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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.

Echocardiographic determinations, left ventricular mass-volume ratio (M/V), left ventricular end-systolic stress (ESS), carotidofemoral pulse wave velocity (PWV), and brachial artery compliance (BAC), deduced from pulsed Doppler measurements and from the Bramwell-Hill equation, were evaluated in 20 patients with sustained essential hypertension in comparison with 20 control subjects of the same age and sex. In hypertensive patients, M/V ratio, ESS, and PWV were significantly increased while BAC was reduced. In the overall population, ESS was directly correlated with PWV (r = 0.73), and M/V ratio was significantly correlated with PWV (r = 0.60), BAC (r = -0.70), and systolic arterial pressure (r = 0.71). No comparable results were observed with diastolic arterial pressure. PWV was unchanged after cadralazine, a dihydralazine-like substance, and was decreased with the same blood pressure reduction following nitrendipine, a new calcium-blocking agent. These results suggest that: (1) the distensibility of large arteries plays an important role in the maintenance of cardiac hypertrophy in hypertension, and (2) antihypertensive drugs may act differently on arterial distensibility with possible consequences on ESS and reversion of left ventricular hypertrophy.

Brachial artery haemodynamics, including arterial diameter, blood flow velocity, blood flow and compliance of the brachial artery may be evaluated non-invasively in man, using pulsed Doppler methods. In patients with sustained untreated essential hypertension, brachial artery diameter is increased, blood flow is normal and arterial compliance is reduced independently of the level of blood pressure. Converting enzyme inhibition may reverse the large artery abnormalities, causing an increase in arterial diameter, blood flow and arterial compliance both in acute and long-term investigations. These changes in large arteries may contribute towards improved cardiovascular morbidity and less mortality in treated hypertensive patients.

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.

The brachial artery diameter and blood flow rate were measured by pulsed Doppler velocimetry in 9 healthy subjects and 24 patients of the same age group with borderline hypertension. To evaluate the results, the patients were divided into two groups according to their cardiac output: high cardiac output group (i.e. patients whose cardiac output was superior to the mean +/- 2 S.D. value in the control population), and normal cardiac output group (i.e. cardiac output lower than that value). Patients in both groups were of the same age and had the same level of blood pressure. The brachial artery diameter and blood flow rate values were the same in the normal cardiac output group and in the control population. However, these values were significantly higher in patients with high cardiac output than in controls (P less than 0.05 and P less than 0.001) and in patients with normal cardiac output (P less than 0.01). These results suggest that the haemodynamic profile in the brachial artery is not the same in all patients with borderline hypertension: there was a tendency to vasoconstriction in patients with normal cardiac output, whereas the brachial artery was clearly dilated in patients with high cardiac output.

Common carotid blood flow has been measured using pulsed Doppler techniques in hypertensive patients over 45 years of age, with and without stenosis of the internal carotid artery. In hypertensive patients without stenosis, arterial diameter remained within the normal range, whereas blood flow velocity and blood flow were significantly reduced. Vascular resistance was significantly increased but did not change markedly after administration of the vasodilating drug isosorbid dinitrate. Patients with hypertension and stenosis of the internal carotid artery were compared with two different populations used as controls: In comparison with hypertensive patients without stenosis of the internal carotid artery, both arterial diameter and blood flow velocity were reduced, leading to a more pronounced decrease in blood flow; and in comparison with normotensive patients with stenosis of the internal carotid artery, common carotid blood flow was more reduced at any degree of stenosis. In a subset of patients, blood flow returned toward normal ranges after endarterectomy. The study suggested that in patients with hypertension without stenosis of the internal carotid artery, the decrease in blood flow is due to a decrease in blood flow velocity with normal arterial diameter despite the elevated blood pressure, and in patients with hypertension and stenosis of the internal carotid artery, blood flow was more reduced than in the normotensive patients with stenosis of the internal carotid artery, suggesting that caution must be taken with indications of antihypertensive treatment.

The haemodynamic pattern of the common carotid artery was studied in men with sustained essential hypertension using pulsed Doppler methods before and after administration of vasodilating drugs. Captopril produced both a fall in vascular resistance and an increase in arterial diameter of the common carotid artery. Isosorbide dinitrate increased markedly the arterial diameter but did not change vascular resistance. Nitrendipine decreased vascular resistance with no change in the arterial diameter. In the common carotid circulation of patients with essential hypertension, vasodilating drugs may either dilate small arteries (nitrendipine), large arteries (isosorbide dinitrate), or both (captopril).

As demonstrated in hypertensive humans on the basis of non-invasive Doppler methods, converting enzyme inhibitors (CEI) dilate not only small arteries but also large arteries, particularly in the brachial and the carotid circulations. The dilating effect of CEI on large arteries is associated with an enhancement of systemic and brachial arterial compliance, implying a particular action of the drug on arterial smooth muscle. Converting enzyme inhibitors are thus able to reverse the reduced arterial compliance observed in patients with essential hypertension.