Plasma catecholamine modulation of alpha 2 adrenoreceptor agonist affinity and sensitivity in normotensive and hypertensive human platelets.

Hollister, Alan S.; Onrot, Jack; Lonce, Suzanna; Nadeau, John; Robertson, David L.

doi:10.1172/jci112452

Cited by 54 publications

(19 citation statements)

References 26 publications

(15 reference statements)

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“…Elevation of catecholamine in blood has been observed both in human and rat hypertension (32,33). However, it has been shown that catecholamine induced aggregation and secretion of human platelets and intensified their responses to various other stimulants (34,35), but did not induce the responses of rat platelets (36). Although our results in rats indicated that hypertension made platelets hypoaggregable in vitro, those data meant that platelet were hyperaggregable in vivo due to the hypertension.…”

Section: Discussioncontrasting

confidence: 50%

Vitamin E Did Not Prevent Platelet Activation, but Prevented Increase of Lipid Peroxides and Renal Dysfunction in DOCA-Salt Hypertensive Rats.

Umegaki¹,

Ichikawa²

1993

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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SummaryChanges in platelet aggregability patterns and lipid perox ide levels and their relationship were examined in DOCA-salt hyperten sive rats during the development of hypertension. In addition, the effect of vitamin E treatment on those changes was also investigated. The blood pressure of the hypertensive rats was 188, 201, 212mmHg on day 11, 17, and 23, respectively.In the hypertensive rats, both aggregability and granule content in platelet decreased on day 12, 18, 24, and marked decreases were observed on day 24. These data suggested the appearance of exhausted platelets, which had been already activated in vivo due to the hypertension. Marked increases in lipid peroxide levels in serum, the heart and the kidney were observed on day 24 in the hypertensive rats.Increase in serum urea nitrogen was also observed in the hypertensive rats on day 24, suggesting the dysfunction of the kidney. Vitamin E treatment did not prevent in vivo platelet activation due to hypertension, but greatly prevented the elevations of lipid peroxides in serum, the heart and the kidney, and serum urea nitrogen.These results suggested that in vivo platelet activation, an increase of lipid peroxides, and renal dysfunction occur in this order due to hypertension, and that the latter two are significantly prevented by vitamin E treatment.

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Section: Discussioncontrasting

confidence: 50%

Vitamin E Did Not Prevent Platelet Activation, but Prevented Increase of Lipid Peroxides and Renal Dysfunction in DOCA-Salt Hypertensive Rats.

Umegaki¹,

Ichikawa²

1993

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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“…Other factors such as decreased baroreceptor reflex-cardiac sensitivity, enhanced pressor responsiveness, 28 and defective a-adrenergic receptors that may mediate it 29 are probably also involved. Thus, while it is possible to deduce from the present studies a number of potential etiological factors in SS subjects, the pathogenesis of the hypertensive process in SR subjects is more obscure.…”

Section: Discussionmentioning

confidence: 99%

Plasma and urinary catecholamines in salt-sensitive idiopathic hypertension.

