***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
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    ***EXAMPLES*** 
    Input: BACKGROUND Recent meta-analyses suggest that once-daily dihydropyridines and angiotensin-converting enzyme inhibitors cause similar decreases in left ventricular ( LV ) mass for comparable decreases in blood pressure ( BP ) . However , some dihydropyridines , such as felodipine-extended release ( ER ) , still increase sympathetic activity and may , therefore , be less effective in decreasing LV mass . OBJECTIVES To evaluate the effects of long term antihypertensive treatment with nifedipine-gastrointestinal therapeutic system ( GITS ) and felodipine-ER compared with enalapril on LV mass relative to the extent of BP control ( assessed by 24 h ambulatory BP monitoring ) and sympathetic activity ( assessed by plasma catecholamine concentrations ) . PATIENTS AND METHODS Enalapril was started at 10 mg/day , felodipine-ER at 5 mg/day and nifedipine-GITS at 30 mg/day , all once daily . Doses were increased to 20 mg/day , 10 mg/day or 60 mg/day , respectively , if the office BP remained 160/90 mmHg or greater at the end of the dosing interval . Evaluable echocardiograms were obtained for 116 patients at the end of the study ( 30 weeks of treatment ) . RESULTS On 24 h ambulatory BP monitoring , nifedipine-GITS caused a consistent decrease in BP throughout the 24 h dosing interval , whereas felodipine-ER caused a more marked fall in BP during the day , and enalapril 's effects diminished during the night and had disappeared by the morning . Only felodipine-ER significantly increased supine and st and ing plasma noradrenaline by more than 50 % similarly after six , 18 , and 30 weeks of treatment . In BP responders ( decrease in systolic BP 10 mmHg or greater ) , enalapril and nifedipine-GITS caused clear decreases in LV mass by 12 to 16 g/m2 , whereas felodipine-ER was less effective ( decrease by only 6 g/m2 , P<0.01 versus enalapril ) . CONCLUSIONS Once-daily dihydropyridines should not be regarded as one homogeneous class and , compared with felodipine-ER , nifedipine-GITS exhibits a better profile regarding 24 h BP control , sympathetic activation and regression of LV mass Objective To compare the effects of amlodipine and nifedipine on heart rate and parameters of sympathetic nerve activity during the acute and chronic treatment periods in order to eluci date their influence on cardiovascular outcome . Design A r and omized and single-blind study . Methods We performed 24 h ambulatory electrocardiography and blood pressure monitoring of 45 essential hypertensive in patients . Plasma and urinary catecholamine levels were measured during the control ( pretreatment ) period , on the first day ( acute period ) and after 4 weeks ( chronic period ) of administration of amlodipine and of short-acting nifedipine or its slow-releasing formulation . The low-frequency and high-frequency power spectral densities and low-frequency : high-frequency ratio were obtained by heart rate power spectral analysis . Results Blood pressure was significantly and similarly reduced by administrations of amlodipine , short-acting nifedipine and slow-releasing nifedipine during the chronic period . The total QRS count per 24 h , which remained constant during the chronic period of administration of slow-releasing nifedipine and was increased by administration of nifedipine , was decreased by 2.8 % by administration of amlodipine . Administration of amlodipine decreased the plasma and urinary norepinephrine levels during the chronic period , whereas the levels were significantly increased by administration of short-acting nifedipine and not changed by administration of slow-release nifedipine . Although low-frequency : high-frequency ratio was increased significantly by administration of short-acting nifedipine and slightly by administration of slow-releasing nifedipine , administration of amlodipine reduced it during the acute and chronic periods . Conclusions Administration of amlodipine did not induce an increase in sympathetic nerve activity in essential hypertensive patients during the chronic period , suggesting that beneficial effects on essential hypertension can be expected after its long-term administration . Administration of slow-releasing nifedipine induces milder reflex sympathetic activation than does that of short-acting nifedipine The sympathetic nervous system ( SNS ) is an important regulator of the circulation . Its activity is increased in hypertension and heart failure and adversely affects prognosis . Although certain drugs inhibit SNS , dihydropyridine calcium antagonists may stimulate the system . Phenylalkylamine calcium antagonists such as verapamil have a different pharmacological profile . We therefore tested the hypothesis of whether amlodipine , nifedipine , or verapamil differs in the effects on muscle sympathetic nerve activity ( MSA ) .  