Why the study?
Does central administration of nicardipine decrease blood pressure and heart rate in spontaneously hypertensive rats?
Does central administration of nicardipine decrease blood pressure and heart rate in spontaneously hypertensive rats?
Central cardiovascular effects of nicardipine in hypertensive rats may result from interaction with dihydropyridine sites within the nucleus tractus solitarii, leading to sympathetic tone withdrawal.
Central nicardipine effects in SHR models are hypothesis-generating; leaves open translation to human hypertension therapy.
The effects of the dihydropyridine (DHP) calcium channel antagonist, nicardipine, on central cardiovascular regulation were investigated by injecting it into the cisterna magna or directly into the nucleus tractus solitarii (NTS), in anesthetized normotensive or spontaneously hypertensive (SHR) rats. Intracisternal injections of nicardipine (1-10 micrograms/kg) dose-dependently decreased blood pressure in SHR; there was no significant change in cardiovascular parameters in normotensive rats. In SHR, nicardipine (100 ng) microinjected bilaterally into the NTS produced hypotension and bradycardia. The same doses of nicardipine intravenously injected did not change either parameter. Previous administration of the beta-adrenoceptor blocking drug, tertatolol (50 micrograms/kg i.v.), prevented the nicardipine-induced bradycardia and hypotension after injection into the NTS. These data suggest that part of the central cardiovascular effects of nicardipine result from an interaction with DHP sites within the NTS leading to a withdrawal of the sympathetic tone.
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Champéroux et al. (1989) studied this question.
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