- Email: [email protected]
G4 A new marker of hypertensive target organ damages: Serum level of hepatocyte growth factor (HGF)
POSTERS: Other Vasoactive Systems— Endothelin, No-Vasopressin, Etc
G1
AJH 1997;1O:178A-182A
G2
INS ULINEMIA.
INSULIN
SENSITIVITY.
JNTRAERYTROCl+E SODIUM (N&) INOBESE(Obj ANDNON OBESE (nOb) HYPERTENSIVE. Sanjdiarri AF, FagundesVGA*, Maweriello ER*, Torres MLG, SpiftefiLP, Moukr MRSG, Dua2tcAVB, -S CM Barrow SG, Franc” tecbettiEA*. HypertensionClinic, CLINEX,Riode JaneiroSteteUnivcraity,RJ, Brazil. Increasein NaiC,due to diminutionof Na-RATPaseand increaseinNa+-H+exchenge, haabeenimplicatedse possible mechanismof hypertensionin insulinresistantpatients. To test this hypothesis we studied 49 hypertensives, age 54.5~2.9y(nOb) and 50.3f2.ly (Ob), atler 2 weeks washout period. Naicwasdeterminedby Chenmethodandinsulin (Ins) by RIA. The BMI was 32t.9 for Ob (n=29) and 24f.3kg/nf for nOb (n=20),p<.001. SBP,DBP and MBP for Ob were 159~2.9, 102fl.4 and 121~1 .6mmHg respectivelyand 154*2.2, 96~1.5 and 116~1.5mmHgfor nOb, respectively. DBP and MBP were higherin Ob than nOb,p<.05. Fastingirrsulinernie errdtheinaulidglicoseratio was 11.4fl.3mU/rnl end .12f.01 for Ob and 7.8f.9rnU/nrJ and .08t.01 for nOb, p<.01, respectively. A positive correlationwaaobservedbetweentheseparemeterssndBM3 (r=.5, p<.001) No significantcorrelationsofcsaualblood pressoreand fastingIns and Ina/Glicratio were noted. NaiC was 8.7f.3 end 7.9f.2rnEq/cel/lfbrObsnd nOb,respectively, p<.05. However,no correlationwas obsmvedbetweenNaiC andtkadngImsemdIns/GlicretioinObandnObhypertensives. The natriuresisin both groups, with comparablecreatinine clearance,was similar. Weconcludethat the increaseinNaiC mayplayapatbogeneticrole inthe hypertensionof studied patientsalthoughnot relatedto fa.%inginaulinerniaorinsulin sensitivity. insul@ insulinsensitivity,hypertension,obesity, intraerytrocytesodium.
Key Words:
RMA4TIONSHIP BETWSEN 3fVPERSNSULINEMfA AND AMBULATORY BLOOD PRESSURS MONITORING (ASPM) IN LSAN AND OVERWEIGHT MALE HYPERTENSIVXX. CA SWdddrI*, A Benmdd, M Akopkn, AO ~ri, S Cauteruc@ HM Chrnin, D Carrtdo. Hypertendon Program, Buenos Alrss Untversttyechodof Medldne San Marttn Hospltrdand Health Sdence Institute, Buenos. Atres, ArgenSna. To ektdak the role of hypertension as part of a date oflrmrSn resbtance, the rekltonddps of hyprtenston and overwdght wftb hyperbmdlmeudn, glucose tolerance and 24b ABPM were exmnlned tn lean and obese male hypertenslvea. We studbxf 31 hypsrtendve males (syslmSc/dtmtok >140/90 mm Hg)wlthout hypertendve treatment or afkr a &week washout period. To test whether the overrvdghtdegree affeckd the lrIwlb-BP rdattonddp, the poputatronwas dlvtded Into term” of body mass index (BMS)ln MS OI-10), >6 to <28 (n-9), and s26 (n-lZ). HSpand walstdrcumferences were measured and wabuhlpo ratbmwere mkutakd. Casual blood pressure In sltllng podtton was measured In trtpScate; pdtents were Urenmdgned t02&h ABPM. Plasma glucose andlnmMn tsvek were measured dudngan 2.h oral glucose (7ss) tokrance tesL The logadthms of the fa.+tq lmuUrrkvdand tnsusn area were used IrJthe analyses. In the poputatlonas a whoklnctdence of dlpper~ and rion-dtppers was deternrtned. Sttaod@UIXMSkVd S at rjo mtnutes were different (192.S *64.74 mgldLverms 13S* 32.S9 mgld~ P
Kev Words:
bype~smemk,
ambulatoryblood pressure
monitoring, obesity
G3
G4
