Abstract-There is sound experimental evidence that cardiovascular sympathetic afferent fibers mediate cardiovascular reflexes largely excitatory in nature with positive-feedback characteristics. This afferent neural channel is likely to normally participate in the neural regulation of cardiovascular function. The hypothesis, which is the core of this article, is that in some pathophysiological conditions, sympathetic overactivity may be partly due to an emerging excitatory reflex action of cardiovascular sympathetic afferents. In fact, the early phase of congestive heart failure can be characterized by an increase in arterial pressure and heart rate and/or by a diastolic dysfunction, leaving unchanged the cardiac output; in these conditions, in which no baroreceptor deactivation should occur, it is possible that cardiovascular sympathetic afferents with sensory endings in the thoracic low-pressure areas, highly responsive to volume loading, are responsible for mediating the reflex sympathetic excitation. Similarly, during acute myocardial infarction, ventricular sympathetic afferents are likely to mediate a reflex sympathetic overactivity, which is known to facilitate sudden death. Finally, numerous reports have described in essential arterial hypertension an increased sympathetic activity that may be due, at least in part, to the reinforcing action of sympathosympathetic reflexes. Thus, in pathophysiological conditions, cardiovascular sympathetic afferents would mediate a reflex sympathetic overactivity independently of baroreceptive mechanisms, and such an absence of a homeostatic purpose would provide a better rationale for some beneficial effects of therapeutic correction. Key Words: heart failure Ⅲ ischemia Ⅲ hypertension, arterial Ⅲ heart rate Ⅲ reflex Ⅲ lung T he present article will attempt to support the hypothesis that in the early phase of congestive heart failure and other pathophysiological conditions, such as myocardial ischemia and arterial hypertension, sympathetic excitation seems devoid of an ultimate homeostatic purpose, and its genesis may be, in part, attributable to an enhanced peripheral excitatory function of sympathetic afferent fibers.In physiological conditions, the cardiovascular neural regulation is likely to result from a complex interaction of central integration and peripheral inhibitory and excitatory reflexes. [1][2][3] In this interplay, cardiovascular sympathetic afferent fibers mediate a reflex action that is largely excitatory in nature 1 (Figure). When a sympathetic excitation is part of an integrated physiological pattern with a clear ultimate purpose, such as emotion, the central neural and, in particular, diencephalic mechanisms 4 are likely to play a predominant role. However, the central command is also likely to be reinforced by a synergistic enhancement of peripheral excitatory reflex mechanisms, accompanied by a simultaneous attenuation of mechanisms exerting an inhibitory action. 3,4