Forty-three patients ( 31 men , 12 women ) with mild to moderate hypertension were r and omly assigned to 1 drug for 8 weeks . Blood pressure , heart rate , and MSA ( by microneurography ) were measured at baseline and after 8 weeks of treatment . All calcium antagonists led to a similar decrease in blood pressure of 5.0±1.5 to 6.4±1.4 mm Hg at 8 weeks ( P < 0.001 versus baseline ) . There were no significant differences in MSA between groups . With amlodipine  , MSA averaged 49±3 bursts/min ( 3 versus baseline ) ; with nifedipine , 48±3 bursts/min ( 2 versus baseline ) ; and with verapamil , 49±2 bursts/min ( all , P = NS ) . With verapamil  , norepinephrine decreased by 4 % but tended to increase by about one third with amlodipine or nifedipine ( P = NS ) . Thus , in hypertension slow release forms of verapamil , nifedipine , and amlodipine exert comparable antihypertensive effects and do not change MSA , although there was a trend toward decreased MSA and plasma norepinephrine  with verapamil This study aim ed to compare the effects of two long-acting dihydropyridine calcium channel blockers ( CCBs ) with different pharmacologic properties , lercanidipine and nifedipine Gastro-Intestinal Therapeutic System ( GITS ) , in the chronic treatment of essential hypertension . After a 4-week placebo run-in period , 60 patients of both sexes were r and omly treated with lercanidipine 10 to 20 mg or nifedipine GITS 30 to 60 mg taken orally for 48 weeks , according to a double-blind , parallel group design . For the first 4 weeks of treatment , the lowest dose of each drug was used , followed by higher doses if diastolic blood pressure ( BP ) was > 90 mm Hg . At the end of the placebo period and after 4 , 8 , 12 , 24 , and 48 weeks of active treatment BP , heart rate ( HR ) , and plasma norepinephrine ( NE ) levels were assessed . Lercanidipine and nifedipine GITS similarly reduced BP values after 48 weeks ( -21.7/15.9 mm Hg and -20.7/14.6 mm Hg , respectively , both P < .001 v placebo ) , with no change in HR . Despite the similar lack of effect on HR , the two drugs displayed different influences on plasma NE , which was significantly increased by nifedipine GITS ( + 56 pg/mL , P < .05 v placebo ) but not by lercanidipine . These findings suggest that 1 ) sympathetic activation occurs during chronic therapy with nifedipine GITS but not with lercanidipine , which might be related to the different pharmacologic characteristics of the two CCBs at the doses evaluated ; and 2 ) nifedipine GITS seems to activate peripheral but not cardiac sympathetic nerves , consistent with differing regulation of cardiac and peripheral sympathetic activity Intravenous , sublingual , or aerosolized nitroglycerin was administered to 19 patients with coronary artery disease during clinical ly indicated cardiac catheterization . Eight blood sample s were collected over 15 min from each patient , and analyzed for content of nitroglycerin , 1,2‐glycerol dinitrate , and 1,3‐glycerol dinitrate .  Simultaneously , heart rate ( HR ) , systolic blood pressure ( SBP ) , and left ventricular end‐diastolic pressure ( LVEDP ) were recorded . Plasma concentrations of nitroglycerin  were highest after intravenous injection and lowest after sublingual tablets . Metabolite concentrations were highest after intravenous injection at early time‐points ; at later time‐points , no betweengroup differences could be detected . SBP was minimally affected by intravenous nitroglycerin but was significantly reduced by sublingual and aerosolized formulations . Minor fluctuations in HR were observed in association with all three formulations . LVEDP was reduced by all three formulations of nitroglycerin but most rapidly by the intravenous form . Overall , no differences were detected in hemodynamic responses caused by sublingual and aerosolized nitroglycerin . Efficacy of sublingual and aerosolized nitroglycerin in patients undergoing cardiac catheterization is equivalent Objective To compare the acute and chronic