Abstract
Dihydropyridines (DHPs) exert a powerful coronary vasodilator action, but whether they actually affect the coronary vasomotor effects elicited by an increase in cardiac sympathetic drive is controversial. We assessed the effects of the DHP calcium antagonist amlodipine on coronary hemodynamics and vascular response to sympathetic activation in patients with coronary heart disease. In the control condition, mean arterial pressure (MAP, aortic catheter), heart rate (HR, ECG), rate-pressure product (RPP), coronary sinus blood flow (CBF, thermodilution) and coronary vascular resistance (CVR) (ratio between MAP and CBF) were measured in all our case series (13 patients with angiographically documented severe coronary artery disease) before and during a 2-min cold pressor test (CPT) and a 30-s diving (D) and, in the 8 patients of this case series who were smokers, also before and during smoking a cigarette (S, nicotine content 1.0 mg for 10 min). The same protocol used in control condition was repeated 30 min after intravenous (i.v.) bolus administration of 11 mg amlodipine. CPT, diving, and smoking increased MAP and RPP and caused a marked and significant increase in CVR (+12.1 ± 4.8, +30.4 ± 6.8, and +16.8 ± 7.2%, respectively). Amlodipine reduced MAP, increased CBF, and caused a marked decrease in CBF. The drug did not modify responses to CPT and diving or pressure and HR responses to smoking, whereas the smoking-induced increase in coronary vascular resistance was attenuated after amlodipine administration (+3.2 ± 2.7%, p <0.05 vs. control condition). Thus, amlodipine does not attenuate the sympathetic coronary vasoconstrictor effects of CPT and diving. However, owing to marked reduction in baseline coronary vasomotor tone, sympathetic stimuli elicit less peak coronary vasoconstriction after administration than before administration of amlodipine. The drug also attenuates coronary vasoconstriction to smoking, presumably because this stimulus is not entirely sympathetic.
| Original language | English |
|---|---|
| Pages (from-to) | 875-882 |
| Number of pages | 8 |
| Journal | Journal of Cardiovascular Pharmacology |
| Volume | 24 |
| Issue number | 6 |
| Publication status | Published - 1994 |
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Keywords
- calcium antagonists
- cigarette smoking
- coronary artery disease
- sympathetic coronary vasoconstriction
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Pharmacology
Cite this
Effects of amlodipine on coronary hemodynamics and vascular responses to sympathetic stimulation in patients with coronary heart disease. / Saino, A.; Pomidossi, G.; Perondi, R.; Gregorini, L.; Rimini, A.; Alessio, P.; Zanchetti, A.; Mancia, G.
In: Journal of Cardiovascular Pharmacology, Vol. 24, No. 6, 1994, p. 875-882.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Effects of amlodipine on coronary hemodynamics and vascular responses to sympathetic stimulation in patients with coronary heart disease
AU - Saino, A.
AU - Pomidossi, G.
AU - Perondi, R.
AU - Gregorini, L.
AU - Rimini, A.
AU - Alessio, P.
AU - Zanchetti, A.
AU - Mancia, G.
PY - 1994
Y1 - 1994
N2 - Dihydropyridines (DHPs) exert a powerful coronary vasodilator action, but whether they actually affect the coronary vasomotor effects elicited by an increase in cardiac sympathetic drive is controversial. We assessed the effects of the DHP calcium antagonist amlodipine on coronary hemodynamics and vascular response to sympathetic activation in patients with coronary heart disease. In the control condition, mean arterial pressure (MAP, aortic catheter), heart rate (HR, ECG), rate-pressure product (RPP), coronary sinus blood flow (CBF, thermodilution) and coronary vascular resistance (CVR) (ratio between MAP and CBF) were measured in all our case series (13 patients with angiographically documented severe coronary artery disease) before and during a 2-min cold pressor test (CPT) and a 30-s diving (D) and, in the 8 patients of this case series who were smokers, also before and during smoking a cigarette (S, nicotine content 1.0 mg for 10 min). The same protocol used in control condition was repeated 30 min after intravenous (i.v.) bolus administration of 11 mg amlodipine. CPT, diving, and smoking increased MAP and RPP and caused a marked and significant increase in CVR (+12.1 ± 4.8, +30.4 ± 6.8, and +16.8 ± 7.2%, respectively). Amlodipine reduced MAP, increased CBF, and caused a marked decrease in CBF. The drug did not modify responses to CPT and diving or pressure and HR responses to smoking, whereas the smoking-induced increase in coronary vascular resistance was attenuated after amlodipine administration (+3.2 ± 2.7%, p <0.05 vs. control condition). Thus, amlodipine does not attenuate the sympathetic coronary vasoconstrictor effects of CPT and diving. However, owing to marked reduction in baseline coronary vasomotor tone, sympathetic stimuli elicit less peak coronary vasoconstriction after administration than before administration of amlodipine. The drug also attenuates coronary vasoconstriction to smoking, presumably because this stimulus is not entirely sympathetic.
AB - Dihydropyridines (DHPs) exert a powerful coronary vasodilator action, but whether they actually affect the coronary vasomotor effects elicited by an increase in cardiac sympathetic drive is controversial. We assessed the effects of the DHP calcium antagonist amlodipine on coronary hemodynamics and vascular response to sympathetic activation in patients with coronary heart disease. In the control condition, mean arterial pressure (MAP, aortic catheter), heart rate (HR, ECG), rate-pressure product (RPP), coronary sinus blood flow (CBF, thermodilution) and coronary vascular resistance (CVR) (ratio between MAP and CBF) were measured in all our case series (13 patients with angiographically documented severe coronary artery disease) before and during a 2-min cold pressor test (CPT) and a 30-s diving (D) and, in the 8 patients of this case series who were smokers, also before and during smoking a cigarette (S, nicotine content 1.0 mg for 10 min). The same protocol used in control condition was repeated 30 min after intravenous (i.v.) bolus administration of 11 mg amlodipine. CPT, diving, and smoking increased MAP and RPP and caused a marked and significant increase in CVR (+12.1 ± 4.8, +30.4 ± 6.8, and +16.8 ± 7.2%, respectively). Amlodipine reduced MAP, increased CBF, and caused a marked decrease in CBF. The drug did not modify responses to CPT and diving or pressure and HR responses to smoking, whereas the smoking-induced increase in coronary vascular resistance was attenuated after amlodipine administration (+3.2 ± 2.7%, p <0.05 vs. control condition). Thus, amlodipine does not attenuate the sympathetic coronary vasoconstrictor effects of CPT and diving. However, owing to marked reduction in baseline coronary vasomotor tone, sympathetic stimuli elicit less peak coronary vasoconstriction after administration than before administration of amlodipine. The drug also attenuates coronary vasoconstriction to smoking, presumably because this stimulus is not entirely sympathetic.
KW - calcium antagonists
KW - cigarette smoking
KW - coronary artery disease
KW - sympathetic coronary vasoconstriction
UR - http://www.scopus.com/inward/record.url?scp=0028648820&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0028648820&partnerID=8YFLogxK
M3 - Article
C2 - 7898068
AN - SCOPUS:0028648820
VL - 24
SP - 875
EP - 882
JO - Journal of Cardiovascular Pharmacology
JF - Journal of Cardiovascular Pharmacology
SN - 0160-2446
IS - 6
ER -