ORALS: Diabetes, Insulin, and the Heart
ALOOSTERONEAFFECTS LEFTVENTRICULAR STRUCTURE ANDFUNCTIONIN ESSENTIALHYPERTENSION. H.P. Schobel,K, Hilgera,C. Getzkeand R.E. Schmiader. Dept. of Medicine/ Nephrology,Unheraityof Germany. Erlengen-NUnberg, In experiments aldotierone has been found to increese collegen content in the myocardium. This potentially mighteffect
Isfi ventricular structuresnd functfonin vtvo.To snslyzethe in humens 2-D guided M-mode pathcgenetic roleofeldoaterone echocerdiography snd 24-hour ambulatory blood pressure montiortng (ASPM) were performed in 26 normotenaNe male whke healthywnlrcdaubjecla (sge: 26 * 3 YIS.) end 31 msle whfie palianta(age: 25 *3 yre.) with mild eaaentiel hypertension (WHO slage I or 11).In parallel 24-hour urinary sodium excretion, urinary eldoeterone and serum sldoelerone concentretton were measured at beaaline and atlar aalt loading with tablets to auppreaa sldoetarone. Serum and urfnaiy aidoatemne concentrations at baseline were not related to left ventrfcuiar structure or functton. Changes in urinary sodium excretion correlated nagativeiywith chenges in sidoalerone concentration (r = - 0.28; p < 0.05) for ail eubjects Lfrinsry sldoeterone concentration efter salt ioading decreased significantly in normotenaive (10.96 vs 7.44 pg I 24h; p -= 0.02), but not in hypertandvesubjects (9.34 w 10.51 pg /24h; n.s.). In contralto the findings at baaeline, urinary aidoalerone concentrstfon sfter saitioadingvae relaladto ieftventricular mass (r = 0.28; p < 0.05) and impaired midwall fretionai fiber shortening (r = - 0.33; p < 0.02), even after taking ASPM into account. Consistently, the lower the decresaa ofaerum aidosterone after salt ioading the greater was ieft ventricular maaa (r= 0.26; p < 0.05). The latter was significantonly for hypertensive subjects (r= 0.44; p < 0.02), independentlyof ABPM. Conciueively, we found that in hypertensive subiecla an
inadequate suppression of aldoeterone in responseto highorei salt intakeimpactsstructuraland funtionei left ventricular changesindependently ofambulatory bloodpressure.Thus,our resultssupportexparfmentai data,thataidoeterone sffecfe left ventricular structure andfunction inhumensasweli. Key Words:
aldoaterone, salt, left ventricular hypertrophy, essential hypertanaion.
EFFECTS OF ACUTE HYPERINSULINEMIA ON SYMPATHETIC RESPONSES TO MENTAL STRESS. ~ E Fossum, A Moan”, G Nordby”, IK Eids, and SE Kjeldsen”. Department of Internal Medicine, Lfllevaal Hospital, Oslo, Norway. It has been suggested that insulin resistance is related to increased sympathetic nervous system
(SNS) activity and conversely that hyperinsulinemia may activate the SNS. Therefore, we aimed at investigating the effect of acute hyperinsulinemia on SNS responsesto mental stress. Healthy 21-year old men (n=18) underwent 5 min of intense arithmetic mental stresstest (MST) prior to and at the end of 120 min of isoglycemic glucose clamping. BP, HR and catecholamines were measured 6 times from announcement to the end of MST. Insulin cone. was raised from 119+10 to 752&35 pmoi/L while glucose remained at it’s fasting level. While BP, HR and epinephrine (Epi) remained unchanged during clamp, Norepi increased from 1011*82 to 1178*104 pmol/L (P=.04).There were highly significant (pc.0001) increases in BP and HR in response to MST, however, no difference in response with and without insulin in max values and area under the curve. The Norepi responsesto MST-1 and MST-2 were almost identical (p=.7), and neither could we see any difference in Epi response (p=.3). Thus, in these experiments in healthy young men with rather bdsk responsesin BP, HR, Norepi and Epi to MST we cannot detect any evidence supporting that insulin acutely activates the SNS. Kay Worda:
insulin, mental
stress,
sympathetic.
