[Central and peripheral hemodynamic effects of nifedipine administered orally and sublingually in essential arterial hypertension]. / Effets hémodynamiques centraux et périphériques de la nifédipine administrée par voie oral et par voie sublinguale dans l'hypertension artérielle essentielle.

The central and peripheral haemodynamic effects of the administration of 10 mg nifedipine sublingually in 6 patients with essential hypertension were compared with those observed after the administration of one 20 mg slow release tablet of nifedipine in 7 other hypertensive patients of the same age. The circulatory effects in the forearm were studied by pulsed Doppler velocimetry which allowed simultaneous measurement of the diameter of the brachial artery and of the velocity of blood flow. Both forms of administration significantly reduced the blood pressure by a significant reduction in total peripheral resistance. This reduction in total peripheral resistance was more significant (p less than 0.001 vs p less than 0.01) and more rapid with sublingual administration and was associated with a greater increase in heart rate and cardiac output. Both forms of administration induced an increase in brachial arterial blood flow due to a simultaneous increase in vessel calibre and velocity of blood flow. The results of this study show that both forms of administration act directly on the vessel wall of the arterioles and great arteries leading to a fall in blood pressure associated with an increase in peripheral blood flow. Sublingual nifedipine would seem to be the drug of choice for the treatment of hypertensive crises, whilst the slow release preparation with its lesser baroreflex stimulation would appear better suited for the long-germ treatment of essential hypertension.

The effect of acute and chronic nicardipine therapy on forearm arterial haemodynamics in essential hypertension.

By using simultaneous recording curves obtained with pulsed Doppler velocimetry and strain gauge mechanography, forearm arterial haemodynamics were studied in 26 patients with mild to moderate essential hypertension. Fifteen patients received a single oral dose of nicardipine 40 mg, and 11 patients were treated with nicardipine 30 mg three times daily for 3 months. In both groups of patients there was a similar and significant (P less than 0.001) reduction in mean, systolic, and diastolic pressures. There was a slight increase in heart rate (P less than 0.05) after the single dose, but no change after 3 months of treatment. The diameter, blood velocity, and blood flow of the brachial artery increased significantly in both treatment groups. The decrease in forearm vascular resistance was significant for both treatment groups. Brachial artery compliance increased (P less than 0.01) and characteristic impedance decreased (P less than 0.01) after both single-dose and long-term therapy with nicardipine. In patients who received nicardipine for 3 months, there were close correlations between the baseline serum calcium level and the percent change in vascular resistance (r = -0.73, P less than 0.01), blood flow (r = 0.89, P less than 0.001), and blood velocity (r = 0.91. P less than 0.001) of the forearm. No correlation was found between the baseline serum calcium and the change in arterial pressure. This study provided evidence that the blood-pressure-lowering effect of nicardipine was accompanied by a direct vasodilatory action in the small and large arteries of the forearm. An increase in peripheral blood flow with concomitant improvement of arterial compliance are the consequences of these arterial actions.

Comparison of oral MK 421 and propranolol in mild to moderate essential hypertension and their effects on arterial and venous vessels of the forearm.

The efficacy of MK 421 and propranolol was compared in 48 patients with mild to moderate hypertension. Each patient was randomly assigned to receive 1 of the drugs for 12 weeks. Additionally, a subgroup of 28 patients underwent studies of forearm arterial and venous circulation by means of pulsed Doppler and mercury-in-silastic plethysmography. Both drugs reduced supine and standing blood pressure (BP) (p less than 0.001). Propranolol reduced heart rate (p less than 0.001), while MK 421 did not change it. Brachial artery diameter, blood velocity and flow increased after MK 421 (p less than 0.001), but were not changed after propranolol therapy. Forearm vascular resistance decreased after MK 421 (p less than 0.001) and after propranolol (p less than 0.05). Forearm venous tone was unaffected on MK 421, but increased after propranolol (p less than 0.01). Thus, in moderate hypertension, 3 months of treatment with MK 421 or propranolol similarly decrease BP, but affect the forearm circulation differently: MK 421 dilates both the brachial artery and the arterioles of the forearm, but does not affect the venous vessels, and propranolol causes little arterial change but increases the forearm venous tone.

Large arteries in hypertension: acute effects of a new calcium entry blocker, nitrendipine.

Acute effects of a new calcium entry blocker, nitrendipine, on large arteries of the forearm were studied by using arterial pulse strain gauge mecanography and pulsed Doppler velocimetry of the brachial artery in 13 mild to moderate essential hypertensive patients. Ninety minutes after nitrendipine ingestion, patients exhibited significant decreases in blood pressure without changes in heart rate; increases in brachial artery diameter and decreases in brachial to radial pulse wave velocity; increases in arterial compliance and decreases in characteristic impedance; and increases in brachial artery blood velocity and flow and decreases in forearm vascular resistance. Lastly, amplitude of pulse pressure was decreased by nitrendipine and negatively correlated to the level of arterial compliance. These results suggest that nitrendipine exerts a direct benefit effect on the hypertensive large arteries whose two main consequences are a decrease in pulsatility of arterial pressure and an increase in arterial flow.