Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We cultured smooth muscle cells from rat renal preglomerular arterioles by injecting a suspension of iron oxide into the left ventricle, separating the arterioles magnetically, and growing cells from explants. In passaged cultures we ascertained vascular smooth muscle purity of > 98% by morphology; contraction to norepinephrine and angiotensin; positive immunofluorescence staining through the sixth passage with monoclonal antibodies to smooth muscle-specific alpha- and gamma-isoactins, myosin, and desmin; and the absence of von Willebrand factor. Angiotensin II (10(-12)-10(-5) M) induced dose-dependent DNA synthesis and proliferation of subcultured (three times) arteriolar smooth muscle cells from a growth-arrested state (p < 0.01). Angiotensin II (10(-5) M) also induced the cells to express c-fos mRNA. We find no previous report of culture of smooth muscle cells from renal preglomerular arterioles. Our findings also provide evidence that angiotensin II is mitogenic to arteriolar muscle cells and thus may be involved in their hyperplasia accompanying hypertension.
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PMID:Culture of renal arteriolar smooth muscle cells. Mitogenic responses to angiotensin II. 139 76

HYPERTENSION AND RENAL DISEASE: In experimental models of renal disease not only protein intake and hyperlipidaemia but also hypertension may contribute to the progressive deterioration in renal function; in these models an imbalance in intrarenal haemodynamics appears to be a particularly important factor. ANTIHYPERTENSIVE THERAPY: A reduction in arterial pressure can alter the course of human chronic renal disease. However, it is not clear whether any one class of antihypertensive drug is superior to any other class in these patients. Angiotensin converting enzyme (ACE) inhibitors may prevent the progression from incipient to overt diabetic nephropathy and afford better protection than conventional treatment. In patients with non-diabetic renal disease there is no unequivocal evidence for a protective effect. In renal transplant recipients, mainly those taking cyclosporine, ACE inhibitors are equally effective compared to calcium antagonists in the control of hypertension, but their renal effects in transplant recipients without renal artery stenosis have not yet been assessed.
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PMID:Antihypertensive therapy in renal disease and transplantation. 140 37

Angiotensin converting enzyme inhibitors (ACEI) are believed to protect remnant kidney, but all previous studies used the ligation model which causes severe hypertension, and very few have compared drugs in rats having similar control of blood pressure (BP). We compared rats with uremia obtained by 70% excision of total renal mass, a model which causes mild, late hypertension. Study I compared the effects of enalapril (E), cicletanine (C) and placebo (P) in uremic (U) rats fed a 0.50% (normal-high) Na diet. Study II compared the effects of E, C, P, and guanfacine (G) in U rats fed a diet restricted to 0.25% Na (normal-low). In study I, UP rats developed progressive hypertension (140, 146, 160 and 166 mm Hg at 3, 6, 9 and 12 weeks), proteinuria (240 mg/day at 9 and 12 weeks) which were not affected by E or C. The occurrence of end-stage renal disease (ESRD) led to the sacrifice of all rats after three months. All three groups had similar severe renal lesions (over 25% sclerosed glomeruli in 5 of 10 UP, 9 of 14 UE, 7 of 14 UC rats, with huge cystic tubular dilatations). In study II, rats could be sacrificed later (6 months) and had evidence of less severe renal disease. All the drugs tested prevented hypertension throughout the study (P less than 0.001), with lowest values in UE rats. E and G, but not C, reduced proteinuria. Renal damage was reduced with E and G, but not with C, despite similar BP in C and G rats. Thus, in contrast with what was obtained in the ligation model, ACEI affected neither the BP nor the renal lesions of rats made uremic by renal excision and fed a 0.50% Na diet. Moderate Na restriction improved the consequences of nephron loss and restored the anti-hypertensive effect of drugs. However, these drugs had a different effect on renal preservation: it was dramatic with E, good with G, and undetectable with C.
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PMID:Renal effect of anti-hypertensive drugs depends on sodium diet in the excision remnant kidney model. 140 18

Using the nuclear medicine procedures it is possible to evaluate the renovascular hypertension via the captopril test. Decreased renal blood flow due to stenotic vessel may produce a variety of findings on the renogram using both OIH-I131 and DTPA-Tc99m. Delayed transit time and excretion also may be detected. In this situation the sensitivity and specificity of Nuclear Medicine for RAS detection is very low. Using Captopril test is possible to detect enhanced modification on the shape of renogram due to Angiotensin Converting enzyme inhibition.
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PMID:[Diagnostic imaging in renal vascular diseases: old and new ways. Role of nuclear medicine]. 141 90

