- Email: [email protected]
Different vascular response patterns to cold pressor test in two newly defined subtypes of human hypertension
130A
POSTERS: Arterial Structure and Compliance
P-303 IN VIVO INHIBITION OF ERK1/2-DEPENDENT SIGNALING PATHWAYS IMPROVES VASCULAR FUNCTION IN SHR R. M. Touyz, C. Deschepper, Q. N. Diep, J. B. Park, G. He, E. L. Schiffrin. 1Clinical Research Institute of Montreal, Univ of Montreal, QC, Canada Extracellular signal-regulated kinases (ERK1/2) influence vascular smooth muscle cell growth and contractility, important factors in blood pressure regulation. This study was designed to investigate whether short-term in vivo inhibition of the ERK1/2 pathway influences vascular function and blood pressure in SHR. SHR (6/group) and WKY (5/group) were injected subcutaneously with either PD98059, selective MEK1/2 inhibitor (20g/g body weight), or vehicle. Blood pressure was measured by tellemetry for 24 hours after injection. Rats were then killed and small mesenteric arteries mounted as pressurized systems for morphometric analysis and assessment of endothelial function and Ang II-induced contractility. ERK1/2 phosphorylation was measured by Western blot assays using protein extracts from small mesenteric arteries. In vivo MEK1/2 inhibition significantly decreased (p⬍0.01) ERK1/2 phosphorylation in both groups, with greater effects in SHR than WKY. In SHR, PD98059 improved Ach-induced relaxation (98% vs 62%, PD98059 vs vehicle) and decreased Ang II-induced contraction by 35%. In PD98059treated WKY, Ang II-stimulated contraction was only slightly reduced (15%). Vascular structure and blood pressure were not significantly altered by PD98059 in either group. In conclusion short-term in vivo inhibition of MEK1/2 improves endothelial function and vascular contractility in resistance arteries of SHR, suggesting a role for ERK1/2dependent signaling pathways in altered vascular function in genetically hypertensive rats.
AJH–April 2001–VOL. 14, NO. 4, PART 2
P-305 VASCULAR AND BLOOD PRESSURE MODIFICATIONS IN TURNER’S SYNDROME J. P. Baguet, S. Douchin, J. P. Siche´, A. M. Rossignol, F. Tremel, J. M. Mallion. 1Dept. of Cardiology and Internal Medicine, Grenoble University Hospital, France We studied blood pressure (BP) and carotid structural parameters in patients with Turner’s syndrome as they often have important risk of aortic complications. Twenty four patients with Turner’s syndrome (mean age 17⫾7years) and 25 healthy women as controls (mean age 19⫾4years) had clinic and ambulatory 24-hour BP measurements and vascular assessment with ultrasound to assess carotid walls and measurement of carotid-femoral pulse wave velocity (PWV). The Turner patients were smaller than the controls (141⫾15 cm vs 163⫾8 cm, p⬍0.001). Lipid profiles were similar. Systolic BP (SBP) was identical in both groups, but diastolic BP (DBP) was more elevated in the Turner patients. Thus, clinical (39⫾8 vs 47⫾11 mmHg, p⬍0.01) and ambulatory pulse pressure (PP) were lower in the Turner group. Arterial stiffness tended to be lower in the Turner group (PWV ⫽ 6.5⫾1.3 m/s vs 7.1⫾1.1 m/s, NS). Likewise, common carotid cross-sectional area (CSA) tended to be greater in Turner’s (9.4⫾1.5 vs 9.0⫾1.2, NS). When corrected for height or body surface area the carotid parameters, intimamedia thickness (IMT), luminal diameter and CSA, were higher in Turner’s (p⬍0.001). IMT and CSA related to body surface area were negatively and independently related to SBP and DBP (p⬍0.01). Turner’s syndrome is associated with an elevation in DBP with reduction of the PP. Aortic stiffness tends to be less in this population, probably related to tissue dysplasia. Unless indexed to height or body surface area, there is no significant remodelling of the carotid artery in Turner’s.
