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

Isradipine, a new calcium channel blocker, was given to 32 patients with mild to moderate essential hypertension. After a run-in period of three weeks, 32 patients were randomized double-blindly to six weeks' treatment with either isradipine 2.5 mg twice daily or isradipine 5.0 mg once daily in a modified release formulation. Based on conventional 'clinic' BP measurements 12 or 24 hours postdose, the two treatments resulted in clinically relevant BP reduction (16/11 and 19/15 mmHg) without reflex tachycardia. No differences were seen between the groups. Efficacy increased throughout the study period. By determination of the 24 hour BP profile with a noninvasive method, the two groups were comparable during the placebo period, and no differences were seen between the two treatments. Both treatments resulted in satisfactory BP reduction during 24 hours (daily reduction of 4/6 and 12/9 mmHg twice daily and once daily dosing respectively). One third of the patients had 'white-coat' hypertension based on ambulatory daytime mean BPs, compared with conventional measurements. No relationship was found between the initial BP lowering effect and the effect after long-term treatment with isradipine in either dose.
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PMID:A randomized comparison of isradipine slow release given once daily with isradipine twice daily on 24 hour blood pressure in hypertensive patients. 183 Jan 8

Earlier clinical trials demonstrated the anti-hypertensive effect of amlodipine, a new calcium channel blocker of the dihydropyridine type. In the present comparative study, we investigated the anti-hypertensive effect of amlodipine in comparison with a combination of nifedipine and mefruside. In both groups, the anti-hypertensive effect was comparable. Normalization of the supine diastolic blood pressure was observed in 72.3% of patients treated with amlodipine and in 66.6% of those patients in the combination group. Both drugs were generally well tolerated, with a somewhat higher incidence of side effects being observed in the combination group. The study shows that amlodipine monotherapy in mild-to-moderate hypertension is equally as effective as combination therapy with nifedipine/mefruside, with amlodipine being superior in terms of tolerability.
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PMID:[Therapy of mild to moderate hypertension. Efficacy and tolerance of Amlodipine in comparison with the combination nifedipine/mefruside]. 183 Feb 87

Hypertensive diabetic rats develop a cardiomyopathy characterized by systolic and diastolic ventricular dysfunction, myocardial hypertrophy and fibrosis, pulmonary congestion and a very high mortality rate. Alterations in contractile proteins and sarcoplasmic reticular calcium (Ca2+) transport in diabetic myocardium and their partial reversal with verapamil suggest that calcium channel blockade may prevent death from congestive heart failure in hypertensive diabetic rats. A large group of rats with renovascular hypertension and streptozotocin diabetes were divided into four groups: untreated animals (Group 1) and animals treated with 100 (Group 2), 300 (Group 3) or 600 (Group 4) mg/kg per day of sustained release diltiazem mixed in their food. Treatment was begun shortly after the onset of hypertension and diabetes. Mortality rates after 4 months were 59% (19 of 32), 53% (17 of 32), 27% (7 of 26) and 35% (12 of 34) in Groups 1, 2, 3 and 4, respectively; the mortality rate in age-matched control rats was 5% (1 of 19). The reductions in mortality rates in Groups 3 and 4 were statistically significant. Diltiazem did not change systolic blood pressure, serum glucose concentration, heart rate or left ventricular mass. There was a trend to decreased left ventricular interstitial fibrosis and perivascular fibrosis in diltiazem-treated animals. Ventricular collagen concentration was similar in untreated hypertensive diabetic and control rats; levels were higher in hypertensive diabetic rats that died than in those that survived. There was a trend to decreased collagen concentration as diltiazem dose increased. Myosin isoenzyme distribution was not changed in Groups 3 and 4 (in comparison with Group 1). In all hypertensive diabetic groups, rats that died had a higher blood pressure, heart rate, relative left ventricular mass, lung weight and lung water than did survivors. The mortality rate was two to three times higher among rats with an initial blood pressure greater than or equal to 180 mm Hg. The beneficial effects of diltiazem on survival were most significant among rats with severe hypertension.
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PMID:Beneficial effects of diltiazem on the natural history of hypertensive diabetic cardiomyopathy in rats. 183 34

