Chemoreceptors are responsible for signaling vasoconstriction, vasodilation, bronchoconstriction, and bronchodilation. The consequent asphyxia stimulates peripheral chemoreceptors which induce an increasing peripheral vasoconstriction and bradycardia. Sensory afferent nerves trigger a systemic sympathetic activation leading to marked vasoconstriction. Endothelial cells are responsible for releasing vasoconstriction and vasodilator factors, thus modifying tone. Without this hypoxic pulmonary vasoconstriction, shunt and its hypoxic effects would worsen. Ciclosporin causes hypertension by inducing vasoconstriction in the kidneys and increasing sodium reabsorption. Ang-II is a peptide hormone which increases blood pressure by initiating vasoconstriction and aldosterone secretion. Angiotensin is a peptide hormone that causes vasoconstriction and an increase in blood pressure. Angiotensin II causes the local release of prostaglandins, which, in turn, antagonize renal vasoconstriction. Cocaine and its metabolites may cause arterial vasoconstriction hours after use. The renin-aldosterone-angiotensin system can be activated, leading to further vasoconstriction and damage. Following administration, marked peripheral vasoconstriction and bradycardia are noted. Hypertension is due to an increase in vascular resistance and vasoconstriction. Vasospasm refers to a condition in which an arterial spasm leads to vasoconstriction. RCVS is diagnosed by detecting diffuse reversible cerebral vasoconstriction.