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

Thirty patients with mild to moderate essential hypertension entered a randomised double-blind parallel group study for 6 months to compare the effects of the new calcium channel blocker nicardipine 90 mg/day and propranolol 240 mg/day. Both drugs reduced systolic and diastolic blood pressures significantly in the supine and in standing positions. After 6 months of treatment, nicardipine had reduced the supine systolic and diastolic blood pressures by 16 and 17 mm Hg, respectively, and propranolol by 15 and 12 mm Hg. While propranolol treatment led to a marked decline in heart rate, nicardipine caused a small but statistically significant increase in heart rate throughout the study. Both drugs reduced blood pressure during maximal exercise, but propranolol had a greater effect. During exercise nicardipine did not affect the heart rate, whereas propranolol dramatically reduced it. Nicardipine did not produce any ECG changes at rest or during exercise. The side-effects for nicardipine were mild and were related to the vasodilatation induced by the drug. No abnormalities in routine blood chemical tests were found for either of the drugs. Nicardipine appears to be an effective single drug treatment for mild to moderate hypertension.
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PMID:Nicardipine in the treatment of essential hypertension controlled 6-month-study comparing nicardipine with propranolol at rest and during exercise. 331 37

Differences in the degree of attenuation by the calcium entry blocker, nicardipine, of the pressor responses to alpha-1 (phenylephrine) and alpha-2 (UK 14.304) adrenoceptor agonists was investigated in pentobarbital-anesthetized, normotensive Sprague-Dawley (SD) or Wistar Kyoto (WKY) rats, and spontaneously hypertensive rats (SHR), treated with the ganglionic blocking agent, pentolinium. Following administration of the ganglionic blocking agent, pentolinium, nicardipine produced a significant fall in blood pressure in SHR but not in SD or WKY rats. Nicardipine had no effect on the basal blood pressure of pithed SHR. In rats treated with the ganglionic blocking agent, pentolinium, nicardipine produced parallel shifts to the right in the dose-response curves for phenylephrine but had no effect on maximal responses to phenylephrine. The decrease in the ED50 of phenylephrine was greater in the SHR than in normotensive rats. Nicardipine produced a decrease in both the ED50 and the maximal response to the alpha-2 adrenoceptor agonist, UK 14.304. The decrease in the maximal response was greater in SHR than in WKY normotensive rats but the change in ED50 for UK 14.304 was greater in WKY than in SHR. SD normotensive rats gave intermediate results. We conclude that the inhibition of alpha-adrenoceptor-mediated pressor responses by nicardipine is generally more pronounced in SHR than in normotensive rats. This suggests that hypertension may be accompanied by an increase in the sensitivity of peripheral resistance beds to calcium entry blockers.
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PMID:Greater vasodepressor sensitivity to nicardipine in spontaneously hypertensive rats (SHR) compared to normotensive rats. 340 21

The involvement of cholinergic mechanisms in the central cardiovascular effects of a dihydropyridine, nicardipine, was investigated in pentobarbital-anaesthetized normotensive dogs. Nicardipine (1 microgram/kg) injected intracisternally (i.c.) induced a rise in both blood pressure and heart rate. This induced hypertension was suppressed by pretreatment with intravenous (i.v.) atropine or i.c. methylatropine but not i.v. methylatropine. I.c. methylatropine reduced nicardipine-induced tachycardia. These results demonstrate the involvement of cholinergic pathways in the central cardiovascular effects of i.c. nicardipine in dogs and suggest a functional interaction between dihydropyridine binding sites and cardiovascular cholinergic mechanisms in the brain.
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PMID:Involvement of cholinergic mechanisms in the central cardiovascular actions of nicardipine in dogs. 342 47

In 10 patients with moderate to severe hypertension, the hemodynamic effects of ergometric exercise and nicardipine, a dihydropyridine calcium channel antagonist, were characterized under basal conditions and after 1 week of therapy. The responses of plasma renin activity and catecholamines were also assessed. Nicardipine induced significant reductions of systolic, diastolic and mean blood pressure under conditions of rest and peak exercise (p less than 0.001), mediated by reversal of vasoconstriction (p less than 0.001). Overall, cardiac index and stroke volume index responses were not significantly altered by nicardipine. Although rest pulmonary wedge pressure was unchanged (6 +/- 3 to 5 +/- 4 mm Hg), peak exercise pulmonary wedge pressure decreased from 24 +/- 22 to 7 +/- 5 mm Hg (p less than 0.001) with nicardipine therapy. This effect of nicardipine on pulmonary wedge pressure was present across all work loads studied, and was accompanied by reduction of peak exercise pulmonary artery pressure from 43 +/- 10 to 25 +/- 7 mm Hg (p less than 0.001). Oxygen consumption was unchanged, associated with reduction of arteriovenous oxygen difference (p less than 0.02). Both plasma renin activity (p less than 0.05) and norepinephrine (p less than 0.005) were significantly increased with nicardipine therapy. Thus, nicardipine produced significant blood pressure reduction by reversal of vasoconstriction in patients with essential hypertension. The preservation of cardiac output, with markedly reduced pulmonary wedge pressure, indicated that nicardipine improved ventricular performance in response to reversal of vasoconstriction.
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PMID:Systemic and pulmonary hemodynamic responses to nicardipine during graded ergometric exercise in patients with moderate to severe essential hypertension. 362 70

