Heat stress is a major environmental factor which perturbs working in safety. In humans, heat stress increases the occurrence of orthostatic syncope and induces marked reductions in orthostatic tolerance. Several mechanisms, including an altered baroreflex responsiveness in heart rate (HR) and peripheral vasomotion, are involved in orthostatic intolerance. In the present review, we discuss the effects of heat stress on the baroreflex function in controlling HR and peripheral vasomotion. The present findings from human studies suggest that (1) heat stress slows the arterial baroreflex responses in HR and peripheral vasomotion and decreases the responses to rapid hypotensive stimulation, (2) heat stress reduces the sensitivity of the spontaneous baroreflex control of HR during orthostasis but not during supine rest, (3) central blood volume decreases with increasing skin blood flow and the sensitivity of the integrative baroreflex control of total peripheral vascular resistance is reduced in heat-stressed humans, and (4) the reduced baroreflex sensitivity of total peripheral vascular resistance may be partly due to the reduction in skin vasoconstrictor response. The altered baroreflex responsiveness in HR and peripheral vasomotor control as well as central hypovolemia are related to orthostatic intolerance in a hot environment.