AJH 1997;1O:28A
INADEQUATE SUPPRESSION OF ANGIOTENSiN II MOOIFIES LEFT VENTRICULAR STRUCTURE IN HUMANS. ~ K. Hilgera,A. Klingbeil,H.P. .%hobel, and R.E. Schmiedef. Oapt. of Medicine / Nephrology, Universityof Erlangen-Niinberg,Germany. In experiment angiotenainil (A H) haa growth stimulatingeffecte.To determinethe pathogeneticrole of angiofenein II inhumanswe performed2-D guidedM-mode echocardiogrephy and 24-hourambulatorybloodpraseurs monitoring (ABPM)in57 youngmale Caucasians(age: 25 * 3yTa.)withnormalor mildlyelevatedbloodpressure(WHO stageI andN).In parallel24-hoururinarysodiumexcretion, angiotensin II concentration (by radioimmunoaasay), plaamareninactivityand serumaldosteroneconcentration were meaeuredfirst on ad Iibitumealt intaka and second after high oral salt intake (aim: sodium excretion > 200 mmol I 24h). Confirmatoryto previouedata, body mase index(r ❑ 0,43; p < 0.001) and ABPM (systolic:r = 29, p < 0.05; diaatolic:r ❑ 0.25; p < 0.05) correlated with Iefl ventricularmaae in our studycohort.A II concentrationat baeelinewas not raiatedto Iefl ventricularstructure.The iowerthe physiologic decreaseof A II afler salt loadingthe greaterwas Iefl ventricularmass, even afler takingASPM into account(r = 0,45; p < 0.001). A II concentrationafler salt loading was related to Iefl ventricular mass independentlyof ABPM (r = 0.37; p < 0.01). Consistently, when the studycohortwas divided into tertilea (by A il concentration),Iefl ventricularmass differed significantly belwaentheupparandlcwertertile(273i 33 vs 224 i 34 g,
p < 0.001).
In conclusionwe found that inadequate suppressionof angiotensinII afler salt loadingis relatedto left ventricular structure independentlyof ambulatory blood pressure. Thus, angiotensin II exerts trophic effects on the myocardiumin humana. Key Words:
angiotensin H, left ventricular essential hypertension.
hypertrophy,
RSLAlTONSHIPOFGET4DS@ ETHNK2TY,ANDR3SKFACTORS TOIMPROVE.MENTINCORONARY~FfJNCITON AFTER INTRACORONARYINFUSION OF L-ARGININE. & Houehto~*, PA Kuhner, DS Strogatz, AA Carr*, Albany Medical College, Albany, NY. Endothelialdysfunctionof the coronaryartties maybe present in the absence of overt coronary artery disease, especially in relation to classical coronary risk factors. The purpose of our study was to investigate the relationship of gender, etfmicity, and established coronary risk fsctors to improvement in endotbelisl function after intracoronary L-arginine infusion in patients with chest pain. Endothelial function was tested in the usual manna utilizing intracoronary infusion of acetylcholine (10’8,10’, 10+ Molar) and quantitative coronary angiogmphy. L-ars (3200 mcmoles) was then infied over 5 to 10 minutes and the peak infusion of ACh repeated. Testingwas conductedin 28 women and 49 men (25 Atlican and 52 WhiteAmericans). Most patients(68’%)had angiographicaflynormal arteries. fn 26 subjects, cndotbelium dependent coronary reserve (EDCRF)increasedtlom 1.9~ 0.7to 2,6f0,9 (p=O.003)atler L-arg. fn 51 subjects EDCFRdid not incrcasc after L-arg (2.3 A 0.9 tn 2.2 t 0.S). Fsctnrspredictivcorsuggesdveofsigniticantacute improvement incndothelialfunctionafterL-argweremale gcndcr(p=O.14),baseline EDCFRS2.2:1 (P=O.09),and absenceof hypertension&O.04S). The combinationofmalc Senderand baseline EDCFRs 2.2:1 was highly predictive nf enhanced endotbelial function after L-erg &fJ.007). African American race and the classical risk factors tobacco use snd hyperlipidcmiadidnotindepcndcntfypredictimpmvcmsntailerL-arg. Conclusions: Acute improvement in coronsry endothclial function afcer intracoronary L-erg can be demonstrated in certain subjects undcrgningcardisccath because of chest pain. Though classical risk fectors did not independently predict such improvcmsnt, the combination ofmalc gender and depressed baseline EDCFRs 2.2:1 was highly predictive of enhanced endothelial function after Larg. This finding may suggest s therapeutic approsch in men with coronaryendotbelialdysfunction. Kay
words:
Endotbelium,vasodilatic.n,gender, L-arginine