***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 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: BACKGROUND Structural and functional alterations of the vasculature may contribute to complications of hypertension . Because angiotensin II may be pivotal in some of these vascular abnormalities , we tested the hypothesis that the angiotensin type 1 ( AT(1 ) ) receptor antagonist losartan , in contrast to the beta-blocker atenolol , would correct resistance artery abnormalities in patients with essential hypertension . METHODS AND RESULTS Nineteen untreated patients with mild essential hypertension ( 47+/-2 years , range 30 to 65 years ; 57 % male ) were r and omly assigned in double-blind fashion to losartan or atenolol treatment for 1 year . Nine age/sex-matched normotensive subjects were also studied . Both treatments reduced blood pressure to a comparable degree ( losartan , from 149+/-4.1/101+/-1.6 to 128+/-3.6/86+/-2.2 mm Hg , P<0.01 ; atenolol , from 150+/-4.0/99+/-1.2 to 130+/-3.2/84+/-1.4 mm Hg , P<0.01 ) . Resistance arteries ( luminal diameter 150 to 350 microm ) dissected from gluteal subcutaneous biopsies were studied on a pressurized myograph . After 1 year of treatment , the ratio of the media width to lumen diameter of arteries from losartan-treated patients was significantly reduced ( from 8.4+/-0.4 % to 6.7+/-0.3 % , P<0.01 ) . Arteries from  atenolol-treated  patients exhibited no significant change ( from 8 . 3+/-0.3 % to 8.8+/-0.5 % after treatment ) . Endothelium-dependent relaxation ( acetylcholine-induced ) was normalized by losartan ( from 82.1+/-4.9 % to 94.7+/-1.1 % , P<0.01 ) but not by atenolol ( from 80 . 4+/-2.7 % to 81.7+/-4.6 % ) . Endothelium-independent relaxation ( by sodium nitroprusside ) was unchanged after treatment . CONCLUSIONS The AT(1 ) antagonist losartan corrected the altered structure and endothelial dysfunction of resistance arteries from patients with essential hypertension , whereas the beta-blocker atenolol had no effect To investigate the time course of cardiovascular structural changes in patients with essential hypertension after angiotensin-converting enzyme ( ACE ) inhibition  , we determined left ventricular structure , minimal vascular resistance in the forearm as an index of resistance vessel structure and stiffness beta of carotid artery in 15 essential hypertensive subjects during a placebo period and after 2 , 6 , and 12 months of temocapril treatment .  Blood pressure decreased within 2 weeks , and the antihypertensive effects were noted throughout the 12-month administration period . Left ventricular mass index decreased significantly after 2 months ( 120+/-12 to 106+/-9 g/m2 ; p < 0.01 ) and was normalized after 12 months ( 88+/-6 g/m2 ) . Postischemic minimal vascular resistance in the forearm decreased gradually from 2.1+/-0.5 to 1.6+/-0.4 PRU at month 12 of temocapril treatment . In contrast , increased stiffness index beta of carotid artery was not altered during a 1-year treatment period ( 11.4+/-4.9 to 11.6+/-3.8 at month 12 of treatment ) . These data indicated that the regression of structural changes of left ventricle and arterioles occurred gradually and progressively for 1-year treatment with ACE inhibition , but large arteries were not affected Seventeen male untreated mild essential hypertensive patients aged 41 + /- 2 years agreed to participate in a double-blind r and omized trial to test the effects of antihypertensive treatment on the structure and function of subcutaneous resistance arteries . Patients were treated with either 50 to 100 mg/d atenolol or 2.5 to 5 mg/d cilazapril .  