Introduction: 

Nicotine is a classical ganglion-stimulating/blocking agent. Presently will be given a summary of earlier and recent data about Nicotine-effect on rat blood pressure (Front. Rad. Ther. Oncol. 31, 22-35/1997; Proc. Rad. Res. I., 434/1995; Strahlenther. 151, 549-554/1976).

Method: 

Registration by Statham element on Rikadenki recorder (see introd.).

Results: 

Nicotine (5-170 mg/kg), similar to mercaptoethylguanidine (MEG: 200-400 mg/kg), transformed acetylcholine-depressor (ACH: 1-2 mg/kg) into a biphasic depressor/pressor reaction (dR/pR). Nicotine potentate MEG-effect: This inhibitor of Ca⁺⁺-independent isoform of NO-synthase augmented also pR of non- (AHR-602, MCN-A-343: 1-100 mg/kg) and nicotinic-like (DMPP: 15-120 mg/kg) ganglion-stimulating agents and of vasopressin (5-100 mU/kg) in normal and spinal rats. MEG blocked dR after peripheral, but transformed it into dR/pR after central vagal electrical stimulation (CVS: 55 Hz, 2 ms, 5 s, 5 V), whereby vasopressin antagonized this effect (also ACH-dR). MEG inverted serotoninergic dR (5-HT-liberation from thrombocytes by nicotine) into pR.

Conclusion: 

Nicotine excites/inhibits (dose-dependently) via nicotinic cholinergic receptors CNS-structures/preganglionic cholinergic sympathetic neurons, responsible for cardio-vascular regulation leading to biphasic CVS-/ACH-dR/pR as well as to sensitisation of central adrenergic and cholinergic (+vasopressin) neurons and of sympathicus (presynaptical neurons) to non- and nicotine-like ganglion-stimulating-agents. Nicotine-effects incl. complex interaction of hormonal/drug-factors could induce non-calculable vasoconstriction leading to cerebral apoplexy and cardial angiospasms.