title: Pima Indian males have lower beta-adrenergic sensitivity than Caucasian males.
abstract: The sympathetic nervous system controls cardiovascular homeostasis and regulates energy metabolism. Pima Indians, a population with a low prevalence of hypertension and a high prevalence of obesity, have low sympathetic nervous activity, compared with Caucasians. Preliminary findings suggest that they may also have a low beta-adrenergic sensitivity. We studied beta-adrenergic sensitivity in 87 nondiabetic normotensive individuals [52 Pima Indians (35 males/17 females) and 35 Caucasians (24 males/11 females)], matched for age and body weight. Chronotropic sensitivity to beta-adrenergic stimulation was assessed by the dose of isoproterenol necessary to increase heart rate by 25 beats per minute [chronotropic dose-25 (CD25)]. Despite a similar basal heart rate and arterial blood pressure, Pimas tended to have lower beta-adrenergic sensitivity than Caucasians (CD25 = 2.37 +/- 2.27 vs. 1.57 +/- 1.38 microg, P = 0.07; mean +/- SD). This difference was significant in males (CD25 = 3.03 +/- 2.39 vs. 1.85 +/- 1.56 microg, P = 0.02) but not in females (CD25 = 1.01 +/- 1.17 vs. 0.96 +/- 0.61 microg, P = 0.99). In males only, CD25 was positively correlated to percent body fat (r = 0.36, P < 0.01). After adjustment for percent body fat, beta-adrenergic sensitivity was still significantly lower in Pima than in Caucasian males (CD25 = 3.44 +/- 2.24 vs. 2.57 +/- 1.60 microg, P = 0.05). In conclusion, our data suggest that increased adiposity is accompanied by decreased beta-adrenergic sensitivity in males only. However, at each level of adiposity, Pima Indian males have lower beta-adrenergic sensitivity than Caucasian males. In combination with a low sympathetic nervous system activity, a reduced beta-adrenergic sensitivity may contribute to the low prevalence of hypertension and the high prevalence of obesity observed in Pima Indians.
authors.affiliation: Clinical Diabetes and Nutrition Section, National Institute of Diabetes Digestive and Kidney Diseases, National Institutes of Health, Phoenix, Arizona 85016, USA.
authors.forename: P A
authors.initials: PA
authors.lastname: Tataranni
authors.forename: L
authors.initials: L
authors.lastname: Christin
authors.forename: S
authors.initials: S
authors.lastname: Snitker
authors.forename: G
authors.initials: G
authors.lastname: Paolisso
authors.forename: E
authors.initials: E
authors.lastname: Ravussin
mesh_terms: D000318:Adrenergic beta-Agonists / Q000494:pharmacology*; D000328:Adult; D001130:Arizona; D002316:Cardiotonic Agents / Q000494:pharmacology*; D005260:Female; D006801:Humans; D007198:Indians, North American / Q000235:genetics*; D007545:Isoproterenol / Q000494:pharmacology*; D008297:Male; D009765:Obesity / Q000453:epidemiology; D015995:Prevalence; D012727:Sex Characteristics; D044465:White People / Q000235:genetics*
chemical_list: D000318:Adrenergic beta-Agonists; D002316:Cardiotonic Agents; D007545:Isoproterenol