effects of nifedipine retard ( NPA ) , nifedipine gastrointestinal therapeutic system ( NGITS ) and amlodipine at trough and peak plasma concentrations of drug on blood pressure and heart rate , and on plasma norepinephrine and epinephrine levels in patients with mild-to-moderate hypertension ( diastolic blood pressure 95–115 mmHg ) . Design and methods After 3 - 4 weeks ' placebo treatment , patients of both sexes were r and omly allocated to be administered 10 or 20 mg NPA twice a day , 30 or 60 mg NGITS once a day , and 5 or 10 mg amlodipine once a day for 6 weeks . Initially , for the first 2 weeks , the lowest dose of each drug was used , but higher doses were administered after 2 weeks if sitting diastolic blood pressure was > 90 mmHg . Patients were evaluated after administration of the first dose and after 6 weeks ' therapy in a hospital setting . Blood sample s were taken for high-performance liquid chromatography measurement of catecholamine and drug levels at various intervals for a period covering trough to peak drug level ranges . Results Administration of all three drugs reduced clinic blood pressure to the same level after 6 weeks ' therapy , but heart rate was increased slightly only with amlodipine ( P < 0.05 ) . Administration of NPA  reduced blood pressure more abruptly whereas administrations of NGITS and amlodipine induced smoother falls after acute and chronic treatments : a significant increase in heart rate was observed with amlodipine after chronic treatment . Both acute and chronic treatments with NPA ( n = 19 ) increased norepinephrine levels ( P < 0.01 ) transiently ( 2 - 4 h ) . In contrast , administration of NGITS ( n = 22 ) did not increase norepinephrine levels and even induced a slight but significant decrease in norepinephrine levels 5 - 6 h after chronic treatments . Although administration of amlodipine ( n = 22 ) did not increase norepinephrine levels transiently either after acute or after chronic administration , it did induce a sustained rise in basal norepinephrine levels by more than 50 % after chronic therapy ( P < 0.01 ) . Plasma epinephrine levels were not increased by any of the treatments and even a slight decrease was observed 4 h after administration of a dose following chronic treatments with NGITS and amlodipine ( P < 0.05 ) . Conclusions The transient increase in norepinephrine levels observed with NPA and the sustained increases in norepinephrine levels observed after chronic treatment with amlodipine suggest that sympathetic activation occurs with those two drugs . The lack of increase in norepinephrine levels after administration of NGITS suggests that this formulation does not activate the sympathetic system . The lowering of epinephrine levels after administrations of NGITS and amlodipine suggests that inhibition of release of epinephrine by the adrenal medulla occurs with longer-acting dihydropyridine formulations N-Type calcium channel antagonists may suppress sympathetic activity . The purpose of this study was to assess the effects of amlodipine and cilnidipine on the cardiac sympathetic nervous system and the neurohormonal status of essential hypertension . 123I-metaiodobenzylguanidine ( MIBG ) cardiac imaging was performed and blood sample s were taken to determine plasma renin activity and plasma norepinephrine concentration before and 3 months after drug administration in 47 patients with mild essential hypertension . Twenty-four of the patients were treated with 5 to 10 mg/d of amlodipine ; the other 23 were treated with 10 to 20 mg/d of cilnidipine . For comparison , 12 normotensive subjects were also studied . No significant differences were found in the basal characteristics between the 2 hypertensive groups . In both hypertensive groups , both the systolic and diastolic 
    Output:
    
Overall , each drug lowered blood pressure  in hypertensive patients in association with only small changes in heart rate ( i.e. < 1 beat/min ) .
Plasma norepinephrine concentrations , as the most widely reported marker of sympathetic nervous system activity , showed greater increases in patients treated with amlodipine than with nifedipine GITS .
The evidence indicates that both these once-daily dihydropyridine CCBs lower blood pressure effectively with minimal effects on heart rate .
There are small differences between the drugs in the extent to which each activates the sympathetic nervous system with an overall non-significant trend in favour of nifedipine GITS