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Reduced β‐adrenergic vasodilation in the Obese Zucker Rat

Obesity is associated with impaired regulation of blood pressure in response to psychosocial stress but the mechanisms remain poorly understood. This study tested the hypothesis that β‐adrenergic reactivity, a component of the stress response, was altered in a rat model of obesity. Cardiac output, mesenteric and hindquarters blood flow, and arterial pressure were monitored in isoflurane‐anesthetized 8 Lean (LZR) and 8 Obese (OZR) Zucker rats. Baseline cardiac output (CO) was elevated in OZR (93+3 vs. 74 + 3 ml/min) but not cardiac index. The increased CO reflected an increased stroke volume (SV, 253 + 17 vs. 175 vs. 10 ul/min) but a decreased heart rate (428 + 10 vs. 372 + 5 bpm). Differences in CO and SV were eliminated by ganglionic blockade with mecamylamine, indicating a sympathetic origin for cardiac differences. Decreases in blood pressure to serial doses of isoproteronol (ISO, 0.01 −0.5ug/kg) were blunted in OZR vs. LZR, as were increases in cardiac output, mesenteric and hindlimb vascular conductance but changes in heart rate were not different in OZR vs. LZR. Taken together, these data indicate a loss of β‐adrenergic receptors and/or signaling in the cardiovascular system in OZR. These perturbations may contribute to the impaired ability of obese patients to regulate blood pressure in the face of environmental stress.