Oral load of tyrosine or L-dopa and plasma levels of free and sulfoconjugated catecholamines in healthy men.

The levels of free and sulfoconjugated catecholamines were measured in the plasma of fasting, recumbent normal subjects before and after an oral load of the catecholamine precursors tyrosine or L-dopa. Basal values of sulfoconjugated catecholamines, measured in plasma samples diluted 1:100 were 7998 +/- 540 pg/ml for dopamine sulfate, 2938 +/- 281 pg/ml for norepinephrine sulfate, and 2958 +/- 288 pg/ml for epinephrine sulfate (n = 37 tests in 15 men); these basal values are higher than those reported previously. Neither free nor sulfoconjugated catecholamine concentrations were changed by a tyrosine load (100 mg/kg) that induced a doubling of the plasma tyrosine level or by a meal low in phenylalanine and tyrosine (but otherwise supplying constituents of normal nourishment) that induced a greater than 50% reduction in the plasma tyrosine concentration. After an oral load of L-dopa (125 mg) the following were observed. (1) An extremely large increase (greater than 100-fold) in dopamine sulfate levels was noted, an increase that was less marked in the same subjects given L-dopa (125 mg) plus the peripheral dopa-decarboxylase inhibitor carbidopa (12.5 mg); as expected, free dopamine concentration also was increased. (2) Neither free nor sulfoconjugated norepinephrine concentrations were altered. (3) Epinephrine sulfate but not free epinephrine concentration was increased (more than ten-fold) after L-dopa ingestion alone; this result was unexpected and has to be confirmed before considering its physiological meaning, if any.

Cardiac hypertrophy and aortic compliance after calcium channel antagonism in hypertension.

Calcium antagonists are potent vasodilators. They improve arterial compliance by their action at the level of the large arteries. Several experimental and clinical studies have shown decreases of varying magnitudes in hypertension-induced cardiac hypertrophy after long term treatment. It appears that the mechanisms of this reduction in cardiac mass are complex. As arterial compliance is one of the determinants of left ventricular hypertrophy in hypertension, it may be considered that an improvement in cardiac mass can result not only from the blood pressure reduction but also from the increase in arterial compliance associated with calcium antagonist treatment in essential sustained hypertension.

Antihypertensive therapy and wave reflections.

Studies of pulsatile arterial hemodynamics have emphasized that the pulsatile component of pulse pressure has two important characteristics: (i) it increases from central to peripheral arteries for a similar value of mean arterial pressure, and (ii) it is dominantly influenced by the amplitude and timing of the backward pressure wave. Although these important aspects of wave reflections have been poorly investigated in the field of hypertension, they may be easily studied noninvasively in humans on the basis of the analysis of the pulse wave contour of carotid and aortic blood pressure. Increased wave reflections returning toward the thoracic aorta during systole may have deleterious consequences on the structure and function of the heart. Some (but not all) antihypertensive drugs may contribute to decrease and/or to delay wave reflections in association with blood pressure reduction.

Effects of antihypertensive drugs on large artery compliance.

The changes in arterial compliance following drug treatment have been studied mainly in hypertension. Physiologically, reduced arterial compliance independently affects blood pressure through an increase in systolic pressure and a decrease in diastolic pressure at any given value of mean arterial pressure. This review summarizes the pharmacological studies performed in recent years on the ability of antihypertensive drugs to modify arterial compliance. For the same decrease in mean arterial pressure, antihypertensive drugs may have differential effects improving arterial compliance (calcium channel blockers, converting enzyme inhibitors, alpha-blockers and some beta-blockers) or causing no change (dihydralazine, diuretics, propranolol) with resulting consequences on cardiac structure and function.

[Acute ischemia of the lower limbs in nephrotic syndrome in a young woman]. / Ischémie aiguë des membres inférieurs au cours d'un syndrome néphrotique chez une jeune femme.

A thirty-year-old woman, who had onset of nephrotic syndrome during the last part of her pregnancy, experienced recurrent acute ischemia of both lower limbs, leading to three conservative surgical procedures one month after delivery. Investigations disclosed no cause of embolism and were suggestive of thrombosis. The arteriography showed a diffuse reduction in diameter of the aorta and iliac vessels without localised stenosis or other vascular lesions. This complication is presumably related to several factors associated with the reduction in arterial diameter: hypovolemia, hyperfibrinemia, hyperlipidemia and abnormalities of hemostasis.