Hypertension has emerged as a frequent side effect in transplant recipients on effective doses of cyclosporine (CsA). To control hypertension in renal transplant patients, calcium channel blockers have been used; some of these, however, have been shown to cause significant increases in CsA levels. These findings point out that possible interactions of each calcium antagonist with CsA deserve investigation. We performed an open, placebo-controlled study in 12 stable renal transplant recipients to determine whether short-term isradipine influences CsA pharmacokinetics. All patients had mild to moderate hypertension and received triple immunosuppressive therapy with CsA, azathioprine, and prednisolone. Throughout a 4-week period of isradipine treatment, blood CsA levels (specific and nonspecific monoclonal antibodies) remained stable. The mean trough specific level was 121 +/- 14 micrograms/L following placebo, compared to 120 +/- 14 micrograms/L during isradipine. Corresponding non-specific values were 465 +/- 68 and 474 +/- 63 micrograms/L. Also, values for Cmax, AUC, and t1/2 were not significantly changed following 4 weeks of isradipine. Mean arterial pressure was significantly reduced at the end of the study. This study implies that isradipine does not influence CsA metabolism. Further studies should be carried out to determine its long-term effects on CsA pharmacokinetics and renal function in transplanted patients.
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PMID:Lack of effect of the calcium antagonist isradipine on cyclosporine pharmacokinetics in renal transplant patients. 183 29

The cardiac organ manifestation of arterial hypertension comprises the myocardium itself with left-ventricular hypertrophy, the interstitium with perivascular and interstitial fibrosis, and the coronary circulation with disease of large and small coronary arteries. The consequences of the sum and interactions of these cardiac organ manifestations have an impact on left-ventricular systolic and diastolic function, the ischemic risk, and the occurrence of arrhythmias in hypertensive patients. As the prognosis of arterial hypertension is determined, to a considerable extent, by these cardiac complications, the aim of treatment of hypertensive heart disease is reversal of the myocardial hypertrophy in order to prevent later progression to hypertensive failure. A further goal of therapy is reversal of hypertensive coronary microangiopathy in order to improve the coronary reserve and to reduce the ischemic risk. Regression of hypertrophy can be induced by suitable antihypertensive drugs (calcium channel blockers of the dihydropyridine type, ACE inhibitors, and sympatholytic substances). While normal systolic function was maintained in the compensated stage of hypertensive hypertrophy and was not significantly influenced by antihypertensive therapy, diastolic function was impaired in a very early stage of arterial hypertension. Both the phase of isovolumic relaxation and the phase of early diastolic filling were imparied, while after long-term antihypertensive treatment with Ca-channel blockers of the dihydropyridine type or ACE inhibitors, only the latter one was improved. From preliminary results there is clinical evidence that hypertensive disease of small coronary arteries can be reversed after long-term antihypertensive treatment with a consequently improved coronary reserve and a reduced ischemic risk. Moreover, to what extent the prognosis of hypertensive heart disease can be improved by reversal of myocardial hypertrophy and disease of small coronary arteries is yet unknown.
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PMID:Long-term treatment in arterial hypertension for protecting hypertrophic myocardium. 183 50

By the extracellular recording technique, the action potentials and spontaneous contractions of the isolated rat longitudinal portal vein strips were simultaneously recorded in the presence of varying concentrations of electrolytes, various vasoactive agents, and hormones, and the mechanisms regulating the force and frequency of spontaneous contraction of the vascular smooth muscle were investigated. A longitudinal stretch (-200% of the initial length), a higher [K+]0 (-30 mM), a lower [Na+]0, epinephrine, acetylcholine or ouabain increased both force and frequency of the phasic contractions. A lower [Na+]0 or ouabain raised basal tone of the muscle in addition to the above effects. A higher [Ca++]0 increased the contractile force, while it decreased the frequency. A lower [Ca++]0, calcium channel blocker or VIP reduced the contractile force but increased the contractile frequency. A bigger force and a higher frequency of the phasic contractions were exhibited in the portal vein strips isolated from rats with CCl4-induced experimental portal vein hypertension. They were similar to responses of the strips from the intact rats to stretch, ouabain, or higher [Ca++]0 in the presence of lower [Na+]0. These results suggest that an initiation and force of the phasic and tonic contractions depend on extracellular Ca++ concentration and influx of Ca++, and frequency of the phasic contractions, mainly on membrane potential rather than on extracellular Ca++ concentration. In the portal hypertension, permeability of the cell membrane to Ca++ is possibly increased.
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PMID:[Regulatory mechanisms for the spontaneous contractile force and frequency of the rat portal vein]. 184 Aug 65

