title: Abnormal vascular reactivity in growth hormone deficiency.
abstract: BACKGROUND
  The reason why patients with growth hormone (GH) deficiency (GHD) are at increased risk for premature cardiovascular death is still unclear. Although a variety of vascular risk factors have been identified in GHD, little is known regarding vascular reactivity and its contribution to premature arteriosclerosis.
  
  
  RESULTS
  We assessed vascular function in 7 childhood-onset, GH-deficient nontreated patients (age 22+/-3 years, body mass index [BMI] 25+/-1 kg/m(2)) and 10 healthy subjects (age 24+/-0.4 years, BMI 22+/-1 kg/m(2)) by using strain gauge plethysmography to measure forearm blood flow in response to vasodilatory agents. The increase in forearm blood flow to intrabrachial infusion of the endothelium-dependent vasodilator acetylcholine was significantly lower in GH-deficient nontreated patients than in control subjects (P:<0.05). Likewise, forearm release of nitrite and cGMP during acetylcholine stimulation was reduced in GH-deficient nontreated patients (P:<0.05 and P:<0.002 versus controls). The response to the endothelium-independent vasodilator sodium nitroprusside was also markedly blunted in GH-deficient patients compared with control subjects (P:<0.005). To confirm that abnormal vascular reactivity was due to GHD, we also studied 8 patients with childhood-onset GHD (age 31+/-2 years, BMI 24+/-1 kg/m(2)) who were receiving stable GH replacement therapy. In these patients, the response to both endothelium-dependent and -independent vasodilators, as well as forearm nitrite and cGMP, release was not different from that observed in normal subjects. Peak hyperemic response to 5-minute forearm ischemia was significantly reduced in GH-deficient nontreated patients (17.2+/-2.6 mL x dL(-1) x min(-1), P:<0.01) but not in GH-treated patients (24.8+/-3.3 mL x dL(-1) x min(-1)) compared with normal subjects (29.5+/-3.2 mL x dL(-1) x min(-1)).
  
  
  CONCLUSIONS
  The data support the concept that GH plays an important role in the maintenance of a normal vascular function in humans.
authors.affiliation: Departments of Internal Medicine and Cardiovascular Sciences and of Endocrinology, University Federico II, Naples, Italy.
authors.forename: B
authors.initials: B
authors.lastname: Capaldo
authors.forename: V
authors.initials: V
authors.lastname: Guardasole
authors.forename: F
authors.initials: F
authors.lastname: Pardo
authors.forename: M
authors.initials: M
authors.lastname: Matarazzo
authors.forename: F
authors.initials: F
authors.lastname: Di Rella
authors.forename: F
authors.initials: F
authors.lastname: Numis
authors.forename: B
authors.initials: B
authors.lastname: Merola
authors.forename: S
authors.initials: S
authors.lastname: Longobardi
authors.forename: L
authors.initials: L
authors.lastname: Saccà
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000328:Adult; D001783:Blood Flow Velocity / Q000187:drug effects; D001794:Blood Pressure / Q000187:drug effects; D001808:Blood Vessels / Q000187:drug effects / Q000503:physiopathology*; D006152:Cyclic GMP / Q000097:blood; D004305:Dose-Response Relationship, Drug; D005260:Female; D005542:Forearm / Q000098:blood supply; D013006:Growth Hormone / Q000172:deficiency* / Q000627:therapeutic use; D020249:Hormone Replacement Therapy; D006801:Humans; D007511:Ischemia / Q000503:physiopathology; D008297:Male; D009573:Nitrites / Q000097:blood; D009599:Nitroprusside / Q000494:pharmacology; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D009573:Nitrites; D014665:Vasodilator Agents; D009599:Nitroprusside; D013006:Growth Hormone; D006152:Cyclic GMP; D000109:Acetylcholine