ARTERIAL PRESSURE DEPENDENCY OF TISSUE NITRIC OXIDE (NO) ACTIVITY WITHIN AUTOREGULATORY RANGE IN CANINE KIDNEY. D .S.A. Maiid, S.A. Omoro, and M. Godfrey. Tulane University School of Medicine, New Orleans, LA. It has baan suggeated that an alteration in NO production rata may play a role in aodium excration (U..V) responses to acuta changea in ranal arterial preaaure (RAP). However, previous attempts to meaaure intrarenal NO activity have remained mostly indirect. Wa have measured the renal tiasue NO activity directly uaing a NO-aelective microelectrode (200 #m in diameter, Intar Medical Co. Ltd., Nagoya, Japan) insartad in the renal cortex of anesthetized dogs. The NO-electroda waa responsive to intrarenal bolus injections of NO agonists acetylcholine, bradykinin, ATP and to NO donor, S-nitroso-n-acaty lpanicillamine (SNAP). Intra-arterial administration of the NO synthasa inhibitor, nitro-L-arginine (NLA; 50 pg/kg/min) decreased renal tiasue NO concentration by 422+91 nM (P< .05; n = 6). Infusions of SNAP (1 ,2, and 3 pg/kg/min for 25 rein) in NLA treated doga (n= 4) reaultad in dose-dependent changea in renal tissue NO activity which showed positive correlation with changes in urinary excretion rate of NO metabolizes, nitratelnitrite (U NOi/N02 “V., r= .62, .1 >P> .05) and U.,V .78, P< .01). Stepwise reductions in RAP (144+3 to k= 73* 2 mmHg; n= 10) within autoregulatory range elicited decreasas in NO concentration in renal tissue (slope, 1 1.8* 1.7 nM.mmHg”’) which were positively correlated with changes in RAP (r= .45; P< .05), U~03,~o;V (r= .64, P< .005) and U..V (r= .46; P< .05). These results indicate the applicability of the NO-electroda for in-vivo assessment of intrarenal NO activity. These data are consistent with the hypothesis that acute changas in RAP elicit parallel changes in intrarenal NO activity which may directly alter tubular sodium reabsorption rate to manifest the phenomenon of presaura natriuresis.
A NEW MARKEROF HYPERTENSNETARG~ ORGAN DAMAGES:SERUMLEVELOF HEPATOCYTE GROWTHFAfXOR(HGF). S. Nakarmsrs, A. Moriguchi, R. Morishits,J. Higaki, and T. Ogihsra. Departmentof Genatrk Medicine,OsakaUniversityMedical School, Suita, JapaN. Errdothali#dyafiiction of hypertensivepatientsis weftknown. HGF has beenpreviouslyreportedas a novel rnemlxxofendo2be bum.specificgrowthfactorswhose ” -nic aetivityiatbemost potentemongbFGF, VlX3Fimd variouscytokines Recentfindingsshow thatHGF Cotrtributeto proteck or repairingof vascularerrdothelird cetis. If so, aerrrmELGFlevelmightbe elevatedin response tmmdcdhelislceErdardamageinducedby hypaxnsion. To teatthis hypothesk, we measuredserumlevelof HGF in hypertensivepatien& Fitly sevennorrnotensives(31 mrdes arrd26females, 5%2 y.o.), mrtreated69hypertensive pedentsgroup(37 malesand 32 females,62fiy.o.), and agematehed 102hypertensivepatientswith aedbyptensive tteatment(54 matesand 48 fernales,60*1 y.o.) were studied. SerumHGF soncentmtimrin hypertensivepatientswith cmnpticetion(0.91&k13 nghnl)was significantlyhigher tha2s2batinpstisrMwithoutcomplication(0.49*0.03 rig/ml, p@lOl). However, semm HGF levelin treated hypectenaivepadents(0.31*0.03nghnl) was decreasedto the sameexterttsearxsmol group (0.32+0.02ng/ml). These resultssrsggeaLtbataerumconcenfmxion of HGF, a novel endothelialspmKc growthfactor, is significantlyelevated withpmgre@mtofhypertmssion. We concludethat meaaummentofaeruns HGF concentrationis clinicallyuseful for as amarkerof hypertensivetargetorgan damages.
