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

AGE-RELATED CARDIOVASCULAR CHANGES: Age-related changes in vascular structure and function may contribute to isolated systolic hypertension and target-organ damage. These include cardiac hypertrophy, systolic as well as diastolic dysfunction, congestive heart failure, coronary artery disease, cardiac arrhythmias, cerebrovascular diseases, peripheral vascular diseases and renal insufficiency. POTENTIAL ADVANTAGES OF CALCIUM ANTAGONISTS IN THE ELDERLY: Dihydropyridine calcium anatagonists have been advocated as first choice agents for the treatment of hypertension in the elderly on the grounds that (1) they may be more active in lowering blood pressure because of the predominantly low renin status in elderly hypertensives, (2) they may be better tolerated because side effects related to the activation of the sympathetic system may be less frequent because of attenuation of baroflexes during ageing and (3) they may have beneficial effects on a variety of concomitant cardiovascular diseases which are frequently present in the elderly. These assumptions, however are not always proven in clinical practice. ADVANTAGES OF NICARDIPINE: Additional to its potent vasodilatator action, nicardipine has anti-ischemic effects in both the coronary and the cerebral circulation, including antiplatelet and hemorrheological effects, and protection at ther cellular level against calcium overload and ischemia. The results of a large number of studies in cerebrovascular insufficiency suggest that nicardipine, may favourably affect the cerebral circulation and may improve the patient's cognitive function. Nicardipine may decrease left ventricular mass by about 4-12% and may reduce both the frequency and the severity of arrhythmias. The anti-anginal effects of nicardipine are well established. The drug is also able to decrease the progression of new atherosclerotic lesions in coronary arteries and is consequently potentially beneficial in elderly hypertensives with coronary artery disease. Nicardipine has no clinically significant negative inotropic effect. Nevertheless, in congestive heart failure, the use of calcium antagonists is usually not recommended because of the lack of clinical benefit and of possible harmful effects, including sympathetic and renin-angiotensin system stimulation. Although kidney protection may be provided by a strict and long-term control of blood pressure, the effects of nicardipine on long-term protection of renal function are not clear at present. RECENT CONTROVERSY CONCERNING SHORT-ACTING CALCIUM ANTAGONISTS: Much-debated recent case-control studies suggest that hypertensive patients treated with short-acting calcium antagonists may have an increased incidence of myocardial infarction and possibly of cardiovascular and total mortality. However, only well designed prospective comparative trials can answer this question.
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PMID:Concomitant diseases in elderly hypertensives: the position of nicardipine. 912 Jun 65

Eight preterm infants were given intravenous nicardipine, a calcium channel blocker, to treat systemic hypertension (renal artery thrombosis (n = 3); dexamethasone for management of bronchopulmonary dysplasia (n = 2); unexplained (n = 3). Nicardipine doses ranged from 0.5 to 2.0 micrograms/kg/min and were given for three to 36 days (mean (SD) 15.9 (10.3) days). Systolic blood pressure had significantly decreased after 12 and 24 hours of nicardipine treatment (-17 (17)% and -21 (10)%, respectively). Diastolic blood pressure significantly decreased after 24 hours of treatment (-22 +/- 16%). The decrease in blood pressure remained significant over the subsequent days of treatment. No hypotension or other clinical side effects were observed. It is concluded that intravenous nicardipine could be a first line treatment for hypertension in preterm infants.
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PMID:Intravenous nicardipine in hypertensive preterm infants. 913 93

Nicardipine, a dihydropyridine type calcium channel blocker, was infused into 4-, 6-, and 23-wk-old spontaneously hypertensive (SH) and age-matched normotensive Wistar-Kyoto (WKY) rats (under sodium thiobutabarbital anesthesia and ventilation, n = 4) through the left femoral vein, resulting in the reduction of blood pressure. In each rat, mean arterial blood pressure, heart rate, and the concentration of plasma catecholamines (CAs), norepinephrine (NE), and epinephrine (E) were concomitantly determined, and the correlations between these three variables were studied. During the infusion of nicardipine, the plasma concentration of CAs was measured with an automatic detection system in blood samples collected from the right femoral artery of each rat. The reduction in blood pressure induced by nicardipine brought about an increase in plasma CA levels. The blood pressure correlated well with the logarithm of plasma NE or E concentration according to the formula Y= -alpha log (X) + m (Y, blood pressure; X, concentration of plasma NE or E; a, slope; and m, intercept). The slopes (as) of 6-wk-old and 23-wk-old SH rats were significantly greater than those of aged-matched WKY rats, meaning that the increment in plasma CAs in response to a decrease in blood pressure was smaller in SH than in WKY rats of similar ages. However, no significant differences were found between the as of 4-wk-old SH and WKY rats. We conclude that the increment in the baroreflex-mediated sympathetic activity in response to a drop in blood pressure induced by nicardipine is similar or greater in prehypertensive SH than in normotensive WKY 4-wk-old rats, while the increment becomes smaller in SH rats with the onset of hypertension (6-wk-old rats), and is much less in fully hypertensive adult (23-wk-old) SH rats than in age-matched WKY rats. On the basis of these findings and previous data obtained by neurography, we conclude that plasma CAs can be used to evaluate baroreflex-mediated sympathetic activity countering the blood pressure reduction caused by calcium antagonists.
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PMID:Age-related weakening of baroreflex-mediated sympathetic activity in spontaneously hypertensive rats in response to blood pressure reduction. 978 97

