Prenatal environment exerts profound influences on the development of an organism and stressful events during pregnancy can bring about long-term physiological/behavioral alterations in the offspring. Epidemiological evidence points to a relationship between intrauterine growth restriction (IUGR), body weight at birth, and adult cardiovascular disease. Experimental research employed different models of IUGR, including altered maternal nutrition, exposure to elevated glucocorticoids, and reduced placental perfusion, all of which can program, when acting during sensitive temporal windows of foetal life, alterations in cardiovascular regulation and stress sensitivity. Original data are presented indicating that prenatal psychological stress (intermittent restraint) does not induce in the rat adult offspring changes of plasma corticosterone levels, cardiac autonomic modulation, and circadian rhythmicity of heart rate (HR), body temperature (T) and physical activity (Act) at rest. However, prenatally stressed rats--when further stimulated in adulthood--exhibit prolonged adrenocortical stress responsivity, disturbed circadian rhythmicity of HR, T, and Act, and increased adrenal weight. This evidence supports the idea that prenatal stress per se does not change dramatically a given structure or function, but it affects resilience and renders the animal more susceptible to pathophysiological outcomes when further insults occur during adulthood.