Key Worda:
pressure natriurasis, nitric oxide electrode, renal tissue nitric oxide, sodium axcration
Key words:
HGF, Ersdotheliaicell, Hypertension,Organdamage
G1
AJH 1997;1O:178A-182A
G2
INS ULINEMIA.
INSULIN
SENSITIVITY.
JNTRAERYTROCl+E SODIUM (N&) INOBESE(Obj ANDNON OBESE (nOb) HYPERTENSIVE. Sanjdiarri AF, FagundesVGA*, Maweriello ER*, Torres MLG, SpiftefiLP, Moukr MRSG, Dua2tcAVB, -S CM Barrow SG, Franc” tecbettiEA*. HypertensionClinic, CLINEX,Riode JaneiroSteteUnivcraity,RJ, Brazil. Increasein NaiC,due to diminutionof Na-RATPaseand increaseinNa+-H+exchenge, haabeenimplicatedse possible mechanismof hypertensionin insulinresistantpatients. To test this hypothesis we studied 49 hypertensives, age 54.5~2.9y(nOb) and 50.3f2.ly (Ob), atler 2 weeks washout period. Naicwasdeterminedby Chenmethodandinsulin (Ins) by RIA. The BMI was 32t.9 for Ob (n=29) and 24f.3kg/nf for nOb (n=20),p<.001. SBP,DBP and MBP for Ob were 159~2.9, 102fl.4 and 121~1 .6mmHg respectivelyand 154*2.2, 96~1.5 and 116~1.5mmHgfor nOb, respectively. DBP and MBP were higherin Ob than nOb,p<.05. Fastingirrsulinernie errdtheinaulidglicoseratio was 11.4fl.3mU/rnl end .12f.01 for Ob and 7.8f.9rnU/nrJ and .08t.01 for nOb, p<.01, respectively. A positive correlationwaaobservedbetweentheseparemeterssndBM3 (r=.5, p<.001) No significantcorrelationsofcsaualblood pressoreand fastingIns and Ina/Glicratio were noted. NaiC was 8.7f.3 end 7.9f.2rnEq/cel/lfbrObsnd nOb,respectively, p<.05. However,no correlationwas obsmvedbetweenNaiC andtkadngImsemdIns/GlicretioinObandnObhypertensives. The natriuresisin both groups, with comparablecreatinine clearance,was similar. Weconcludethat the increaseinNaiC mayplayapatbogeneticrole inthe hypertensionof studied patientsalthoughnot relatedto fa.%inginaulinerniaorinsulin sensitivity. insul@ insulinsensitivity,hypertension,obesity, intraerytrocytesodium.
Key Words:
RMA4TIONSHIP BETWSEN 3fVPERSNSULINEMfA AND AMBULATORY BLOOD PRESSURS MONITORING (ASPM) IN LSAN AND OVERWEIGHT MALE HYPERTENSIVXX. CA SWdddrI*, A Benmdd, M Akopkn, AO ~ri, S Cauteruc@ HM Chrnin, D Carrtdo. Hypertendon Program, Buenos Alrss Untversttyechodof Medldne San Marttn Hospltrdand Health Sdence Institute, Buenos. Atres, ArgenSna. To ektdak the role of hypertension as part of a date oflrmrSn resbtance, the rekltonddps of hyprtenston and overwdght wftb hyperbmdlmeudn, glucose tolerance and 24b ABPM were exmnlned tn lean and obese male hypertenslvea. We studbxf 31 hypsrtendve males (syslmSc/dtmtok >140/90 mm Hg)wlthout hypertendve treatment or afkr a &week washout period. To test whether the overrvdghtdegree affeckd the lrIwlb-BP rdattonddp, the poputatronwas dlvtded Into term” of body mass index (BMS)ln MS OI-10), >6 to <28 (n-9), and s26 (n-lZ). HSpand walstdrcumferences were measured and wabuhlpo ratbmwere mkutakd. Casual blood pressure In sltllng podtton was measured In trtpScate; pdtents were Urenmdgned t02&h ABPM. Plasma glucose andlnmMn tsvek were measured dudngan 2.h oral glucose (7ss) tokrance tesL The logadthms of the fa.+tq lmuUrrkvdand tnsusn area were used IrJthe analyses. In the poputatlonas a whoklnctdence of dlpper~ and rion-dtppers was deternrtned. Sttaod@UIXMSkVd S at rjo mtnutes were different (192.S *64.74 mgldLverms 13S* 32.S9 mgld~ P
Kev Words:
bype~smemk,
ambulatoryblood pressure
monitoring, obesity
G3
G4