Angiotensin converting enzyme inhibitors (ACEI) are used increasingly to treat cardiovascular diseases, and so, therefore, the number of patients scheduled for surgery and treated preoperatively with these drugs. Haemodynamic instability has sometimes been observed during anaesthesia in these patients, leading some authors to discontinue ACEI administration before anaesthesia. However, recent physiological data concerning the renin angiotensin system (RAS) and ACEI pharmacological data may increase our understanding of the mechanisms of cardiovascular interaction between ACEI and anaesthesia. The RAS is involved in blood pressure regulation when extracellular fluid volume is decreased and in case of hypovolaemia, by inducing vasoconstriction and longterm volume regulation. Arterial vasoconstriction is the target for ACEI. However, venoconstriction may maintain venous return and cardiac output in spite of reduced blood volume. On the other hand, ACEI treatment impedes cardiac adaptation to acute changes in extracellular fluid volume. This effect may be increased by underlying pathology (especially in hypertension) as well as by anaesthesia. A combination of an increased sensitivity to acute changes in ventricular load due to treatment with ACEI and anaesthesia in hypertensive patients or in patients with cardiac failure may carry a high risk of hypotension. Specific studies on haemodynamic tolerance of anaesthesia in patients chronically treated with ACEI are required to assess the prevalence of this risk and how to manage it.
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PMID:[Anesthetic consequences of hemodynamic effects of angiotensin converting enzyme inhibitors]. 141 79

Angiotensin II-induced phosphorylation of proteins was examined in isolated myocytes from hearts of Dahl rats. A high salt diet induced cardiac hypertrophy in Dahl salt-sensitive rats. Angiotensin II-induced phosphorylation of a 42-kd protein (pp42) was detected by two-dimensional electrophoresis in hypertrophic but not normal ventricular myocytes. Angiotensin II stimulation was time-dependent, with a peak effect at 30 minutes. The half-maximal and maximal concentrations of angiotensin II that stimulated pp42 phosphorylation were 1 and 10 nM, respectively. Phosphorylation of pp42 was a function of cardiac hypertrophy. Phorbol 12-myristate 13-acetate-induced phosphorylation of pp42 indicates the possibility of an association between protein kinase C and the signal transduction pathway of angiotensin II-induced pp42 phosphorylation. Ionomycin and A23187 (both at 1 microM) did not stimulate phosphorylation of pp42. Angiotensin II produced a small increase in the synthesis of myocyte proteins in both normal and hypertrophic cells as shown by [35S]methionine incorporation. However, this increase could not account for the increase in the phosphate content of pp42. This protein was not an isoform of actin nor was it of platelet origin. These results raise the possibility that angiotensin II may play a role in the activation of factors in hypertrophic myocytes; however, further study is required to define a link between phosphorylation of pp42 and the hypertrophic process.
Hypertension 1992 Nov
PMID:Angiotensin II-induced protein phosphorylation in the hypertrophic heart of the Dahl rat. 142 15

Transcatheter arterial infusion chemotherapy is one of the most useful therapeutic procedures for gynecologic malignancies. Recently, several reports have been published about Angiotensin II-induced hypertension chemotherapy and the efficacy of the method, but there have been no reports to evaluate an application for gynecologic malignancies. We evaluate the usefulness of the method for gynecologic malignancies demonstrating the changes of hemodynamics of the tumor using 81mKr scintigraphy. Thirteen patients with pathologically confirmed gynecologic malignancies were evaluated by angiography and continuous infusion of 81mKr via the catheter with and without Angiotensin II. At first, continuous infusion of 81mKr was performed under the superselective catheterization of the uterine artery. The radioactivities in the ROI were counted. Then, withdrew the catheter from the uterine artery to the internal iliac artery, and again continuously infused 81mKr and counted the radioactivities in the same ROI. Finally, keeping the catheter in the internal iliac artery, Angiotensin II and 81mKr were infused simultaneously. And counted the radioactivities. The radioactivities were highest when the catheter tip was placed in uterine arteries and lowest when the catheter tip was placed in internal iliac arteries. But radioactivities in the ROIs were definitely increased when Angiotensin II was used, even if the catheter tip was keeping in the internal iliac arteries. The optimal catheter position of transcatheter arterial chemotherapy for gynecologic malignancies is at proximal uterine artery. Since Angiotensin II-induced hypertension may increase blood flow of tumors, it seems to have indication for post-operative cases, highly advanced cases and cases with difficulties to perform superselective catheterization.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[81mKr scintigraphic evaluation of hemodynamics in gynecologic malignancies under condition of angiotensin II-induced hypertension]. 143 80