Blood pressure before treatment was 148 + /- 6/99 + /- 1 and 147 + /- 2/99 + /- 1 mm Hg , respectively . At 1 year of treatment blood pressure was 131 + /- 4/85 + /- 2 and 132 + /- 2/87 + /- 1 mm Hg , respectively . Resistance arteries ( 200 to 400 microns lumen diameter ) dissected from subcutaneous gluteal biopsies obtained before treatment and at 1 year showed that the media-lumen ratio of arteries from patients treated with cilazapril was reduced to 6.31 + /- 0.21 % from 7.54 + /- 0.31 % before treatment ( P < .05 ) , still slightly but significantly larger ( P < .05 ) than the media-lumen ratio of resistance arteries of normotensive control subjects ( 5.15 + /- 0.30 % ) . In contrast , in arteries from patients treated with atenolol there was no significant change with treatment ( 7.97 + /- 0.60 % before and 8.07 + /- 0.45 % after 1 year of treatment ) . Active wall tension responses to endothelin-1 were blunted in hypertensive patients and normalized in the cilazapril-treated patients . Depressed active media stress responses to norepinephrine , arginine vasopressin , and endothelin-1 were accordingly normalized in the patients receiving cilazapril as the media width became thinner but were unchanged in those taking atenolol . ( ABSTRACT TRUNCATED AT 250 WORDS Our study attempted to evaluate the importance of changes in the circulating renin-angiotensin-aldosterone system ( RAAS ) and in hemodynamics in relation to observed changes in cardiovascular structure . We studied previously untreated men ( n = 28 ) with essential nonmalignant hypertension and a supine casual diastolic blood pressure > 95 mm Hg on three to four separate ( > 1-week interval ) occasions measured in triplicate . We used intraarterial blood pressure , dye-dilution technique , plethysmography ( h and s ) , eye-ground photos , M-mode echocardiography , radio immunoassays , and multiple regression analysis . Patients were r and omized to 6 months of double-blind treatment with either enalapril or hydrochlorothiazide , following 4 to 6 weeks on placebo . We found that enalapril blocked the plasma angiotensin converting enzyme ( ACE ) with a secondary increment in plasma renin activity ( PRA ) and reductions in angiotensin II ( AII ) and aldosterone . Blood pressure was lowered through a reduction in total peripheral resistance ( TPR ) .  Hydrochlorothiazide increased PRA , AII , and aldosterone , and lowered blood pressure mainly through a reduction in cardiac output .  Enalapril was significantly more effective than hydrochlorothiazide in reversing structural changes in the retinal and h and vasculature as well as in the heart . A reduction in cardiac hypertrophy was seen even in the occasional enalapril-treated patient , in whom little or no reduction in blood pressure occurred . In the stepwise regression analyses , the changes in retinal and h and vascular structure were most strongly related to various changes in the RAAS , explaining 15 to 34 % of the variance . For the changes in cardiac structure , the type of therapy ( enalapril or hydrochlorothiazide ) appeared to be the most important factor , explaining between 29 and 50 % of the variance . The changes in cardiac structure were even more strongly related to changes in the RAAS for the enalapril treated patients and explained up to 55 % of the variance in cardiac structure . It can be concluded that the reversal of structural vascular changes during antihypertensive therapy was more dependent on the blockade of the RAAS than on lowering of the blood pressure In a double-blind r and omized trial , the effects of treatment with an angiotensin-converting enzyme ( ACE ) inhibitor ( perindopril ) and a beta-blocker ( atenolol ) on small artery structure were compared in previously untreated essential hypertensive patients . Subjects ( diastolic blood pressure > or = 100 and < or = 120 mm Hg ) were r and omly assigned to treatment for 12 months with either perindopril ( n = 13 , 4 to 8 mg/d ) or atenolol ( n = 12 , 50 to 100 mg/d ) ; the dosage was adjusted upward and in some cases combined ( n = 5 , perindopril ; n = 2 , atenolol ) with thiazide diuretic to achieve target blood pressure ( diastolic blood pressure below 90 mm Hg ) . Before and at the end of treatment , gluteal biopsies were taken under local anesthetic ; from these biopsies , two small arteries were dissected and mounted on a myograph for morphometry . The reduction in blood pressure with  atenolol  ( drop in mean blood pressure 