ARTERIAL PRESSURE DEPENDENCY OF TISSUE NITRIC OXIDE (NO) ACTIVITY WITHIN AUTOREGULATORY RANGE IN CANINE KIDNEY. D .S.A. Maiid, S.A. Omoro, and M. Godfrey. Tulane University School of Medicine, New Orleans, LA. It has baan suggeated that an alteration in NO production rata may play a role in aodium excration (U..V) responses to acuta changea in ranal arterial preaaure (RAP). However, previous attempts to meaaure intrarenal NO activity have remained mostly indirect. Wa have measured the renal tiasue NO activity directly uaing a NO-aelective microelectrode (200 #m in diameter, Intar Medical Co. Ltd., Nagoya, Japan) insartad in the renal cortex of anesthetized dogs. The NO-electroda waa responsive to intrarenal bolus injections of NO agonists acetylcholine, bradykinin, ATP and to NO donor, S-nitroso-n-acaty lpanicillamine (SNAP). Intra-arterial administration of the NO synthasa inhibitor, nitro-L-arginine (NLA; 50 pg/kg/min) decreased renal tiasue NO concentration by 422+91 nM (P< .05; n = 6). Infusions of SNAP (1 ,2, and 3 pg/kg/min for 25 rein) in NLA treated doga (n= 4) reaultad in dose-dependent changea in renal tissue NO activity which showed positive correlation with changes in urinary excretion rate of NO metabolizes, nitratelnitrite (U NOi/N02 “V., r= .62, .1 >P> .05) and U.,V .78, P< .01). Stepwise reductions in RAP (144+3 to k= 73* 2 mmHg; n= 10) within autoregulatory range elicited decreasas in NO concentration in renal tissue (slope, 1 1.8* 1.7 nM.mmHg”’) which were positively correlated with changes in RAP (r= .45; P< .05), U~03,~o;V (r= .64, P< .005) and U..V (r= .46; P< .05). These results indicate the applicability of the NO-electroda for in-vivo assessment of intrarenal NO activity. These data are consistent with the hypothesis that acute changas in RAP elicit parallel changes in intrarenal NO activity which may directly alter tubular sodium reabsorption rate to manifest the phenomenon of presaura natriuresis.
A NEW MARKEROF HYPERTENSNETARG~ ORGAN DAMAGES:SERUMLEVELOF HEPATOCYTE GROWTHFAfXOR(HGF). S. Nakarmsrs, A. Moriguchi, R. Morishits,J. Higaki, and T. Ogihsra. Departmentof Genatrk Medicine,OsakaUniversityMedical School, Suita, JapaN. Errdothali#dyafiiction of hypertensivepatientsis weftknown. HGF has beenpreviouslyreportedas a novel rnemlxxofendo2be bum.specificgrowthfactorswhose ” -nic aetivityiatbemost potentemongbFGF, VlX3Fimd variouscytokines Recentfindingsshow thatHGF Cotrtributeto proteck or repairingof vascularerrdothelird cetis. If so, aerrrmELGFlevelmightbe elevatedin response tmmdcdhelislceErdardamageinducedby hypaxnsion. To teatthis hypothesk, we measuredserumlevelof HGF in hypertensivepatien& Fitly sevennorrnotensives(31 mrdes arrd26females, 5%2 y.o.), mrtreated69hypertensive pedentsgroup(37 malesand 32 females,62fiy.o.), and agematehed 102hypertensivepatientswith aedbyptensive tteatment(54 matesand 48 fernales,60*1 y.o.) were studied. SerumHGF soncentmtimrin hypertensivepatientswith cmnpticetion(0.91&k13 nghnl)was significantlyhigher tha2s2batinpstisrMwithoutcomplication(0.49*0.03 rig/ml, p@lOl). However, semm HGF levelin treated hypectenaivepadents(0.31*0.03nghnl) was decreasedto the sameexterttsearxsmol group (0.32+0.02ng/ml). These resultssrsggeaLtbataerumconcenfmxion of HGF, a novel endothelialspmKc growthfactor, is significantlyelevated withpmgre@mtofhypertmssion. We concludethat meaaummentofaeruns HGF concentrationis clinicallyuseful for as amarkerof hypertensivetargetorgan damages.
Key Worda:
pressure natriurasis, nitric oxide electrode, renal tissue nitric oxide, sodium axcration
Key words:
HGF, Ersdotheliaicell, Hypertension,Organdamage