Suppressive Effect of Captopril on Platelet Aggregation in Essential Hypertension

Someya, Noriyuki; Morotomi, Yasuyuki; Kodama, Kazuhisa; Kida, Osamu; Higa, Toshinobu; Kondo, Koichi; Tanaka, Kenjiro

doi:10.1097/00005344-198409000-00016

Cited by 55 publications

(19 citation statements)

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“…Patients on captopril therapy had decreased platelet aggregation in response to ADP, epinephrine, collagen, and arachidonic acid 6 ; however, platelet aggregation induced by epinephrine, ADP, and collagen in patients on quinapril therapy and by ADP and arachidonic acid in patients on lisinopril therapy was unchanged. 7,8 Recently, the effect of fosinopril on platelet aggregation was evaluated by using collagen and ADP in hypertensive patients.…”

Section: Discussionmentioning

confidence: 91%

Combination of Fosinopril and Pravastatin Decreases Platelet Response to Thrombin Receptor Agonist in Monkeys

Hale

Craver

Berrier

et al. 1998

ATVB

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Abstract-Both angiotensin-converting enzyme (ACE) inhibitors and 3-hydroxy-3-methylglutaryl coenzyme A (HMGCoA) reductase inhibitors have been shown to decrease cardiovascular morbidity and mortality. Results from clinical trials have suggested that HMG-CoA reductase inhibition might exert a beneficial effect independent of its lipid-lowering effect, and ACE inhibition may exert a benefit independent of blood-pressure lowering. To test the hypothesis that such an effect might be mediated by alteration in platelet reactivity, we studied 55 monkeys receiving both, 1, or neither of the ACE inhibitor fosinopril and the HMG-CoA reductase inhibitor pravastatin. Platelet responsiveness to collagen and to the thrombin receptor agonist (TRA) SFLRRN-NH 2 was determined by aggregometry. For each agonist, the maximum rate and extent of aggregation were measured for each dose, and the concentration required for half-maximal response (C 50 ) was determined. Each drug, when given alone, slightly decreased the dose of agonist required to produce 50% response in the rate and extent of platelet aggregation relative to control. The combination of the 2 drugs, however, produced a significant increase in the dose of TRA required to produce 50% response in the rate and extent of aggregation relative to either drug alone or the control group. This was not true for collagen. The magnitude of the change relative to the control group, 47% for rate and 30% for extent of aggregation, could confer considerable protection by changing the threshold for thrombin-induced platelet aggregation and, thus, decrease thrombosis. (Arterioscler Thromb Vasc Biol. 1998;18:1643-1646.)Key Words: angiotensin-converting enzyme inhibitors Ⅲ platelet aggregation Ⅲ 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors C ardiovascular disease is the leading cause of death in the United States. 1 Most of the morbidity and mortality of this disease results from the rupture of atherosclerotic plaques in the vessel wall. This event leads to exposure of the thrombogenic inner components of the plaque to circulating blood, resulting in platelet activation and aggregation and activation of the coagulation system. Subsequently, a thrombus forms.2 The use of angiotensin-converting enzyme (ACE) inhibitors and lipid-lowering drugs has decreased cardiovascular morbidity and mortality below that expected from the resulting mild reduction in blood pressure and minor reduction in severity of coronary stenosis.2-4 Therefore, in addition to their well-known actions, these drugs probably have other protective effects on the processes that lead to cardiovascular disease and thrombosis. It is possible that these drugs may affect platelet function.In this randomized trial, we studied platelet responsiveness to collagen and a thrombin receptor agonist (TRA) in monkeys that were treated with an ACE inhibitor, a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, both drugs, or neither drug. Methods MaterialsThe highly purified peptide TRA SFLRRN-NH 2 (PMIS387) wa...

