Key result
Intracerebroventricular diltiazem lowers BP, HR, and sympathetic nerve activity in rats.
Why the study?
Does centrally administered diltiazem reduce blood pressure and sympathetic nerve activity in urethane-anaesthetized rats?
Does centrally administered diltiazem reduce blood pressure and sympathetic nerve activity in urethane-anaesthetized rats?
Diltiazem exerts central vasodepressor effects by decreasing sympathetic outflow, potentially mediated through the AV3V area.
Central diltiazem effects in rats are hypothesis-generating; leaves open any human translation or therapeutic relevance.
The effects of a calcium channel blocker, diltiazem, on central cardiovascular regulation were investigated by injecting it intracerebroventricularly (i.c.v.) in urethane-anaesthetized rats. The blood pressure decreased immediately after the injection returning to baseline level 20-30 min later. Both heart rate and abdominal sympathetic nerve activity decreased correspondingly. Diltiazem injected intravenously (i.v.) decreased both blood pressure and heart rate without affecting sympathetic nerve firing. Although the central pressor responses to carbachol and prostaglandin E2 were not affected by i.c.v. pretreatment with diltiazem, diltiazem attenuated the pressor responses to angiotensin II. Furthermore, electrical lesioning of the anteroventral third ventricle (AV3V) area significantly attenuated the depressor responses to diltiazem injected i.c.v. These results suggest that diltiazem injected i.c.v. affects the central nervous system to decrease sympathetic outflow, and thereby to attenuate the central vasopressor effects of angiotensin II in the brain AV3V area.
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IYODA et al. (1985) studied this question. Diltiazem was evaluated on Blood pressure, heart rate, and sympathetic nerve activity. Intracerebroventricular injection of diltiazem in rats decreased blood pressure, heart rate, and sympathetic nerve activity, and attenuated central pressor responses to angiotensin II.
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