title: Platelet hyperactivity in hypertensive older patients is controlled by lowering blood pressure.
abstract: OBJECTIVE
  Patients with hypertension tend to have a high prevalence of atherothrombotic accidents. Platelet hyperactivity is frequently associated with hypertension. Because the vascular disease associated with hypertension evolves over the years, we investigated platelet activity parameters in a population of older hypertensive patients with no other risk factors for cardiovascular disease.
  
  
  METHODS
  We studied 34 older, nonsmoking patients (mean age 74 +/- 5 years) with uncomplicated hypertension before and after the normalization of blood pressure (BP) was achieved with the angiotensin-converting enzyme inhibitor quinapril alone or in combination with the Ca2+ antagonist nifedipine.
  
  
  METHODS
  Platelet aggregation, P-selectin (CD62) expression on the platelet surface, serum levels of Interleukin-1beta (IL-1beta) and of Interleukin-6 (IL-6), as well as plasma levels of soluble P-selectin and Endothelin-1 (ET-1), were analyzed.
  
  
  RESULTS
  All platelet hyperactivity parameters were reduced significantly with the normalization of BP at the end of antihypertensive drug treatment (systolic/diastolic: 186.2 +/- 2.7/103.4 +/- 1.1 mm Hg vs 135.0 +/- 1.3/85.9 +/- 1.9 mm Hg; P < .001). Those factors more strictly associated with endothelium injury, such as ET-1 and IL-6, did not show variations. A significant correlation (Spearman Rank test) was observed among all platelet function parameters and blood pressure values.
  
  
  CONCLUSIONS
  This study demonstrated that even in a population of older hypertensive patients with no other risk factor for atherogenic disease, normalization of blood pressure induces a significant reduction of the parameters of enhanced platelet hyperactivity independent of the action exerted, at the platelet level, by the antihypertensive drugs.
authors.affiliation: Department of Experimental Medicine and Pathology, University La Sapienza, Rome, Italy.
authors.forename: S
authors.initials: S
authors.lastname: Riondino
authors.forename: P
authors.initials: P
authors.lastname: Pignatelli
authors.forename: F M
authors.initials: FM
authors.lastname: Pulcinelli
authors.forename: L
authors.initials: L
authors.lastname: Lenti
authors.forename: C
authors.initials: C
authors.lastname: Di Veroli
authors.forename: V
authors.initials: V
authors.lastname: Marigliano
authors.forename: P P
authors.initials: PP
authors.lastname: Gazzaniga
mesh_terms: D000368:Aged; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D001161:Arteriosclerosis / Q000209:etiology; D001794:Blood Pressure / Q000187:drug effects* / Q000502:physiology; D002121:Calcium Channel Blockers / Q000627:therapeutic use; D019332:Endothelin-1 / Q000097:blood; D005260:Female; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology*; D007375:Interleukin-1 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D007546:Isoquinolines / Q000627:therapeutic use; D008297:Male; D009543:Nifedipine / Q000627:therapeutic use; D019007:P-Selectin / Q000097:blood; D015539:Platelet Activation / Q000187:drug effects / Q000502:physiology*; D010974:Platelet Aggregation / Q000187:drug effects / Q000502:physiology; D015995:Prevalence; D011355:Prodrugs / Q000627:therapeutic use; D000077583:Quinapril; D044005:Tetrahydroisoquinolines
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D000959:Antihypertensive Agents; D002121:Calcium Channel Blockers; D019332:Endothelin-1; D007375:Interleukin-1; D015850:Interleukin-6; D007546:Isoquinolines; D019007:P-Selectin; D011355:Prodrugs; D044005:Tetrahydroisoquinolines; D009543:Nifedipine; D000077583:Quinapril