Key Words: ERK, Resistance arteries, SHR Key Words: Turner’s Syndrome, Hypertension, Carotid Remodeling
P-304 DIFFERENT VASCULAR RESPONSE PATTERNS TO COLD PRESSOR TEST IN TWO NEWLY DEFINED SUBTYPES OF HUMAN HYPERTENSION R. P. Bochmann, A. Vogelgesang, U. Reuter, C. Planitz. 1Dept. of Physiol., Techn. Univ. Dresden, Dresden, Germany In a previous study we have shown that in mild hypertension the peripheral pulse pressure augmentation from brachial to digital artery is either increased (H-20) or diminished (H-0) as compared to control. The aim of this study was to test the hypothesis that the vessel wall properties of the digital artery are essential different in these two subgroups of hypertension. We tested the hypothesis by measuring the local hemodynamic response to the cold pressor test (cpt; immersing the contralateral hand 1 min in ice water). The local pressure response (P) was measured with the FINAPRES device and the compliance of the digital artery was determined from simultaneously measured pressure (⌬P) and volume changes (⌬V) (impedance plethysmography) from neighbouring fingers as C⫽ ⌬V/⌬P. We studied 46 never treated hypertensive patients, 26 H-20 and 18 H-0, (mean age 33 ⫾ 6 years) and 58 age matched healthy subjects. In H-20: during cpt systolic pressure increases from 141⫾18 to 155⫾21 mm Hg, diastolic pressure from 79⫾12 to 89⫾14 mm Hg and digital arterial compliance decreases from 1.9⫾1.0 to 1.3⫾0.7 l/mm Hg per 100 ml tissue (all, p⬍0.01). In H-0: during cpt there is no reaction of local pressure and of local arterial compliance. We conclude, that H-20 is characterised by a decreased local arterial compliance at baseline and a normal vascular response of the digital artery under cpt as compared to control and, in contrast, H-0 shows a nearly normal local arterial compliance at baseline but there is no local vascular response under cpt. Key Words: Vessel wall properties, Cold pressor test, Human hypertension
P-306 ARTERIAL STIFFNESS AS A MARKER OF INTIMA MEDIA TICKENING IN HYPERTENSION Ricardo Armentano, Sebastia´n Graf, Lucas Gamero, Franco Pessana, Laura Brandani, Hugo Baglivo, Ramiro Sa´nchez. 1Favaloro Foundation, Buenos Aries, Argentina, 2Favaloro University, Buenos Aries, Argentina Wall viscosity and inertia showed a high relation with the intima media thickening (IMT) induced by hypertension. We studied 11 normotensive (NT, 49 ⫾ 14y), 11 mild to moderate hypertensive patients (HT, 51 ⫾ 10y) and 8 hypertensive patients after 3 months of effective treatment (TR, 58 ⫾ 18y) with ramipril (5-10 mg/day) to assess if IMT is related to the major mechanical parameters (elasticity, E 10-4 mmHg/mm; viscosity, n 10-4 mmHg s/mm and inertia, M 103 mmHg s2/mm) in a multiple regression analysis (MRA). In the common carotid artery we measured IMT and diameter (automatic B mode images analysis) and pressure (Tonometry). E., n and M were estimated by using a 3 order system modeling identification approach. MRA on the overall population of data (TR⫹NT⫹HT), holding mean pressure constant showed that IMT⫽5.7 E⫹3.0 n ⫹ 8.5 M ⫹ 0.62 (r⫽0.6, p⬍0.05), however a stepwise analysis determine that E is the only significant factor in the IMT (IMT ⫽ 6.4 E ⫹ 0.62, r⫽ 0.6, p⬍0.05). In the simultaneous assessment of mechanical properties, E appears as the only mechanical marker of an IMT process and its treatment by an ACEI inhibitor. Key Words: Arterial wall stiffness, Intima media thickness, wall viscosity
POSTERS: Arterial Structure and Compliance
