The paper outlines the previously unknown smooth muscle insufficiency in terms of its etiology, pathogenesis, diagnosis and treatment. It has been shown that drug administration leads to smooth muscle insufficiency which is eliminated by serotonin both in vitro and in vivo. The clinical manifestations of smooth muscle (SM) insufficiency are eliminated by serotonin, irrespective of whether it has been caused by the use of drugs or impaired smooth muscle innervation. The mechanism of vascular rhythmic oscillations in the microcirculatory bed, the so-called endogenous vasomotility (EV) has been decoded. The mechanism of EV regulation is due to the fact that platelets constantly (continuously) adsorb serotonin from the enterochromaffin cells of the gastrointestinal tract and constantly (continuously) release it into the microcirculatory bed, thereby providing the continuum of entry of the stimulant to the SM fibers which are able to contract at this time. The summation of these contractions of smooth muscle contractions in the microcirculatory bed maintains their vascular tone and yields the pattern of EV. The paper also describes the earlier unknown properties of hemoglobin and myoglobin to cause smooth muscle spasm and to accelerate platelet destruction. A correlation between the EV and vascular platelet hemostasis is described in terms of these properties. The continuous mechanism of EV is impaired and it transforms to intermittent (final) vascular platelet hemostasis.