Caffeine is pharmacologically similar to the other xanthine drugs, such as theobromine and theophylline; however, these three agents differ in the intensity of their actions on various structures. Caffeines CNS and skeletal muscle effects are greater than those of other xanthines. In all other areas, theophylline has greater activity than caffeine, although some studies report that caffeine has greater diuretic effect than theobromine. The increased levels of intracellular cyclic-AMP mediate most of caffeines pharmacologic actions. Caffeine competitively inhibits phosphodiesterase, the enzyme that degrades cyclic 3- 5 adenosine monophosphate. Caffeine stimulates all levels of the CNS. Caffeines cortical effects are milder and of shorter duration than those of amphetamines. In slightly larger doses, caffeine stimulates medullary vagal, vasomotor and respiratory centers, promoting bradycardia, vasoconstriction, and increased respiratory rate.

Caffeine produces a positive inotropic effect on the myocardium and a positive chronotropic effect at the sinoatrial node, causing transient increases in heart rate, force of contraction, cardiac output and heart work. In doses greater than 250 mg, the centrally mediated vagal effects of caffeine may be masked by increased sinus rates, tachycardia, extrasystoles, or other major ventricular arrhythmias may result.

Caffeine constricts cerebral vasculature. In contrast, the drug directly dilates peripheral blood vessels, decreasing peripheral vascular resistance. The effect of this decrease in peripheral vascular resistance (and possibly that of vagal cardiac stimulation) on blood pressure is offset by increased cardiac output (and possibly stimulation of the medullary vasomotor area). The overall effect of caffeine on heart rate and blood pressure depends on whether CNS or peripheral effects predominate. Therapeutic doses of caffeine increase blood pressure only slightly.

Caffeine stimulates voluntary skeletal muscle, increasing the force of contraction and decreasing muscular fatigue. The drug also stimulates gastric acid secretion from parietal cells. Caffeine increases renal blood flow and glomerular filtration rate and decreases proximal tubular reabsorption of sodium and water, resulting in mild diuresis.

Caffeine stimulates glycogenolysis and lipolysis, but increase in blood glucose and in plasma lipids are insignificant in normal patients. Tolerance may develop to the diuretic, cardiovascular, and CNS effects of caffeine.

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