1,721,285 research outputs found
Heterogeneous interference of nicardipine, verapamil, and diltiazem with forearm arteriolar responsiveness to adrenergic stimulation in hypertensive patients.
No full textThe interference of intraarterial nicardipine, verapamil, and diltiazem with the forearm vascular response to graded exogenous norepinephrine was evaluated in hypertensive patients. Nicardipine antagonized the vasoconstrictor effect of norepinephrine in a dose-dependent manner, whereas verapamil was ineffective, suggesting that functional alpha-adrenergic antagonism may participate in the vasodilatory and possibly the antihypertensive effect. Nicardipine also blunted the vasoconstriction to lower-body negative pressure and the action of angiotensin II administered intraarterially. Despite a comparable increase in basal forearm flow, verapamil was less potent than nicardipine in inhibiting vasoconstriction after both stimuli. Therefore nicardipine suppressed preferentially regional vascular reactivity, probably by blockade of the influx of extracellular calcium in response to receptor activation, because both alpha-adrenergic and angiotensin II receptor-mediated vasoconstrictor responses were attenuated. At variance with both nicardipine and verapamil was potentiation of the responses to norepinephrine after the administration of diltiazem. Because intraarterial propranolol abolished that potentiating action and the local vasodilatation to isoproterenol was clearly reduced, diltiazem probably interfered also with beta-adrenergic receptor-mediated vasorelaxing mechanisms in human forearm arterioles. The data further stress the heterogeneity of calcium channel blockers in humans
Analisi dei metodi e delle condizioni per il calcolo dei carichi su velivoli a controllo attivo
No full textReactive hyperemia during short-term blood flow and pressure changes in the hypertensive forearm.
No full textThe aim of the present study was to further validate our method for the determination of minimal forearm vascular resistance after ischemia (13 min arterial occlusion and 1 min hand exercise) in patients with hypertension. This parameter, calculated as the ratio of mean blood pressure (intra-arterial recordings on the experimental side) to forearm blood flow (strain-gauge venous plethysmography), was measured basally and after either increasing (through unrelated vasodilators such as sodium nitroprusside or the calcium antagonist nicardipine in six mild-to-moderate uncomplicated hypertensives) or decreasing (norepinephrine, n = 4) flow without changes in systemic pressure. In spite of the divergent starting flow values, minimal postischemic forearm vascular resistance was unchanged, indicating a lack of relationship with functional arteriolar tone and the achievement of maximal dilatation. In two additional groups of patients, systemic arterial pressure was decreased by approximately equipotent oral doses of either nifedipine, a calcium antagonist (n = 6), or captopril, an angiotension converting enzyme inhibitor (n = 5). Under these conditions, minimal forearm vascular resistance was unchanged from pretreatment values, suggesting that local autoregulatory mechanisms were overridden during the reactive hyperemia, and that the vessel lumen was dependent on the distending pressure. Overall, the data show that our experimental conditions are suitable for measuring minimal forearm vascular resistance as a functional correlate of the morphological status of systemic arterioles in arterial hypertension
Sympathetic vasoconstriction as a mechanism of action of ouabain in forearm arterioles of hypertensive patients.
No full text1. The interaction of ouabain, a Na+/K+ adenosine 5'-triphosphatase inhibitor, with sympathetic mechanisms of vasoconstriction, as well as its possible site(s) of action, were investigated in forearm arterioles of patients with uncomplicated hypertension. 2. Intra-arterial infusion of ouabain per se decreased forearm blood flow without changes in systemic arterial pressure or contralateral flow. However, the vasoconstrictor effect of the glycoside was abolished after local pretreatment with either phentolamine, a competitive alpha-adrenoceptor antagonist, or bretylium tosylate, a neurotransmitter blocker. 3. To exclude a non-specific effect due to the vasodilatation, a similar protocol was performed using histamine, which acts independently of sympathetic mechanisms. The vascular effect of ouabain was maintained in spite of histamine-induced increases in forearm blood flow even greater than those obtained from either blocker. 4. To discriminate between pre- and post-synaptic site(s) of action of ouabain, exogenous noradrenaline was infused intra-arterially after inactivation of local neurotransmitter release by bretylium, thus causing direct postsynaptic vascular alpha-adrenoceptor stimulation. Under these conditions, noradrenaline decreased forearm blood flow irrespective of the presence or absence of ouabain. 5. Thus, local sympatholysis by drugs acting on different levels of the sympathetic neuroeffector junction abolished the effect of ouabain, whereas histamine did not influence it. The data provide positive evidence for an effect of ouabain on sympathetically mediated vasoconstriction. This action is apparently not exerted at a postsynaptic site but possibly by enhancing neurotransmitter release. 6. If a circulating endogenous ouabain-like Na+/K+ adenosine 5'-triphosphatase inhibitor is relevant to the development of hypertension in man, it might act through a similar mechanism
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Calcium entry blockade and alpha-adrenergic vascular reactivity in human beings: differences between nicardipine and verapamil.
No full textThe interference by two unrelated calcium entry blockers, nicardipine and verapamil, with the forearm vascular response to graded exogenous norepinephrine was evaluated in two groups (n = 6 each) of patients with uncomplicated hypertension. Drugs were infused into the brachial artery at systemically ineffective rates and forearm blood flow was measured by venous plethysmography. Nicardipine (1 microgram/dl forearm tissue/min) relaxed forearm arterioles and antagonized the vasoconstrictor effect of norepinephrine, whereas verapamil (1 microgram/dl forearm tissue/min) was ineffective, although vasodilating to a comparable extent. Therefore, functional alpha-antagonism may contribute to the vasodilating and, possibly, the antihypertensive effect of nicardipine but, apparently, not verapamil. The data further stress the heterogeneity of calcium channel entry blockers even in human beings
Climatologia e idrologia nel bacino del Torrente Roglio (Val d'Era-Toscana) in relazione ai processi morfogenetici in atto
No full textThe renin-angiotensin-aldosterone system and blood pressure during oxprenolol treatment in hypertensive patients pretreated with diuretics.
No full textThe interrelationship between PRA, urinary aldosterone excretion, and blood pressure was studied in 11 patients with essential hypertension while receiving a diuretic (1st week) and subsequently a diuretic + oxprenolol (2nd week). The diuretic reduced blood pressure and body weight but increased PRA and aldosterone. Oxprenolol reduced PRA on the 1st day but to a lesser extent on the 7th day. Blood pressure was decreased 1 day after oxprenolol administration, but to a greater extent on the 7th day. Blood pressure decrements were independent of renin suppression, but directly correlated to aldosterone changes. These data suggest that the hypotensive effect of oxprenolol in patients receiving diuretic treatment is independent of its suppression of renin. Aldosterone suppression may instead contribute to the hypotensive effect of the drug
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