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Section: Discussionmentioning

confidence: 91%

Combination of Fosinopril and Pravastatin Decreases Platelet Response to Thrombin Receptor Agonist in Monkeys

Hale

Craver

Berrier

et al. 1998

ATVB

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“…In a recent study, it was suggested that the [ 5Ca2+] uptake elicited by these latter agents reflects calcium mobilisation events at the plasma membrane associated with signal transduction mechanisms and not with changes in intracellular calcium levels . Other clinical trials have shown that administration of the ACEI, captopril, to human subjects diminishes ex vivo platelet aggregation (James et al, 1986;Someya et al, 1984). In turn, in vitro and ex vivo studies have shown that calcium channel blockers, including nifedipine, inhibits platelet aggregation and concomitant thromboxane A2 release .…”

Section: Discussionmentioning

confidence: 99%

“…Recent clinical trials have demonstrated that captopril inhibits ex vivo platelet aggregation (James et al, 1988;Someya et al, 1984) and concomitant thromboxane A2 (TXA2; a proaggregatory eicosanoid) release (James et al, 1988). In a subsequent study, it was shown that captopril inhibited [45Ca2+] uptake by human isolated platelets at concentrations similar to that of verapamil, a conventional calcium channel blocker (Gill et al, 1988).…”

Section: Introductionmentioning

confidence: 99%

Lisinopril and nifedipine administration inhibits the ex vivo uptake of [45Ca2+] by platelets from hypertensive diabetic patients.

Gill

Fonseca

Dandona

et al. 1992

Brit J Clinical Pharma

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1. The effect of administration of the angiotensin converting enzyme inhibitor (ACEI), lisinopril (Carace; 10‐40 mg twice daily) and the calcium channel blocker, nifedipine (Adalat Retard; 20‐40 mg twice daily) on ex vivo [45Ca2+] uptake by platelets from hypertensive diabetic (type 1 and 2) patients was investigated. 2. At the end of at least 3 months treatment, blood was collected prior to the patient taking the morning dose of medication and washed platelets prepared. [45Ca2+] uptake was monitored following the addition of adrenaline, isoprenaline and dibutyryl cAMP (dbcAMP), as well as in unstimulated (zero) platelets. 3. Both nifedipine and lisinopril significantly inhibited the ex vivo uptake of [45Ca2+] by platelets when this process was stimulated by adrenaline, isoprenaline and dibutyryl cAMP. Basal uptake was also inhibited in both groups. 4. These data consolidate the hypothesis that ACE inhibitors may possess calcium channel/calcium mobilisation blocking properties. Apart from its hypertensive action, lisinopril may also reduce platelet activity via modulation of calcium dynamics, thereby reducing the incidence of vascular complications associated with diabetes mellitus.

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“…12 A clinically significant inhibition of platelet aggregation has been demonstrated in patients receiving captopril, which may contribute to a possible cardioprotective effect associated with this medication. 13 This concept of cardioprotection resulting from captopril use is theoretical at present but may be a factor to consider in the selection of vasodilating agents and, in particular, in the selection of an angiotensin converting enzyme inhibitor.…”

Section: Supplement I Hypertension Vol 13 No 5 May 1989mentioning

confidence: 99%

Alternatives to traditional first-line antihypertensive treatment: unresolved questions and therapeutic dilemmas. A personal approach.

Zusman

1989

Hypertension

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The best antihypertensive regimen for use in patients with mild-to-moderate hypertension has not been determined. When nonpharmacological treatment of hypertension fails, initial drug treatment with diuretic drugs, sympatholytic agents (including /3-adrenergic receptor blockers), or vasodilators will result in satisfactory blood pressure control. However, each of these therapies has effects that are independent of their antihypertensive activity and that should be considered before a selection is made for initial therapy.

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Suppressive Effect of Captopril on Platelet Aggregation in Essential Hypertension

Cited by 55 publications

References 0 publications

Combination of Fosinopril and Pravastatin Decreases Platelet Response to Thrombin Receptor Agonist in Monkeys

Combination of Fosinopril and Pravastatin Decreases Platelet Response to Thrombin Receptor Agonist in Monkeys

Lisinopril and nifedipine administration inhibits the ex vivo uptake of [45Ca2+] by platelets from hypertensive diabetic patients.

Alternatives to traditional first-line antihypertensive treatment: unresolved questions and therapeutic dilemmas. A personal approach.

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