P-303 IN VIVO INHIBITION OF ERK1/2-DEPENDENT SIGNALING PATHWAYS IMPROVES VASCULAR FUNCTION IN SHR R. M. Touyz, C. Deschepper, Q. N. Diep, J. B. Park, G. He, E. L. Schiffrin. 1Clinical Research Institute of Montreal, Univ of Montreal, QC, Canada Extracellular signal-regulated kinases (ERK1/2) influence vascular smooth muscle cell growth and contractility, important factors in blood pressure regulation. This study was designed to investigate whether short-term in vivo inhibition of the ERK1/2 pathway influences vascular function and blood pressure in SHR. SHR (6/group) and WKY (5/group) were injected subcutaneously with either PD98059, selective MEK1/2 inhibitor (20g/g body weight), or vehicle. Blood pressure was measured by tellemetry for 24 hours after injection. Rats were then killed and small mesenteric arteries mounted as pressurized systems for morphometric analysis and assessment of endothelial function and Ang II-induced contractility. ERK1/2 phosphorylation was measured by Western blot assays using protein extracts from small mesenteric arteries. In vivo MEK1/2 inhibition significantly decreased (p⬍0.01) ERK1/2 phosphorylation in both groups, with greater effects in SHR than WKY. In SHR, PD98059 improved Ach-induced relaxation (98% vs 62%, PD98059 vs vehicle) and decreased Ang II-induced contraction by 35%. In PD98059treated WKY, Ang II-stimulated contraction was only slightly reduced (15%). Vascular structure and blood pressure were not significantly altered by PD98059 in either group. In conclusion short-term in vivo inhibition of MEK1/2 improves endothelial function and vascular contractility in resistance arteries of SHR, suggesting a role for ERK1/2dependent signaling pathways in altered vascular function in genetically hypertensive rats.
AJH–April 2001–VOL. 14, NO. 4, PART 2
P-305 VASCULAR AND BLOOD PRESSURE MODIFICATIONS IN TURNER’S SYNDROME J. P. Baguet, S. Douchin, J. P. Siche´, A. M. Rossignol, F. Tremel, J. M. Mallion. 1Dept. of Cardiology and Internal Medicine, Grenoble University Hospital, France We studied blood pressure (BP) and carotid structural parameters in patients with Turner’s syndrome as they often have important risk of aortic complications. Twenty four patients with Turner’s syndrome (mean age 17⫾7years) and 25 healthy women as controls (mean age 19⫾4years) had clinic and ambulatory 24-hour BP measurements and vascular assessment with ultrasound to assess carotid walls and measurement of carotid-femoral pulse wave velocity (PWV). The Turner patients were smaller than the controls (141⫾15 cm vs 163⫾8 cm, p⬍0.001). Lipid profiles were similar. Systolic BP (SBP) was identical in both groups, but diastolic BP (DBP) was more elevated in the Turner patients. Thus, clinical (39⫾8 vs 47⫾11 mmHg, p⬍0.01) and ambulatory pulse pressure (PP) were lower in the Turner group. Arterial stiffness tended to be lower in the Turner group (PWV ⫽ 6.5⫾1.3 m/s vs 7.1⫾1.1 m/s, NS). Likewise, common carotid cross-sectional area (CSA) tended to be greater in Turner’s (9.4⫾1.5 vs 9.0⫾1.2, NS). When corrected for height or body surface area the carotid parameters, intimamedia thickness (IMT), luminal diameter and CSA, were higher in Turner’s (p⬍0.001). IMT and CSA related to body surface area were negatively and independently related to SBP and DBP (p⬍0.01). Turner’s syndrome is associated with an elevation in DBP with reduction of the PP. Aortic stiffness tends to be less in this population, probably related to tissue dysplasia. Unless indexed to height or body surface area, there is no significant remodelling of the carotid artery in Turner’s.
