Low blood pressure may also be attributed to heat stroke which can be indicated by absence of perspiration, light headedness and dark colored urine.Other medications can produce hypotension by different mechanisms. Chronic use of alpha blockers or beta blockers can lead to hypotension. Beta blockers can cause hypotension both by slowing the heart rate and by decreasing the pumping ability of the heart muscle.Decreased cardiac output despite normal blood volume, due to severe congestive heart failure, large myocardial infarction, heart valve problems, or extremely low heart rate (bradycardia), often produces hypotension and can rapidly progress to cardiogenic shock. Arrhythmias often result in hypotension by this mechanism.Excessive vasodilation, or insufficient constriction of the blood vessels (mostly arterioles), causes hypotension. This can be due to decreased sympathetic nervous system output or to increased parasympathetic activity occurring as a consequence of injury to the brain or spinal cord. Dysautonomia, an intrinsic abnormality in autonomic system functioning, can also lead to hypotension. Excessive vasodilation can also result from sepsis, acidosis, or medications, such as nitrate preparations, calcium channel blockers, or AT1 receptor antagonists (Angiotensin II acts on AT1 receptors). Many anesthetic agents and techniques, including spinal anesthesia and most inhalational agents, produce significant vasodilation.Lower blood pressure is a side effect of certain herbal medicines, which can also interact with several medications. An example is the theobromine in Theobroma cacao, which lowers blood pressure through its actions as both a vasodilator and a diuretic, and has been used to treat high blood pressure.
Despite a moderately high pretreatment relapse rate in the patient group prior to treatment (1.3/year pre-enrollment; 1.2/year during a three-month baseline period), no relapses occurred between months 6 and 24 on minocycline. Also, despite significant MRI disease-activity pretreatment (19/40 scans had gadolinium-enhancing activity during a three-month run-in), the only patient with gadolinium-enhancing lesions on MRI at 12 and 24 months was on half-dose minocycline. Levels of interleukin-12 (IL-12), which at high levels might antagonize the proinflammatory IL-12 receptor, were elevated over 18 months of treatment, as were levels of soluble vascular cell adhesion molecule-1 (VCAM-1). The activity of matrix metalloproteinase-9 was decreased by treatment. Clinical and MRI outcomes in this study were supported by systemic immunological changes and call for further investigation of minocycline in MS.The overall antidepressant effect size of minocycline compared to placebo in a meta-analysis was -0.78, indicative of a potential antidepressant effect.In ongoing research and trial minocycline demonstrated efficacy and seems a promising neuroprotective agent in acute stroke patients, especially in AIS subgroup. Further RCTs are needed to evaluate the efficacy and safety of minocycline among ICH patients. Data from cellular and animal models
PARP1 inhibition Ki = 13.8 nM
Neuroprotection IC50 = 10 nM
Microglia full inhibition = 20 nM
Suppression of the mouses locomotor activity = 0.5 mg/kg

References
External links
"Minocycline". Drug Information Portal. U.S. National Library of Medicine.