin levels and prevented inner retinal blood vessel growth. Quantitative in situ hybridization revealed that the expression of vascular endothelial growth factor and its type 2 receptor in the inner retina and proliferating blood vessels were increased in rats with retinopathy of prematurity. Lisinopril reduced both retinal vascular endothelial growth factor and its type 2 receptor mRNA in retinopathy of prematurity rats, whereas losartan had no effect. It is predicted that agents that interrupt the renin-angiotensin system may play an important role as retinoprotective agents in various forms of proliferative retinopathy.
Hypertension 2000 Dec
PMID:Retinal neovascularization is prevented by blockade of the renin-angiotensin system. 1111 32


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>

---