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1.
Clin Pharmacol Ther ; 83(1): 122-9, 2008 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-17522594

RESUMO

We examined the effect of -58 C/T and BE1 +9/-9 polymorphisms in the bradykinin B2 receptor gene on forearm vascular resistance (FVR) before and during intrabrachial artery infusion of the B2 receptor-, endothelium-dependent agonist bradykinin and the endothelium-independent agonist sodium nitroprusside in 228 normotensive subjects. In 166 white Americans, systolic blood pressure (SBP) and pulse pressure were highest in the BE1 +9/+9 group (118+/-2 and 51+/-2 mm Hg, respectively; P<0.05 versus -9/-9 for either), intermediate in the +9/-9 group (114+/-1 and 49+/-1 mm Hg, P<0.05 versus -9/-9 for pulse pressure), and lowest in the -9/-9 group (110+/-2 and 44+/-2 mm Hg). In 62 black Americans, FVR was 25% higher in the BE1 +9/+9 group compared with the BE1 +9/-9 and -9/-9 groups at baseline (P=0.038) or during bradykinin (P=0.03). Increased SBP or vascular resistance may contribute to increased left ventricular mass reported previously in individuals with the BE1+9/+9 genotype.


Assuntos
Negro ou Afro-Americano/genética , Pressão Sanguínea/genética , Antebraço/irrigação sanguínea , Polimorfismo Genético , Receptor B2 da Bradicinina/genética , Resistência Vascular/genética , População Branca/genética , Adulto , Velocidade do Fluxo Sanguíneo/efeitos dos fármacos , Pressão Sanguínea/efeitos dos fármacos , Bradicinina/administração & dosagem , Relação Dose-Resposta a Droga , Feminino , Frequência do Gene , Genótipo , Humanos , Infusões Intra-Arteriais , Masculino , Nitroprussiato/administração & dosagem , Fenótipo , Receptor B2 da Bradicinina/agonistas , Fluxo Sanguíneo Regional/genética , Resistência Vascular/efeitos dos fármacos , Vasodilatadores/administração & dosagem
2.
Cardiovasc J S Afr ; 11(3): 138-143, 2000 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-11447475

RESUMO

BACKGROUND: Valvular heart disease is the most important cardiac manifestation of systemic lupus erythematosus (SLE). We performed a study to determine the presence of valvular heart disease in our patients with SLE. METHODS: We performed clinical, electrocardiographic, transthoracic echocardiographic and laboratory evaluations in 24 patients with SLE. The echocardiographic findings were compared with those of 10 age- and sex-matched volunteers. RESULTS: None of the 24 patients had obvious symptoms of cardiac origin. Valvular abnormalities were common. Valvular thickening was the most predominant finding (more than 50%), followed by mitral valvular regurgitation (12.5%) and pericardial effusions (12.5%). Valvular abnormalities were uncommon in the control group. CONCLUSION: Valvular heart disease is common in our patient population with SLE, although haemodynamically significant valvular dysfunction is rare.

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