Mechanism of lipid enhancement of alpha1-adrenoceptor pressor sensitivity in hypertension
| Autor: | Crystal A. Gadegbeku, M Zakarea Shrayyef, Brent M. Egan, Timothy P. Taylor |
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| Rok vydání: | 2006 |
| Předmět: |
Agonist
Male medicine.medical_specialty Physiology medicine.drug_class medicine.medical_treatment Blood Pressure Hyperlipidemias Baroreflex Fatty Acids Nonesterified chemistry.chemical_compound Phenylephrine Internal medicine Receptors Adrenergic alpha-1 Hyperlipidemia Internal Medicine medicine Humans Antihypotensive agent Triglycerides Triglyceride Mechanism (biology) business.industry Middle Aged medicine.disease Endocrinology Blood pressure chemistry Hypertension Female Vascular Resistance Cardiology and Cardiovascular Medicine business Adrenergic alpha-Agonists circulatory and respiratory physiology medicine.drug |
| Zdroj: | Journal of hypertension. 24(7) |
| ISSN: | 0263-6352 |
| Popis: | Plasma lipids enhance alpha1-adrenoceptor pressor sensitivity, impair baroreflex function, and correlate with increased blood pressure. This clinical study was designed to determine whether the enhanced alpha1-pressor sensitivity induced by acute hyperlipidemia is primarily mediated by increased vascular alpha1 responsiveness, reduced baroreflex sensitivity (BRS) or both.Regional alpha1-adrenoceptor vasoreactivity was measured using a graded brachial artery infusion of the alpha1 agonist, phenylephrine, in seven subjects with stage 1 hypertension. Forearm blood flow was estimated from venous occlusion plethysmography. The phenylephrine dose-forearm blood flow response curve was used to determine alpha1-vascular reactivity (slope of the dose-response curve) and sensitivity, EC50 (phenylephrine dose inducing 50% maximal response). BRS (ms/mmHg) was measured as the slope of the progressive rise in systolic blood pressure and the resultant lengthening in the subsequent R-R interval after systemic intravenous boluses of phenylephrine. Subsequently, plasma lipids were raised with a 1-h systemic co-infusion of intralipid and heparin, after which measurements of regional vasoreactivity and BRS were repeated.Mean arterial pressure was 109 +/- 4 versus 110 +/- 3 (P = NS), vasoreactivity was -0.71 +/- 0.10 versus -0.82 +/- 0.10 (P = NS) and log EC50 was 1.47 +/- 0.29 versus 1.52 +/- 0.34 nmol/l (P = NS) before and after raising non-esterified fatty acids, respectively. In contrast, mean BRS was acutely reduced from 8.2 +/- 2.1 to 6.2 +/- 1.8 ms/mmHg (P = 0.02) after the lipid infusion.These findings suggest that in hypertensive patients, the primary mechanism for short-term alpha1-pressor hypersensitivity in response to hyperlipidemia is via the acute impairment of BRS. |
| Databáze: | OpenAIRE |
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