aortic coarctation/аргинин

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Elevated arginine vasopressin and lowered atrial natriuretic factor associated with hypertension in coarctation of the aorta.

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Impairment of humoral and neural regulation of blood pressure may contribute to preoperative and postoperative hypertension in coarctation of the aorta and may also affect the release of vasopressin and atrial natriuretic factor. Because vasopressin and atrial natriuretic factor have potent

Blockers of the L-arginine-nitric oxide-cyclic GMP pathway facilitate baroreceptor resetting.

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We investigated the role of nitric oxide on rapid (25- and 40-minute) baroreceptor resetting during the onset of acute hypertension in rats treated with NG-nitro-L-arginine, an inhibitor of nitric oxide synthesis, and methylene blue, an inhibitor of guanylate cyclase. The effect of treatment with

[The effect of L-arginine on the development of experimental cardiac hyperfunction and hypertrophy].

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It was shown, in the investigation on laboratory rats with experimental aortic coarctation, the development of myocardial hyperfunction and hypertrophy before and under the influence of the N kappa--predecessor--L-arginine. It was found that on the 14-20 day after coarctation weight of the heart,

Enhanced responses to L-arginine in aortic rings from rats with angiotensin-dependent hypertension.

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We contrasted, in normotensive and hypertensive rats, the effect of L-arginine on isometric tension of phenylephrine-contracted rings of aorta bathed in Krebs' bicarbonate buffer on cyclic guanosine monophosphate content of aortic rings and on blood pressure. L-Arginine had no effect on isometric

Contribution of constrictor prostanoids to the calcium-dependent basal tone in the aorta from rats with aortic coarctation-induced hypertension: relationship to nitric oxide.

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Rings of thoracic aortae taken from rats made hypertensive by aortic coarctation express a calcium-dependent basal tone. We investigated whether this basal tone is mediated by prostanoids. To this end, we contrasted the effects of indomethacin, an inhibitor of cyclooxygenase, and of ifetroban, an

Acute aortic coarctation hypertension: role of vasopressin and angiotensin II.

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The role of vasopressin (AVP) and angiotensin II (ANG II) in the onset of acute (45 min) aortic coarctation hypertension was studied in conscious rats. Changes in mean carotid pressure (MCP) and heart rate (HR) were measured in four groups of rats. Control rats presented a hypertensive response that

Role of nitric oxide in ginsenoside Rg(1)-induced protection against left ventricular hypertrophy produced by abdominal aorta coarctation in rats.

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Ginsenoside Rg(1) (Rg(1)), one of the active components of Panax ginseng, has been reported to promote endogenous nitric oxide (NO) production in some tissues, and to inhibit left ventricular (LV) hypertrophy in rats. This study aimed to investigate whether Rg(1)-induced inhibition of rat LV

Mechanical and neuro-humoral factors in acute aortic coarctation hypertension.

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The hemodynamic responses and the role of renal nerves in the physiopathogenesis of acute (45 min) aortic coarctation hypertension were studied in conscious rats. The hemodynamic responses elicited by aortic constriction in intact and bilaterally nephrectomized rats were analyzed by means of

Long-term inhibition of nitric oxide synthase potentiates effects of anandamide in the rat mesenteric bed.

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In rat isolated mesenteric beds, anandamide induced a concentration-dependent reduction (0.01-50 microM) of the contractile responses elicited by bolus administration of noradrenaline. The anandamide-induced reductions of noradrenaline responses were unmodified by the in vitro exposure to the nitric

Vascular responsiveness to nitric oxide synthesis inhibition in hypertensive rats.

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We contrasted in normotensive and hypertensive rats the effect of inhibition of nitric oxide synthesis on isometric tension development by aortic rings bathed in Krebs' bicarbonate buffer. NG-Nitro-L-arginine methyl ester (L-NAME) (3 x 10(-4) mol/L) increased tension (82 +/- 11% of the response to

Involvement of nitric oxide and potassium channels in the reduction of basal tone produced by blockade of thromboxane A2/prostaglandin H2 receptors in aortic rings of hypertensive rats.

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This study was designed to investigate involvement of potassium channels in the action of nitric oxide facilitating reduction of basal tone by thromboxane A2/prostaglandin H2 receptor blockade with ifetroban in rings of thoracic aorta taken from rats with aortic coarctation-induced hypertension.

Nitric oxide and the depressor response to angiotensin blockade in hypertension.

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We investigated the contribution of nitric oxide to the short-term blood pressure reduction caused by interruption of the renin-angiotensin system in angiotensin-dependent hypertension. The blood pressure of rats made hypertensive by coarctation of the aorta between the renal arteries at their

Endocrine dysfunction in a patient with PHACE syndrome, including port-wine stain of the right periorbital area.

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OBJECTIVE To report a case of PHACE syndrome-Posterior fossa brain abnormalities, Hemangioma (usually facial), Arterial anomalies, Coarctation of the aorta along with cardiac defects, and Eye abnormalities-in a 16-year-old female patient with a port-wine stain of the right periorbital area present

Peripheral hypertension and alterations in pulmonary vascular regulation.

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We have recently reported in normal isolated-perfused rat lungs that low basal tone appears to be regulated by nitric oxide (NO)-dependent and -independent mechanisms of soluble guanylate cyclase activation. In this study, we examined the role of NO in the regulation of pulmonary artery (PA) tone

[Role of nitric oxide in the modulation of the vascular response to angiotensin II in hypertensive rats].

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Vasorelaxant activity induced by nitric oxide has been associated with a regulator activity on the blood pressure. In the present study we evaluated the nitric oxide contribution of the regulation of angiotensin II-induced vasoconstriction in normotensive rats and aortic coarctation-induced

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