To explore the role of calcium channels in hypertension, dihydropyridine ([3H]PN200-110) binding to heart, brain, and skeletal muscle microsomes of 4-, 8- and 15-week-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats was measured. At a constant Ca2+ ion concentration (pCa 3.0), maximal binding (Bmax) of dihydropyridine binding to heart and brain microsomes was significantly enhanced in 8- and 15-week-old SHR compared with WKY rats (p less than 0.01), whereas this phenomenon was not observed in 4-week-old SHR and WKY rats. Bmax and dissociation constant (Kd) values for skeletal muscle microsomes from SHR showed no difference compared with WKY rats irrespective of age. Dihydropyridine binding to heart microsomes, brain microsomes, and solubilized skeletal muscle microsomes exhibited strong calcium dependence. The Ca2(+)-dependent dihydropyridine binding curves for heart showed a Hill slope, and pK 0.5 values for 15-week-old SHR and WKY rats were 0.70 +/- 0.12 and 4.66 +/- 0.12 versus 0.72 +/- 0.12 and 5.66 +/- 0.08 (n = 4, mean +/- SD), respectively, indicating that 15-week-old SHR require 10-fold higher calcium concentration than WKY rats to promote dihydropyridine binding. The pK 0.5 values of calcium for brain and solubilized skeletal muscle calcium channels in 15-week-old SHR were also significantly lower than in WKY rats. This difference first became apparent in SHR and WKY rats as early as 4 and 8 weeks after birth. These results suggest that enhancement of calcium channel density might occur in the heart and brain of SHR in response to elevated blood pressure and that reduced calcium sensitivity of dihydropyridine binding to calcium channels might be a primary characteristic of this rat strain.
Hypertension 1991 Feb
PMID:Reduced calcium sensitivity of dihydropyridine binding to calcium channels in spontaneously hypertensive rats. 184 42

We administered a calcium channel blocker, nicardipine 0.01 mg.kg-1 i. v. bolus or 5 micrograms.kg-1.min-1 i. v. infusion before induction with thiamylal or modified NLA (thiamylal, droperidol and butorphanol) to prevent hypertension at intratracheal intubation, and measured blood pressure and heart rate before and after intubation. Blood pressure of all experimental groups was significantly reduced in comparison with the control group right after intubated. Nicardipine is effective to prevent hypertension at intubation.
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PMID:[Prevention of hypertension at intubation with intravenous nicardipine]. 187 47

Currently, calcium channel blockers are being used increasingly for the treatment of hypertension in the elderly. Several case reports in the dental literature suggest that patients treated with the calcium channel blockers manifest gingival hyperplasia similar to that seen in patients taking phenytoin (Dilantin, Parke-Davis). A small study of 89 patients undertaken at the Westside Veterans Administration Medical Center, Chicago seems to indicate that nifedipine and diltiazem do indeed cause gingival hyperplasia. A total of 83% of the patients studied receiving nifedipine showed evidence of hyperplastic tissue and 74% of those on diltiazem were found to have hyperplastic tissue.
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PMID:Gingival hyperplasia: a side effect of nifedipine and diltiazem. 188 59

Spontaneously hypertensive rats (SHR) that underwent uninephrectomy (UNX) at six weeks of age were randomly assigned to receive no treatment, the calcium channel blocker, nifedipine, or the angiotensin converting enzyme inhibitor, enalapril. Both drugs reduced systemic blood pressure, however, blood pressure tended to be greater in rats given nifedipine than in those on enalapril. After six months, proteinuria and the relevance of glomerula sclerosis were significantly reduced in the two treated groups compared to values observed in untreated SHR. Kidney weight was also reduced by therapy, suggesting that both enalapril and nifedipine inhibited compensatory kidney growth. Micropuncture studies performed in similarly treated groups of rats, but at 11 weeks of age, revealed that PGC was elevated in untreated UNX SHR and reduced by both nifedipine and enalapril. These findings support the hypothesis that glomerular hypertension and renal hypertrophy are important risk factors for glomerular injury. They suggest that calcium blockers are as effective as angiotensin converting enzyme inhibitors in preventing progressive kidney damage.
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PMID:Effects of nifedipine and enalapril on glomerular structure and function in uninephrectomized SHR. 189 65


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