Nicardipine is a new calcium ion antagonist with vasodilating properties which has been shown to be effective in the treatment of hypertension and angina. We have studied its effect on systolic and diastolic left ventricular function in patients with mild to moderate degrees of congestive heart failure. Ten male patients with New York Heart Association Class II and III heart failure underwent acute treatment with an intravenous infusion of nicardipine (10 mg over 10 minutes). A nuclear probe was used to monitor left ventricular ejection fraction, peak filling rate, and relative cardiac output. Blood pressure and heart rate were also measured. The blood pressure (mean +/- SD) fell from 133 +/- 26/86 +/- 11 mmHg to 103 +/- 22/69 +/- 13; the heart rate rose from 67 +/- 9 beats/min to 85 +/- 10; left ventricular ejection fraction from 31 +/- 7 to 38 +/- 6%; relative cardiac output from 24 +/- 9 to 41 +/- 11; peak filling rate from 1.18 +/- 0.4 end-diastolic volume per second to 1.82 +/- 0.4 (p less than 0.001 in all cases) at the end of infusion. After 4 weeks of chronic treatment in eight patients (20 mg to be taken three times daily (tds) in one and 40 mg tds in 7), the blood pressure and heart rate had returned to baseline values but the improvements in left ventricular ejection fraction, relative cardiac output, and peak filling rate were sustained; this was associated with functional improvement in all 8 patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute and chronic effects of nicardipine on systolic and diastolic left ventricular performance in patients with heart failure: a pilot study. 372 49

Nicardipine is a new slow channel calcium blocker. It has been shown to be effective in the treatment of hypertension and angina pectoris. Nine patients with mild to moderate left ventricular failure were given intravenous infusions of nicardipine and the haemodynamic effects measured. In patients receiving 20 mg of nicardipine, mean cardiac index rose to a peak 1.81 X min-1 X m-2 (64%) above the preinfusion level, stroke volume index rose by 12 ml X m-2 (35%) and heart rate rose by 16 beats X min-1 (20%). There was a significant fall in systemic vascular resistance of 50% manifested by a reduction of 22 mm Hg in systolic blood pressure (18%) and 18 mm Hg in diastolic blood pressure (22%). Pulmonary vascular resistance fell by 45%. Mean pulmonary artery pressure and capillary wedge pressure did not change significantly. This study suggests that concomitant mild to moderate left ventricular failure is not a contra-indication to nicardipine therapy in patients with angina.
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PMID:The acute haemodynamic effects of nicardipine in patients with chronic left ventricular failure. 374 13

Fifty patients with mild essential (primary) hypertension entered a double-blind, parallel-group study with either nicardipine 30 mg three times daily or placebo, randomly assigned as monotherapy for 6 weeks. At the end of 6 weeks, the nicardipine-treated group had a statistically significant reduction in mean supine systolic/diastolic pressure of 21.2/15.0 mm Hg (P less than 0.001) compared with the nonsignificant reduction of 0.7/2.9 mm Hg in the placebo-treated group. The difference in mean response between the nicardipine- and placebo-treated groups was significant (P less than 0.001). In the nicardipine-treated group, the reduction in mean standing systolic/diastolic blood pressure, 17.9/13.8 mm Hg, was significant (P less than 0.001), whereas in the placebo-treated group the change was +3.0/-1.5 mm Hg. The difference between the two treatment groups was significant (P less than 0.001). In both treatment groups, changes in pulse rate were minor, and there was no evidence of tachyphylaxis occurring with nicardipine. Adverse experiences were minor in all cases except for one patient with muscle pain during treatment with nicardipine. Patients who received nicardipine showed a mean increase of 52% in plasma renin activity (PRA) after 6 weeks (P less than 0.01). Initial basal or stimulated PRA did not correlate with blood pressure reduction on nicardipine. Nicardipine 30 mg three times daily is a well-tolerated and effective antihypertensive agent.
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PMID:Nicardipine hydrochloride in essential hypertension--a controlled study. 389 78

