Tachycardia

Elevated heart rate is a frequent comorbidity of dissociative symptoms.

ACE-inhibitors, apparent hypoxanthine (i) analogues have been noted to reduce some cases of unexplained tachycardia, putatively by decreasing bradykinin metabolism, increasing available bradykinins. Reduction in xanthines as a secondary effect of decreased xanthine precursor (hypoxanthine) may mediate this correlation. IMG

Glycopyrrolate is xanthine similar in chemical structure and is used to combat bradycardia. Glycopyrrolate does not cross the blood brain barrier, so will not affect centrally mediated xanthine-associated symptoms like dissociation. IMG

Along with beta blockers, calcium channel blockers are first line agents for the treatment of tachycardia. Dihydropyridine calcium channel blockers are similar to PNP-precursors, and may act via PNP inhibition, decreasing xanthine by decreasing conversion of xanthosine to xanthine. IMG

Considering Parkinson's disease as a purine-wasting syndrome, it is notable that bradycardia is a common finding, limiting use of beta blockers for dyskinesia: PMID 12535472, perhaps indicative of decreased xanthine as the homeostatic mechanism seeks guanine.

Like a-methyl-DOPA, L-DOPA is associated with decreased HR PMID 24715569.