Key Words: ERK, Resistance arteries, SHR Key Words: Turner’s Syndrome, Hypertension, Carotid Remodeling
P-304 DIFFERENT VASCULAR RESPONSE PATTERNS TO COLD PRESSOR TEST IN TWO NEWLY DEFINED SUBTYPES OF HUMAN HYPERTENSION R. P. Bochmann, A. Vogelgesang, U. Reuter, C. Planitz. 1Dept. of Physiol., Techn. Univ. Dresden, Dresden, Germany In a previous study we have shown that in mild hypertension the peripheral pulse pressure augmentation from brachial to digital artery is either increased (H-20) or diminished (H-0) as compared to control. The aim of this study was to test the hypothesis that the vessel wall properties of the digital artery are essential different in these two subgroups of hypertension. We tested the hypothesis by measuring the local hemodynamic response to the cold pressor test (cpt; immersing the contralateral hand 1 min in ice water). The local pressure response (P) was measured with the FINAPRES device and the compliance of the digital artery was determined from simultaneously measured pressure (⌬P) and volume changes (⌬V) (impedance plethysmography) from neighbouring fingers as C⫽ ⌬V/⌬P. We studied 46 never treated hypertensive patients, 26 H-20 and 18 H-0, (mean age 33 ⫾ 6 years) and 58 age matched healthy subjects. In H-20: during cpt systolic pressure increases from 141⫾18 to 155⫾21 mm Hg, diastolic pressure from 79⫾12 to 89⫾14 mm Hg and digital arterial compliance decreases from 1.9⫾1.0 to 1.3⫾0.7 l/mm Hg per 100 ml tissue (all, p⬍0.01). In H-0: during cpt there is no reaction of local pressure and of local arterial compliance. We conclude, that H-20 is characterised by a decreased local arterial compliance at baseline and a normal vascular response of the digital artery under cpt as compared to control and, in contrast, H-0 shows a nearly normal local arterial compliance at baseline but there is no local vascular response under cpt. Key Words: Vessel wall properties, Cold pressor test, Human hypertension
P-306 ARTERIAL STIFFNESS AS A MARKER OF INTIMA MEDIA TICKENING IN HYPERTENSION Ricardo Armentano, Sebastia´n Graf, Lucas Gamero, Franco Pessana, Laura Brandani, Hugo Baglivo, Ramiro Sa´nchez. 1Favaloro Foundation, Buenos Aries, Argentina, 2Favaloro University, Buenos Aries, Argentina Wall viscosity and inertia showed a high relation with the intima media thickening (IMT) induced by hypertension. We studied 11 normotensive (NT, 49 ⫾ 14y), 11 mild to moderate hypertensive patients (HT, 51 ⫾ 10y) and 8 hypertensive patients after 3 months of effective treatment (TR, 58 ⫾ 18y) with ramipril (5-10 mg/day) to assess if IMT is related to the major mechanical parameters (elasticity, E 10-4 mmHg/mm; viscosity, n 10-4 mmHg s/mm and inertia, M 103 mmHg s2/mm) in a multiple regression analysis (MRA). In the common carotid artery we measured IMT and diameter (automatic B mode images analysis) and pressure (Tonometry). E., n and M were estimated by using a 3 order system modeling identification approach. MRA on the overall population of data (TR⫹NT⫹HT), holding mean pressure constant showed that IMT⫽5.7 E⫹3.0 n ⫹ 8.5 M ⫹ 0.62 (r⫽0.6, p⬍0.05), however a stepwise analysis determine that E is the only significant factor in the IMT (IMT ⫽ 6.4 E ⫹ 0.62, r⫽ 0.6, p⬍0.05). In the simultaneous assessment of mechanical properties, E appears as the only mechanical marker of an IMT process and its treatment by an ACEI inhibitor. Key Words: Arterial wall stiffness, Intima media thickness, wall viscosity