Magnesium is essential in mechanisms of pulmonary vasomotor control.

Magnesium (Mg2+) is an important cofactor in many intracellular biochemical reactions; however, its role in the signal transduction pathways of pulmonary vascular smooth muscle is poorly defined. The purpose of this study was to examine the following mechanisms of pulmonary vascular smooth relaxation in the presence and in the absence of Mg2+: (1) Endothelium-dependent cGMP-mediated relaxation (response to acetylcholine, ACh), (2) Endothelium-independent cGMP-mediated relaxation (response to sodium nitroprusside, SNP), and (3) beta2-adrenergic cAMP-mediated relaxation (response to isoproterenol, ISO). Dose response curves were generated in isolated rat pulmonary artery rings preconstricted with phenylephrine. With Mg2+, ACh 10(-6) M produced complete ring relaxation but in the absence of Mg2+, only 66% relaxation was produced in response to ACh 10(-6) M (P < 0.05). On the other hand, endothelium-independent cGMP-mediated relaxation (response SNP) was not impaired without Mg2+. Beta2-adrenergic cAMP-mediated relaxation was also impaired in the absence of Mg2+. In the presence of Mg2+, ISO 10(-6) M produced complete relaxation but without Mg2+, only 30% relaxation was produced (P < 0.05). We conclude that Mg2+ is essential for cGMP- and cAMP-mediated mechanisms of pulmonary vasorelaxation. Hypomagnesemia should be avoided to prevent pulmonary vasomotor dysfunction.