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. METHODS AND 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.
RCT Entities:
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. METHODS AND 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-deficientpatients 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: Carmen Gonzalez; Hector Rosas-Hernandez; Brenda Jurado-Manzano; Manuel Alejandro Ramirez-Lee; Samuel Salazar-Garcia; Pedro Pablo Martinez-Cuevas; Aída Jimena Velarde-Salcedo; Humberto Morales-Loredo; Ricardo Espinosa-Tanguma; Syed F Ali; Rafael Rubio Journal: Acta Pharmacol Sin Date: 2015-04-20 Impact factor: 6.150
Authors: R Lorusso; E Pasini; A Cargnoni; C Ceconi; M Volterrani; A Burattin; D Valle; R Ferrari; A Giustina Journal: J Endocrinol Invest Date: 2003-01 Impact factor: 4.256
Authors: Guolian Li; Juan-Pablo Del Rincon; Linda A Jahn; Yangsong Wu; Bruce Gaylinn; Michael O Thorner; Zhenqi Liu Journal: J Clin Endocrinol Metab Date: 2008-01-08 Impact factor: 5.958