Which of the following statement(s) is/are true concerning the neuroendocrine responses to shock?

c. Increased pancreatic secretion of glucagon contributes to glucose intolerance associated with injury and sepsis

d. The renin-angiotensin axis further augments the sympathetic-mediated vasoconstriction

The neuroendocrine response to shock attempts to achieve restoration of effective blood volume, mobilization of metabolic substrates, and maintenance of central profusion. Both peripheral and central afferent stimuli to the central nervous system are involved in inducing this response. Hypotension, associated with a decrease in impulses from the aortic and carotid baroreceptors, disinhibits the vasomotor center. This disinhibition results in increased adrenergic output and decreased vagal activity. Sympathetic nerve endings release norepinephrine, inducing peripheral and splanchnic vasoconstriction which is responsible for greater than 80% of systemic vascular resistance and is a major contributor to maintenance of central organ perfusion and venous return. Plasma levels of both epinephrine and norepinephrine are elevated with injury, and the degree of the catecholamine elevation corresponds to the magnitude of injury. In shock the effects of endogenous epinephrine are largely metabolic. In addition to initiating autonomic nervous activity, the hypothalamus secretes releasing hormones, which induce the stress hormone release of the pituitary. As part of this response, adrenocorticotropic hormone (ACTH) secretion by the anterior pituitary is increased stimulating cortisol secretion by the adrenal cortex. In conjunction with elevated plasma levels of cortisol and epinephrine, increased pancreatic secretion of glucagon accelerates hepatic gluconeogenesis and further aggravates the glucose intolerance that follows injury and sepsis. The secretion of renin is increased in responses to adrenergic discharge and decreased perfusion of the juxtaglomerular apparatus in the kidney. Renin allows formation of angiotensin I in the liver, which is then converted to angiotensin II in the lungs. Angiotensin II is an extremely effective vasoconstrictor that further augments sympathetic-mediated vasoconstriction.