It has been reported that the production of oxygen radicals mediated by xanthine oxidase (XO) is stimulated in hypertensive cardiovascular endothelium, suggesting involvement of oxidative stress in pathogenesis of hypertension. In this study we estimated the effect of nicardipine, a calcium blocker, on the oxidative stress and antioxidant activities in left ventricles from spontaneously hypertensive rat (SHR) and stroke-prone SHR (SHRSP). The activity of XO increased 3.5-fold in SHR and 6.2-fold in SHRSP compared to that in normal controls (WKY). Interestingly, the levels of glutathione (GSH) and the activity of its synthesizing enzyme (gamma-glutamylcysteine synthetase, gamma-GCS) elevated concomitantly in SHR and SHRSP: the level of GSH increased 1.2-fold in SHR and 1.3-fold in SHRSP. The activity of gamma-GCS was elevated 1.5-fold in SHR and 2.4-fold in SHRSP, accompanying an increase in the expression of its mRNA. Treatment of these rats with nicardipine, for 4 weeks improved blood pressure, from 176 +/- 10 to 140 +/- 8 mmHg in SHR, and from 201 +/- 11 to 167 +/- 5 mmHg in SHRSP, respectively, and decreased wet weight of heart, levels of GSH, and the activities of XO and gamma-GCS. Nicardipine reduced the expression of gamma-GCS mRNA. Collectively, these results suggest that reactive oxygen species produced by XO in hypertensive rat heart cause induction of the expression of gamma-GCS and nicardipine plays a role in reducing the oxidative stress in hypertensive heart.
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PMID:Nicardipine normalizes elevated levels of antioxidant activity in response to xanthine oxidase-induced oxidative stress in hypertensive rat heart. 979 May 16

Nicardipine, a dihydropyridine type calcium channel blocker, was infused at two flow-rates into spontaneously hypertensive (SH) and control normotensive Wistar-Kyoto (WKY) rats (young, 6-week-old and adult, 23-week-old, n = 5) under pentobarbital anesthesia, to cause hypotension. Mean arterial blood pressure and the concentrations of plasma amino acids and norepinephrine (NE) were measured before infusion and at each step of the infusion. The reduction in blood pressure caused by nicardipine induced a decrease in plasma L-arginine concentration in both young and adult SH rats, this effect being larger in adult rats. There was no significant change in plasma levels of L-arginine in age-matched WKY rats. The concentration of other amino acids did not change in both rat strains. On the contrary, there was an increase in plasma NE concentration in both SH and WKY rats after infusion with nicardipine. Plasma L-arginine concentration showed a good inverse correlation with the logarithm of plasma NE concentration in SH and WKY rats and the correlation was expressed as Y = -alpha log(X) + m (Y, plasma L-arginine concentration (nmol/mL); X, plasma NE concentration (pmol/mL); alpha, a slope; and m, an intercept). alpha, 43.0 and 4.35 for 23-week-old SH and WKY rats, respectively, and 17.0 and 4.0 for 6-week-old SH and WKY rats, respectively. The present data together with previous data suggest a direct noradrenergic stimulation of the synthesis of nitric oxide (NO) from L-arginine. The findings also indicate an impairment of the L-arginine metabolism or pools in SH rats compared with WKY rats. The deficiency of L-arginine increases with the age of SH rats and could be related to the development and maintenance of hypertension due to inefficient production of NO.
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PMID:Changes of plasma L-arginine levels in spontaneously hypertensive rats under induced hypotension. 1019 40

Calcium channel antagonists are widely prescribed for treatment of hypertension. In this study, we examined whether treatment with the calcium channel antagonists, nicardipine, nifedipine or diltiazem, alters cytochrome P-450 2B or 3A (CYP2B or CYP3A, respectively) expression in rat liver. Western blot analyses were undertaken using antibodies specific for one or several members of these cytochrome P-450 subfamilies. Nicardipine was found to be an effective inducer of CYP3A; in particular, CYP3A23 was increased approximately 36-fold following treatment with 100 mg of nicardipine/kg/day. Nicardipine induced CYP2B forms up to approximately 3.1-fold. Nifedipine did not alter CYP3A expression but did increase CYP2B expression such that total CYP2B, CYP2B1, and CYP2B2v (a splice variant of CYP2B2) were increased approximately 5- to 15-fold after treatment with 100 mg of nifedipine/kg/day, with increases in benzyloxyresorufin O-dealkylase and erythromycin N-demethylase activities, respectively. The distinct differences in cytochrome P-450 induction profile induced by nicardipine and nifedipine suggest that they may enhance cytochrome P-450 expression by different mechanisms unrelated to their effects on calcium channels.
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PMID:Effect of calcium channel antagonists nifedipine and nicardipine on rat cytochrome P-450 2B and 3A forms. 1045 23

