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Patients and animal models of arterial hypertension are characterized by structural and functional abnormalities of the coronary microcirculation. Using a translational approach, we ascertained whether antihypertensive treatment can reverse microvascular remodelling and improve myocardial perfusion.

Nitrendipine is a dihydropyridine calcium antagonist suggested to be a new drug for first-line antihypertensive therapy, possibly active in once-daily administration. In the present study the acute and long-term hypotensive effects of nitrendipine have been evaluated in comparison with those of atenolol in a randomized, double-blind, clinical trial. Twenty-four patients have been studied, and the effects of treatment have been evaluated both at rest and during psychological and physiological stresses. Hemodynamic non-invasive parameters have also been obtained, at rest and during mental arithmetic tests, by a continuous-wave Doppler technique. Preliminary results about the first 13 consecutive patients are reported here. Nitrendipine induced a highly significant acute hypotensive effect (2 h after drug administration), whereas no effect was observed for atenolol except for heart rate. During chronic treatment (5 weeks), nitrendipine showed less hypotensive effect than atenolol when BP values 24 h after the last administration were analyzed, but significantly more effect when values obtained 2 h after drug administration were evaluated. These findings confirm that nitrendipine is effective in decreasing blood pressure, but the once-daily administration may not bring about the maximum effect in all patients. Interesting aspects of this drug, which make the clinical use of this compound safe, are represented by apparent lack in tolerance and rebound, and by the moderate increase in cardiac output associated with the treatment.

Suppression of the renin-angiotensin system (RAS) by angiotensin converting enzyme (ACE) inhibition may induce renal failure in patients with bilateral renal artery stenosis. Recent scintigraphic studies with the glomerular tracer technetium-99m-diethylenetriaminepenta-acetate (99m-Tc DTPA) indicate that in patients with unilateral renal artery stenosis, glomerular filtration rate (GFR) may be markedly reduced in the affected kidney after inhibition of ACE. This finding reflects the important role of the RAS in maintaining GFR (by increasing postglomerular resistance) in states of low renal perfusion pressure. Preliminary observations suggest that this scintigraphic test might be useful in the detection of renovascular hypertension.

We studied the influence of hypertensive (HT) serum on human umbilical vein endothelial cell (HUVEC) and on human umbilical artery smooth muscle cell (HUASMC) proliferation. We also tested the possible influence of the HT serum on vasoconstrictor substances released by HUVECs.Pools of HT and normotensive (NT) sera were collected and used to supplement cell culture medium. Both HUVECs and HUASMCs were conditioned with culture media supplemented with either HT or NT sera. After conditioning, both types of cells were tested for proliferative capacity. Under the same experimental conditions the HUVEC conditioned medium was assayed for angiotensin II (AII) and endothelin 1 (ET,). All and ET, were also assayed after acute exposure to HT serum of HUVEC preconditioned with NT serum.Our results showed that HUVEC and HUASMC conditioned with HT serum substantially enhanced cell proliferation. Preconfluent HUVECs conditioned with HT serum showed higher levels of AZZ and lower levels of ET1 compared with the controls in NT serum. These differences were reduced at confluence. HUVECs conditioned with NT serum showed a transient increase in ET1 levels after acute exposure to HT serum.We suggest that serum from hypertensive patients is able to modulate vascular cell proliferation and possibly the production of vasoactive substances in culture.