Abstract-Spontaneously occurring, parallel fluctuations in arterial pressure and heart period are frequently used as indices of baroreflex function. Despite the convenience of spontaneous indices, their relation to the arterial baroreflex remains unclear. Therefore, in 97 volunteers, we derived 5 proposed indices (sequence method, ␣-index, transfer function, low-frequency transfer function, and impulse response function), compared them with arterial baroreflex gain (by the modified Oxford pharmacologic technique), and examined their relation to carotid distensibility and respiratory sinus arrhythmia. The subjects comprised men and women (nϭ41) aged 25 to 86 years, 30% of whom had established coronary artery disease. Generally, the indices were correlated with each other (except ␣-index and low-frequency transfer function) and with baroreflex gain. However, the Bland-Altman method demonstrated that the spontaneous indices had limits of agreement as large as the baroreflex gain itself. Even in individuals within the lowest tertile of baroreflex gain for whom baroreflex gain appears to be the most clinically relevant, spontaneous indices failed to relate to baroreflex gain. In fact, for these individuals, there was no correlation between any index and baroreflex gain. Forward stepwise linear regression showed that all spontaneous indices and baroreflex gain were related to respiratory sinus arrhythmia, but only baroreflex gain was related to carotid distensibility. Therefore, these data suggest that spontaneous indices are inadequate estimates of gain and are inconsistent with arterial baroreflex function. Key Words: baroreceptors Ⅲ carotid sinus Ⅲ elasticity Ⅲ arrhythmia Ⅲ baroreflex T he arterial baroreflex is a key mechanism for blood pressure homeostasis, is clinically relevant as a predictor of cardiovascular mortality, 1 and is physiologically relevant as an indicator of autonomic control. 2 The sensitivity, or gain, of the arterial baroreflex is calculated routinely from the relation of bradycardic and/or tachycardic responses to increases and/or decreases in systemic arterial pressure. 3 These responses encompass both mechanical and neural aspects of the system. Changes in pressure result in stretch of the aortic arch and the carotid sinus, wherein stretch-sensitive receptors reside. These afferent baroreceptive neurons terminate in the dorsomedial medulla, which in turn signals the neurons composing the efferent autonomic limb of the baroreflex. The resultant cardiac vagal adjustments appropriately regulate heart period to buffer against pressure rises and falls. 2 Arterial baroreflex physiology dictates that both barosensory vessel distensibility and cardiac vagal function critically determine reflex sensitivity. Indeed, a relation between baroreflex gain and carotid stiffness has been shown in healthy young and middle-aged subjects, 4 as well as in hypertensive individuals. 5 Additionally, in patients with coronary disease 6,7 and diabetes, 8,9 both gain and carotid distensibility are prognostically rele...