Captopril is a suitable drug to treat high blood pressure in diabetic patients. This Angiotensin-Converting Enzyme Inhibitor (ACEI) is a vasodilator without tachycardia and saline retention. Furthermore, captopril is one of antihypertensive drugs with less adverse effects. It does not induce metabolic changes, improves glucose tolerance and brake the evolution of renal insufficiency. About 50-60% of patients are under control (DBP < 90 mmHg) with captopril monotherapy. In the present paper, were included 64 women and 16 men with diabetes mellitus and mild-moderate hypertension, I-II phase WHO. The average age (mean +/- S.D.) was 66.6 +/- 9.2 years. All patients were treated with 25 mg/12 h of captopril, for one month. If blood pressure was not under control, captopril treatment enhanced to 50 mg/12 h during second month. After this period of two months, patients under control were got out of this study. 37 patients (46.25%) needed a second drug. In randomized form, 20 patients associated 25 mg HCTZ one time a day (CAP + HCTZ); and 17 patients associated 20 mg/12 h of nifedipine retard (CAP + NIF). The study continued for 4 months more. Both treatments reduced blood pressure in significant form without changes statistical significant in the heart rate, weight, glycemia, cholesterol, triglycerides, c-HDL, uric acid, creatinine, Na+ and K+ blood levels. CAP + HCTZ controlled (DBP < 90 mHg) 85% and CAP + NIF 81.25% of patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Captopril + hydrochlorothiazide versus captopril + nifedipine in the treatment of arterial hypertension in diabetes mellitus type II]. 143 67

We have previously shown that the stimulatory effects of guanine nucleotides, N-ethylcarboxamide-adenosine and other agonists on adenylate cyclase activity were diminished in aorta and heart sarcolemma of spontaneously hypertensive rats (SHR) [Anand-Srivastava (1988) Biochem. Pharmacol. 37, 3017-3022]. In the present studies, we have examined whether the decreased response of these agonists is due to the defective GTP-binding proteins (G-proteins) which couple the receptors to adenylate cyclase, and have therefore measured the levels of G-proteins in aorta and heart from SHR and their respective Wistar-Kyoto (WKY) controls by using pertussis toxin (PT)- and cholera toxin (CT)-catalysed ADP-ribosylations and immunoblotting techniques using specific antibodies against G-proteins. The labelling with [32P]NAD+ and PT identified a 40/41 kDa protein in heart and aorta from WKY and SHR and was significantly increased in the hearts (approximately 100%) and aorta (approximately 30-40%), from SHR as compared with WKY. Immunoblotting revealed an increase in the levels of the G-protein alpha-subunits Gi alpha-2 and Gi alpha-3 in heart and Gi alpha-2 in aorta, whereas no change in Go alpha was observed in heart from SHR and WKY. On the other hand, no differences were observed in CT labelling or immunoblotting of stimulatory G-protein (Gs) in heart and aorta from WKY and SHR. In addition, CT stimulated the adenylate cyclase activity in heart sarcolemma from WKY and SHR to a similar extent. These results were correlated with adenylate cyclase inhibition and stimulation by various hormones. Angiotensin II (AII), atrial natriuretic factor (ANF) and oxotremorine-mediated inhibition was found to be greater in SHR as compared with WKY, whereas the stimulatory effects of adrenaline, isoprenaline, dopamine and forskolin were diminished in SHR aorta as compared to WKY. These results indicate that regulatory protein G(i) is more expressed in SHR, which may be associated with the decreased responsiveness of stimulatory hormones and increased sensitivity of inhibitory hormones to stimulate/inhibit adenylate cyclase activity. It may thus be suggested that the enhanced G(i) activity may be one of the mechanisms responsible for the diminished vascular tone and impaired myocardial functions in hypertension.
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PMID:Enhanced expression of inhibitory guanine nucleotide regulatory protein in spontaneously hypertensive rats. Relationship to adenylate cyclase inhibition. 144 83

Angiotensin-II (AII) stimulates plasminogen activator inhibitor-1 (PAI-1) gene transcription, translation, and protein secretion from astroglial cells derived from normotensive [Wistar-Kyoto (WKY)] rat brain, an effect mediated by AII type 1 (AT1) receptors. Since abnormal expression of the brain AII system has been demonstrated in spontaneously hypertensive (SH) rats, we investigated the regulation of PAI-1 gene expression by AII in astroglial cells from the brains of these animals. AII caused an increase in PAI-1 gene expression in SH rat astroglia in a manner similar to that observed in WKY-derived cultures. However, both the basal and AII-stimulated levels of PAI-1 mRNA in SH rat astroglia were only 20% of those observed in WKY rat astroglial cultures. Consequently, there was a significant reduction in the de novo synthesis and secretion of PAI-1 from astroglia of SH rat brain. The reduced synthesis and secretion of PAI-1 from SH rat brain astroglia was associated with lower numbers of AT1 receptors in these cells. However, the steady state levels of AT1 receptor mRNA were comparable in both WKY and SH rat astroglia. This reduction in AII-modulated PAI-1 levels in SH rat astroglia is consistent with a proposed role of these interactions in the development of hypertension in these animals.
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PMID:Angiotensin-II induction of plasminogen activator inhibitor-1 gene expression in astroglial cells of normotensive and spontaneously hypertensive rat brain. 149 87


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