Previous reports have demonstrated that Cyclosporine A (CyA) chronically administered induces an increase in adenosine plasma concentration by inhibiting adenosine uptake by red blood cells (RBC). We hypothesized that this effect may modulate, by a down regulation, the mRNA expression of adenosine receptors in rat kidney. Since high blood pressure (HBP) is a classical side effect of CyA treatment, nicardipine, a dihydropyridine calcium channel blocker, is often associated with CyA in treatment. To distinguish between the effects of CyA-induced HBP and the effects of CyA by itself, we have evaluated the effects of CyA and/or nicardipine on the mRNA expression of A1 and A2a adenosine receptors. The study was performed on five groups of rats (n= 8) receiving during 21 days either serum saline (0.5 ml i.p), CyA (12 mg/kg/day, i.p), nicardipine (1.2 mg/kg i.p) or nicardipine + CyA. The last (or fifth) group was injected with vehicle (0.5 ml i.p). Blood samples for adenosine assay were collected in the renal artery at day 21, just before the rat kidneys were removed for quantitation of adenosine A1 and A2a mRNA concentration by RT-PCR. We make two conclusions :i) Nicardipine induces a decrease in mRNA expression of A1 but not of A2a adenosine receptors. However, because nicardipine lowered both blood pressure and A1 mRNA expression, it is not possible to conclude if A1 mRNA decrease is implicated in the nicardipine effects on blood pressure.ii) CyA induces an increase in renal artery adenosine concentration and a decrease in mRNA expression of A1 and A2a adenosine receptors.
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PMID:Cyclosporine A and purinergic receptors in rat kidney. 1062 69

Nicardipine is the first dihydropyridine calcium channel blocker capable of intravenous administration. Seven pediatric patients with hypertensive emergencies attributable to various pathological processes were treated with intravenous nicardipine, starting at 1 microg/kg/min. Nicardipine appeared to be safe and effective in controlling hypertension in these patients. Two patients who received nicardipine through peripheral lines developed superficial thrombophlebitis. None of the five patients receiving nicardipine through a central line experienced phlebitis, and no other adverse effects were noted.
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PMID:Nicardipine is a safe and effective agent in pediatric hypertensive emergencies. 1079 49

In the present study, in order to elucidate the role of dihydropyridine (DHP)-sensitive calcium (Ca) channels in the regulation of neurotransmitter release in hypertension, we examined the effects of the DHP-sensitive Ca channel blocker nicardipine on norepinephrine (NE) release in blood vessels of spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats. The stimulation-evoked pressor responses and NE release were significantly greater in the mesenteric arteries of SHR than in the mesenteric arteries of WKY rats. Nicardipine significantly inhibited the stimulation-evoked NE release as well as vasoconstrictor responses in the mesenteric arteries to a greater extent in SHR than in WKY rats. These results demonstrated that nicardipine markedly reduced the stimulation-evoked NE release in blood vessels of SHR, which might suggest that the DHP-sensitive Ca channels could be involved, at least in part, in the regulation of NE release in hypertension.
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PMID:Role of dihydropyridine-sensitive calcium channels in the regulation of norepinephrine release in hypertension. 1181 55

Retinal and choroids arteries changes were investigated ophthalmoscopically and with morphometric techniques in spontaneously hypertensive rats (SHR) of 26 weeks either untreated (control animals) or treated for 12 weeks equi-hypotensive doses of the Ca2+ antagonist nicardipine or of the non-dihydropyridine type vasodilatator hydralazine. Retinal and choroid arteries hypertensive changes were compared with those affecting pial and intracerebral arteries of frontal lobe. Ophthalmoscopic analysis revealed in control SHR a rarefaction of capillaries and a decrease of their length and area. Treatment with nicardipine and to a lesser extent with hydralazine countered ophthalmoscopic changes noticeable in SHR. Morphometric analysis revealed thickening of the wall and luminal narrowing of retinal, choroids, pial, and intracerebral arteries. Anti-hypertensive treatment decreased thickening of the arterial wall and increased luminal narrowing of different arteries investigated. Nicardipine was more effective than hydralazine in countering arterial hypertensive changes in SHR and displayed a vasodilatory activity on small sized retinal and cerebral arteries, that represent a vascular segment not sensitive to hydralazine. Comparative evaluation of the wall-to-lumen ratio revealed a similar pattern between retinal and intracerebral arteries, but not between other arteries investigated. This suggests that analysis of retinal arteries may be predictive of brain intracerebral arteries changes in hypertension.
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PMID:Quantitative image analysis of choroid and retinal vasculature in SHR: a model of cerebrovascular hypertensive changes? 1245 Feb 48


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