Hemorheological and cardiovascular responses to beta-endorphin and naloxone in healthy subjects and in patients with essential hypertension
| Autor: | R. Buoninconti, Roberto Torella, G Verrazzo, A. Tirelli, Dario Giugliano, Ludovico Coppola, Domenico Cozzolino, Riccardo Giunta |
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| Přispěvatelé: | Coppola, L, Cozzolino, Domenico, Giugliano, Dario, Verrazzo, G, Tirelli, Armando, Giunta, Riccardo, Buoninconti, R, Torella, R. |
| Rok vydání: | 1994 |
| Předmět: |
Adult
Male medicine.medical_specialty Platelet Aggregation Endocrinology Diabetes and Metabolism Clinical Biochemistry Blood viscosity Blood Pressure Hematocrit Essential hypertension Cardiovascular System Biochemistry Endocrinology Waist–hip ratio Bolus (medicine) Heart Rate Internal medicine Heart rate medicine Humans medicine.diagnostic_test Naloxone business.industry beta-Endorphin Biochemistry (medical) Fibrinogen Middle Aged Blood Viscosity medicine.disease Adenosine Diphosphate Blood pressure Opioid Hypertension Female Rheology business medicine.drug |
| Zdroj: | The Journal of Clinical Endocrinology & Metabolism. 79:826-830 |
| ISSN: | 1945-7197 0021-972X |
| DOI: | 10.1210/jcem.79.3.8077368 |
| Popis: | The purpose of the present study was to determine if opioid agonism (beta-endorphin) and antagonism (Naloxone) exert rheological and cardiovascular effects in normal humans and in patients with essential hypertension. Eight hypertensive patients were matched for age, sex, and body habitus (body mass index, waist to hip ratio) with eight normotensive healthy subjects. In all subjects, heart rate and blood pressure (continuous automatic recording), blood and plasma viscosity, fibrinogen, hematocrit, and platelet aggregation to ADP were evaluated during an infusion of human synthetic beta-endorphin (0.5 mg/h). On a different day and in randomized order, the subjects were submitted to another beta-endorphin infusion preceded by an i.v. naloxone bolus (5 mg in 5 min). beta-Endorphin and naloxone failed to significantly alter heart rate or blood pressure in both normotensive and hypertensive subjects. In hypertensive patients, beta-endorphin significantly increased blood viscosity and ADP-induced platelet aggregation, but only the former effect was naloxone-sensitive. In normotensive subjects, beta-endorphin caused a transient but significant decrease of platelet aggregation that was reversed by naloxone. These data suggest that beta-endorphin may play some role in the inhibitory control of platelet aggregation in normal subjects. An altered responsiveness of some rheological determinants to beta-endorphin seems to be present in human hypertension. |
| Databáze: | OpenAIRE |
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