et al. 1988

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SUMMARY Nineteen patients with normal renin idiopathic hypertension were arbitrarily classified as salt-sensitive or salt-resistant depending on whether their mean arterial pressure did or did not increase by 8% or more when sodium intake was increased. The responses of the two subsets and of five normal subjects to sodium intakes of 9, 109, and 249 mEq/day given for 7 days were as follows: The salt-sensitive subjects retained more sodium than normal and plasma or urinary norepinephrine did not decrease when they were given a high sodium intake; urinary dopamine was normal but did not increase normally when sodium intake was increased. The salt-resistant subjects excreted sodium normally and plasma and urinary norepinephrine was decreased by 30 and 37%, respectively, when they were given a high sodium intake; urinary dopamine was supernormal and did not increase further when sodium intake was increased. Cumulative sodium retention during the high sodium intake was directly related to the percentage of change in plasma norepinephrine in the hypertensive subjects, suggesting that renal adrenergic activity was a factor in the impaired sodium excretion in the salt-sensitive patients. Cumulative sodium retention and the percentage of change hi plasma norepinephrine were inversely related to urinary dopamine in the hypertensive subjects, suggesting that increased formation of dopamine in renal and neural tissue in the salt-resistant subjects may have been responsible for the differences between the subsets hi renal and adrenergic responses to a high sodium intake. Supernormal sodium retention and a failure to suppress adrenergic activity may explain, hi part, the phenomenon of salt sensitivity of blood pressure in salt-sensitive patients and may also be factors in the pathogenesis of hypertension in this subset. (Hypertension 11: 312-319, 1988) KEY WORDS • plasma norepinephrine • urinary dopamine • blood pressure P ATIENTS with hypertension have been arbitrarily defined as salt-sensitive (SS) or saltresistant (SR) based on the response of blood pressure to manipulations of dietary sodium intake or of body fluid volume.1 " 5 Categorization of patients with idiopathic hypertension by these criteria suggests that 25 to 51 % may be SS. '• 6 Studies that compared SS and SR patients suggest that the difference between

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“…56 In addition, in human essential hypertension an inability to desensitize the a 2 -adrenergic receptor pathway has been described. 57 Finally, we have recently shown that in hypertensive patients insulin is not able to modulate reflex forearm sympathetic vasoconstriction. 58 The physiological implication of our study is that in healthy subjects the ability of insulin to modulate at the peripheral level the adrenergic-mediated reflex vasoconstriction represents a mechanism that buffers the consequences of the reflex activation of the sympathetic system induced by hyperinsulinemia.…”

mentioning

confidence: 98%

Insulin blunts sympathetic vasoconstriction through the alpha 2-adrenergic pathway in humans.

et al. 1994

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We investigated the mechanisms underlying the insulin-induced attenuation of sympathetic forearm vasoconstriction in healthy humans. In 5 subjects, we applied 20 mm Hg lower body negative pressure for 30 minutes in control conditions and during a 60-minute infusion of insulin (0.05 mU/kg per minute) in the brachiaJ artery and measured forearm norepinephrine kinetics and hemodynamics. In 11 subjects, we applied graded lower body negative pressure at 5, 10,15, and 20 mm Hg for 5 minutes each in control conditions and during the simultaneous intrabrachial administration of insulin (0.05 mU/kg per minute) (5 subjects) or insulin plus ouabain (3.5 fig/min per liter) (6 subjects) to investigate whether insulin acts through a potentiation of the vascular smooth muscle Na + ,K + -ATPase. To assess a possible effect of insulin on a specific adrenergic receptor pathway, in a further study group we evaluated (1) the forearm vascular response to intrabrachial infusion of the a,-adrenergic receptor agonist phenylephrine (0.5, 1, and 2 jig/kg per minute; n=7) and of the a 2 -adrenergic receptor agonist BHT-933 (0.5, 1, 2, and 4 jtg/kg per minute; n=9), and (2) the effects of intra-arterial infusion of prazosin (0.5 ^g/100 mL per minute) alone or combined with insulin on the forearm vascular response to

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Plasma catecholamine modulation of alpha 2 adrenoreceptor agonist affinity and sensitivity in normotensive and hypertensive human platelets.

Cited by 54 publications

References 26 publications

Vitamin E Did Not Prevent Platelet Activation, but Prevented Increase of Lipid Peroxides and Renal Dysfunction in DOCA-Salt Hypertensive Rats.

Vitamin E Did Not Prevent Platelet Activation, but Prevented Increase of Lipid Peroxides and Renal Dysfunction in DOCA-Salt Hypertensive Rats.

Plasma and urinary catecholamines in salt-sensitive idiopathic hypertension.

Insulin blunts sympathetic vasoconstriction through the alpha 2-adrenergic pathway in humans.

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