Platelets and Hypertension

Erné, Paul; Tj, Resink; Bürgisser, Ernst; Fr, Bühler

doi:10.1097/00005344-198500076-00017

Cited by 36 publications

(8 citation statements)

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“…Concerning platelet alpha, adrenoceptors, conflicting results have been reported in the literature since increases (Brodde et al, 1985), decreases (Jones et al, 1985), or no change (Erne et al, 1985) in alpha, adrenoceptor number have been reported in hypertensive patients. Concerning platelet alpha, adrenoceptors, conflicting results have been reported in the literature since increases (Brodde et al, 1985), decreases (Jones et al, 1985), or no change (Erne et al, 1985) in alpha, adrenoceptor number have been reported in hypertensive patients.…”

Section: Discussionmentioning

confidence: 99%

Plasma Catecholamines and Adrenoceptors After Chronic Sinoaortic Denervation in Dogs

Valet¹,

Damase‐Michel²,

Jl³

et al. 1989

Fundamemntal Clinical Pharma

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Chronic sinoaortic denervation (SAD) performed by section of both carotid and aortic nerves induced a significant and sustained increase in blood pressure and heart rate in conscious dogs; under our experimental conditions, the values of systolic blood pressure and heart rate were never lower than 190 mmHg and 120 beats/min, respectively. The present long-term study (8 mo) investigated the time-course of plasma catecholamine levels and circulating blood cell adrenoceptor (leukocyte beta 2 and platelet alpha 2) number. Catecholamine plasma levels were highly correlated with the variations of leukocyte beta adrenoceptors (measured by [125I]cyanopindolol binding and characterized as a beta 2 receptor in dogs). These two parameters followed a biphasic pattern after SAD: during the first 2 mo, significant increases in noradrenaline and adrenaline levels were associated with a decrease in leukocyte beta 2 adrenoceptor number; from the 4th month, they slowly returned to normal values, although blood pressure remained elevated. By contrast, platelet alpha 2 adrenoceptor number (measured by [3H]yohimbine binding) did not follow this pattern since it remained lower than before SAD during the whole experiment. Finally, the development (but not the maintenance) of SAD-induced hypertension is associated with an increase in sympathetic tone. Only leukocyte beta 2 (and not platelet alpha 2) adrenoceptors are directly regulated by the endogenous levels of catecholamines.

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Section: Discussionmentioning

confidence: 99%

Plasma Catecholamines and Adrenoceptors After Chronic Sinoaortic Denervation in Dogs

Valet¹,

Damase‐Michel²,

Jl³

et al. 1989

Fundamemntal Clinical Pharma

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“…It is interesting to compare the present results observed in arterial hypertension associated with phaeochromocytoma with the data obtained in human essential arterial hypertension. In fact, conflicting results were reported since some authors found an increase in platelet a2-and in lymphocyte Pz-adrenoceptors [26,27], whereas others described a decrease [28] or even no change [29]. These differences can be explained by the fact that plasma catecholamine levels are not always increased in essential arterial hypertension [30].…”

Section: Discussionmentioning

confidence: 99%

Platelet α₂‐ and leucocyte β₂‐adrenoceptors in phaeochromocytoma: effect of tumour removal

Valet

Damase‐Michel

Chamontin³

et al. 1988

Eur J Clin Investigation

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Abstract. Platelet ct2-and leucocyte P2-adrenoceptors (as well as noradrenaline and adrenaline plasma levels) were studied in five patients with confirmed phaeochromocytoma using tritiated yohimbine and iodated cyanopindolol, respectively, before and after tumour removal. Patients with phaeochromocytoma had a lower leucocyte iodated cyanopindolol binding than control subjects, but no change in platelet tritiated yohimbine binding. Plasma catecholamine levels were higher than controls. Tumour removal induced a return to normal values of leucocyte iodated cyanopindolol binding and a decrease in plasma catecholamine levels. These results underline the potential interest of leucocyte 8-adrenoceptor quantification in the diagnosis and the follow-up of phaeochromocytoma. Pharmacologically, they show that down-regulation occurs in viuo for leucocyte pz-adrenoceptors but not for platelet a2-adrenoceptors.

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“…The platelet l ‐arginine–NO–cGMP pathway has been described elsewhere [24,25], where NO has been described as an inhibitor of platelet adhesion and aggregation. Since platelets influence vascular tone, are promoters of atherosclerosis, and mediators of thromboembolic complications [26,27], their hyperactivity might contribute to increased vascular reactivity associated with CsA‐induced hypertension. Other studies have demonstrated the effects of unbalanced platelet NO synthesis in hypertension [28].…”

Section: Introductionmentioning

confidence: 99%

Impairment of vascular and platelet levels of nitric oxide and cyclic guanosine‐3′,5′‐monophosphate in cyclosporin A‐induced hypertensive rats

Santiago

Reis

Almeida

et al. 2003

Fundamemntal Clinical Pharma

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The therapeutic use of the immunosuppressive agent cyclosporin A (CsA) is associated with arterial hypertension and increased risk of thromboembolism. Impaired endothelium-mediated relaxation is one of the main hypotheses explaining the CsA-induced vascular hyper-reactivity. Since nitric oxide (NO) modulates both vascular and platelet activity, we studied the effects of CsA on the levels of arterial and platelet NO as well as 3',5'-cyclic guanosine monophosphate (cGMP) levels which are influenced by NO. An animal model of CsA-induced hypertension was used. Wistar rats were treated with a clinically relevant, oral dose of 5 mg/kg CsA, daily, for 4 weeks. CsA increased both systolic and diastolic blood pressures compared to non-treated rats (P < 0.01). Nitrite, a NO metabolite, decreased in the entire aorta wall (30%, P < 0.05) and in the aorta wall without the endothelial layer (70 %, P < 0.05) in CsA-treated vs. control groups. cGMP content was also decreased in the CsA-treated group (67%, P < 0.01) vs. control. Taken together, these results suggest a defect on the endothelial NO generation, acceleration of breakdown and/or consumption of NO, as well as marked alterations directly on cGMP metabolism. Conversely, platelet nitrite and cGMP content significantly increased in the CsA-treated rats, which was also observed in in vitro studies of platelet nitrite release following CsA treatment. This suggests a platelet self-regulation mechanism against CsA-induced platelet hyper-reactivity, which, in turn, could compensate vascular impairment.

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Platelets and Hypertension

Cited by 36 publications

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Plasma Catecholamines and Adrenoceptors After Chronic Sinoaortic Denervation in Dogs

Plasma Catecholamines and Adrenoceptors After Chronic Sinoaortic Denervation in Dogs

Platelet α₂‐ and leucocyte β₂‐adrenoceptors in phaeochromocytoma: effect of tumour removal

Impairment of vascular and platelet levels of nitric oxide and cyclic guanosine‐3′,5′‐monophosphate in cyclosporin A‐induced hypertensive rats

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Platelets and Hypertension

Cited by 36 publications

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Plasma Catecholamines and Adrenoceptors After Chronic Sinoaortic Denervation in Dogs

Plasma Catecholamines and Adrenoceptors After Chronic Sinoaortic Denervation in Dogs

Platelet α2‐ and leucocyte β2‐adrenoceptors in phaeochromocytoma: effect of tumour removal

Impairment of vascular and platelet levels of nitric oxide and cyclic guanosine‐3′,5′‐monophosphate in cyclosporin A‐induced hypertensive rats

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Platelet α₂‐ and leucocyte β₂‐adrenoceptors in phaeochromocytoma: effect of tumour removal