28.4 + /- 1.8 mm Hg ) was greater than with perindopril ( 20.6 + /- 1.8 mm Hg , P < .05 ) . Perindopril treatment caused an increase in small artery diameter ( 231 + /- 14 to 274 + /- 13 microns , P < .05 ) and a reduction in the ratio of media thickness to lumen diameter ( 7.94 + /- 0.65 % to 5.96 + /- 0.42 % , P < .05 ) , whereas atenolol had no effect ( 246 + /- 14 to 231 + /- 13 microns and 7.14 + /- 0.47 % to 6.79 + /- 0.45 % , respectively ) . The change in small artery morphology caused by perindopril was not accompanied by any change in media cross-sectional area , suggesting that the change was due to " remodeling . " ( ABSTRACT TRUNCATED AT 250 WORDS In order to investigate whether hypertension-related structural vascular changes may be influenced by antihypertensive treatment , 10 patients were studied suffering from essential arterial hypertension , five males and five females , aged between 34 and 61 years ( mean age : 46.9 + /- 8.13 years ) . All patients received a placebo for 1 week and then captopril , 75 mg b.i.d . for 3 months . After placebo and captopril treatments , the following parameters were evaluated : SBP , DBP , mean blood pressure ( MBP ) , by the formula 1/3 ( SBP + 2 x DBP ) and basal and minimal vascular resistances , respectively obtained by the ratios MBP/rest flow and MBP/peak flow . Blood flows have been obtained by strain gauge plethysmography . A significant decrease in systolic ( P less than 0.025 ) , diastolic ( P less than 0.01 ) and mean blood pressure ( P less than 0.01 ) , basal vascular resistances ( 52 + /- 19 vs 28 + /- 12 A.U. , P less than 0.01 ) and minimal vascular resistances ( 6.3 + /- 2.2 vs 3.9 + /- 2.8 A.U. , P less than 0.025 ) has been observed after captopril treatment in comparison to placebo , whereas rest ( 2.9 + /- 0.7 vs 4.1 + /- 0.9 ml.min-1.100 g-1 , P less than 0.01 ) and peak blood flows ( 21.3 + /- 5.8 vs 29.7 + /- 9.4 ml.min-1.100 g-1 ) significantly increased . These data seem to indicate that antihypertensive treatment with the angiotensin-converting enzyme inhibitor , captopril , is not only efficacious in inducing a significant blood pressure decrease , consequent to the reduction of basal vascular resistance ( due to the vasodilating effects of the drug ) , but is also able to reduce minimal vascular resistance . ( ABSTRACT TRUNCATED AT 250 WORDS We studied the structural and functional characteristics of the vascular bed at calf level in 46 middle aged hypertensive patients ( 20 males and 26 females ) treated with different beta-blockers . After one week of placebo , the patients were divided into three groups : group 1 was treated with labetalol , an alpha-beta-blocker ( 200 mg t.t.d . ) ; group 2 was treated with acebutolol , a cardioselective beta-blocker with intrinsic sympathomimetic activity ( ISA ) ( 200 mg t.t.d . ) ; group 2 was treated with acebutolol , a cardioselective beta-blocker with intrinsic sympathomimetic activity ( ISA ) ( 200 mg t.t.d . ) ; group 3 was treated with metoprolol , a cardioselective beta-blocker without ISA ( 100 mg t.t.d . ) . Before and after placebo , and after three months of active drug treatment , we measured blood pressure , and rest and peak flow at the calf level by strain gauge plethysmography . Basal and minimal vascular resistances were calculated as the ratio between mean blood pressure and rest or peak flow , respectively . A 
    Output:
    
The survey shows that change in blood pressure in indeed a poor indicator of change in resistance vessel structure .
However , it is a remarkably consistent finding that normalization of resistance vessel structure is obtained with therapeutic regimens which reduce blood pressure by vasodilation rather than by lowering cardiac output Thus , to the extent that normalization of resistance vessel structure is deemed a goal of antihypertensive treatment , the survey points towards the importance of considering not only the treatment effect on blood pressure , but also the haemodynamic effects within patients with essential hypertension