Rebound vasodilation

Abelson MB, Butrus SI, Weston JH, Rosner B. Tolerance and absence of rebound vasodilation following topical ocular decongestant usage. Ophthalmology 1984 91 1364-1367. Abelson MB, George M, Garofalo C, et al.An effective treatment for allergy sufferers. Contact Lens Spectrum 1995 10 28-32. 

Rhinitis medicamentosa—Nasal congestion associated with tolerance to and resulting overuse of topical decongestants. Also known as rebound vasodilation or rebound congestion. 

Nitroprusside has a rapid onset of action and a duration of action of less than 10 minutes, necessitating its administration by continuous intravenous infusion. This allows for precise dose titration based on measured clinical and hemodynamic parameters. It, like other vasodilators used in heart failure, should be initiated at a low dose (0.1 to 0.2 mcg/kg per minute) to avoid excessive hypotension and then increased by small increments (0.1 to 0.2 mcg/kg per minute) every 5 to 10 minutes as needed and tolerated. Usually effective doses range from 0.5 to 3 mcg/kg per minute. A rebound phenomenon has been reported after abrupt withdrawal of nitroprusside in patients with heart failure and is apparently due to reflex neurohormonal... 

Tyramine present in certain food and beverages can displace NE from sympathetic nerve endings, causing CV stimulation, but only if its metabolism is inhibited by MAO inhibitors. Patients suffering from HTN commonly discontinue medications (without physician consultation) based on perceived undesirable side effects, such as sexual dysfunction. In the case of clonidine, rebound hypertension and tachycardia, especially with abrupt discontinuance, can be problematic. Discontinuance of thiazide is likely to result in fluid retention with weight gain and unlikely to cause tachycardia and marked increase in BP. Ethanol is an effective vasodilator and tends to decrease BP. Tachyphylaxis refers to the development of a decreased response to drug treatment over a time span of minutes to hours, not years. 

The normal additive hypotensive effects of these drugs result from the two acting in concert at different but complementary sites in the cardiovascular system. Just why antagonism sometimes occurs is unexplained. The hypertensive rebound following elonidine withdrawal is thought to be due to an increase in the levels of circulating catecholamines. With the beta (vasodilator) effects blocked by a beta blocker, the alpha (vasoconstrictor) effects of the catecholamines are unopposed and the hypertension is further exaggerated. 

---