Although transmembrane potential (Em) appears to be an important regulator of vascular smooth muscle (VSM) contractile force in vivo, little is known of the electrophysiological changes in VSM during low flow states. In rats, VSM in small mesenteric veins depolarizes in the compensatory stage of hemorrhagic hypotension while the onset of peripheral vascular decompensation is associated with VSM hyperpolarization. Pretreatment with 30 mg/kg i.v. of methylprednisolone prevents the Em changes in mesenteric veins of hemorrhaged rats and reduces the depolarization of isolated vessels in response to norepinephrine, suggesting that some therapeutic agents may act by modifying the electrophysiological responses of VSM during the stress. Finally, adrenergic depolarization under resting conditions may contribute to a reduced ability of spontaneously hypertensive rats (SHR) to tolerate blood loss by reducing their compensatory venoconstrictor reserve relative to normotensive WKY controls. Although these observations suggest that vascular responses to hypotensive stress are related to the effects of the sympathetic nervous system upon VSM Em, further studies are required fully to elucidate the relative role of Em-dependent and Em-independent mechanisms in controlling active VSM tone during low flow states.
Animals Glucocorticoids