The haemodynamic, antianginal and antihypertensive effects of nicardipine, a vascular selective calcium antagonist, were studied in experimental animals. In the canine isolated coronary artery, nicardipine relaxed potassium-induced contraction and suppressed 3,4-diaminopyridine-induced rhythmic contractions more effectively than nifedipine, verapamil or diltiazem. In anaesthetised rats, nicardipine prevented the elevation of ST segment induced by intracoronary injection of methacholine. In anaesthetised dogs, nicardipine produced a greater vasodilatation in vertebral, carotid, and coronary vessels than in mesenteric, femoral, and renal vessels and did not affect myocardial oxygen consumption. In conscious monkeys, nicardipine given intravenously lowered blood pressure and gave rise to reflex tachycardia but did not prolong the A-V conduction time. Nicardipine given orally lowered blood pressure in spontaneously hypertensive rats (SHR), renal hypertensive rats (RHR), and deoxycorticosterone acetate/salt hypertensive rats (DOCA/Salt), as well as in normotensive rats. Long-term treatment with nicardipine given orally for 12 weeks effectively lowered high blood pressure in the three types of hypertensive rats, reduced cardiac hypertrophy in SHR and DOCA/Salt rats, and prevented mortality from stroke in DOCA/Salt rats. Combined treatment with nicardipine and a beta-adrenoceptor blocking agent (indenolol) showed an antihypertensive effect similar to that obtained with nicardipine alone. Conscious renal hypertensive dogs given repeated oral administration of nicardipine for 14 days did not develop tolerance to the hypotensive activity of nicardipine. Under the same conditions, tolerance to hydralazine developed within 4 days.
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PMID:Cardiovascular pharmacology of nicardipine in animals. 402 53

The effect of nicardipine on experimental hyperlipemia induced by a 1% cholesterol diet in spontaneously hypertensive rats (SHR) was investigated by the change of hemodynamics and the determination of lipid contents of the serum, liver, heart and aorta. Nicardipine increased liver weight and liver weight per body weight ratio, and it decreased heart and kidney weight significantly. Nicardipine inhibited the increase in blood pressure with cholesterol and normal diets. Nicardipine decreased heart rate in SHR fed the normal diet, and it inhibited the increase in heart rate in SHR fed the cholesterol diet. Serum lipid levels significantly increased with the cholesterol diet. Nicardipine significantly increased cholesterol in high density lipoprotein (HDL-C) and phospholipid in HDL (HDL-PL) with cholesterol and normal diets, and it decreased triglyceride and improved the atherogenic index "(total cholesterol-HDL-C)/HDL-C" with the normal diet. Serum GOT and GPT significantly increased with the cholesterol diet. Nicardipine significantly enhanced an increase in GOT and GPT levels with the cholesterol diet. Nicardipine increased phospholipid content in the liver, triglyceride in the heart, and it decreased total cholesterol in the aorta. A morphologic study showed a fatty liver in SHR fed the cholesterol diet, but nicardipine had no effect on the morphological changes in the liver, heart and aorta. These results suggest that nicardipine may prevent atherosclerotic degeneration by the inhibition of hypertension, increase in serum HDL and decrease in total cholesterol in the aorta.
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PMID:[Effect of nicardipine on cholesterol-fed S.H.R]. 405 35

The purpose of this study was to test in double-blind trial the tolerance and antihypertensive effect of nicardipine versus placebo in 32 elderly patients (mean age: 84 years). Nicardipine was given three times a day (mean dose: 69.4 mg per day). After four weeks, nicardipine lowered blood pressure (BP) from 186 +/- 4 mmHg/99.5 +/- 3 mmHg to 150 +/- 6/84 +/- 3 mmHg (p less than 0.001). 10 out of 16 patients were normalized (BP less than 160-95 mmHg). The placebo group remained hypertensive: 181 +/- 7/96 +/- 4 mmHg versus 183 +/- 4/101 +/- 3 mmHg (NS). 3 placebo treated patients were nevertheless normalized. The changes in systolic BP and diastolic BP were significantly greater in the Nicardipine group: respectively -36 +/- 4 versus -2 +/- 6 mmHg (p less than 0.001), -16 +/- 3 versus -5 +/- 4 mmHg (p less than 0.05). Treatment was very well tolerated. Orthostatic hypotension, change in heart rate, variation in biological parameters were never observed. These data agree with Buhler's statement suggesting that calcium channel inhibitors can represent an interesting alternative to diuretics as first line monotherapy in the treatment of hypertension in the elderly.
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PMID:[Treatment of arterial hypertension in the aged with a calcium antagonist: nicardipine]. 644 44


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