The results of the present study suggest that melatonin and n-acetylcysteine improve the baroreflex response in SHR in correlation with the antioxidant effects of these substances.

The present study showed that melatonin exerted a bradycardic and an antihypertensive action in SHR. The enhancement by melatonin of the endothelium-dependent vasodilation (Ach and/or A23187) in mesenteric artery and aorta from SHR and WKY rats and the higher increase in MAP following L-NAME treatment in melatonin-treated SHR suggest the contribution of an improved vascular NOS pathway activity in the hypotensive effect of melatonin.

These results suggest that NAC and melatonin decreased the MAP and heart rate and improved the chronotropic response to isoproterenol in SHRs, in association with an inhibition of sympathetic activity and the restoration of cardiac beta-adrenoceptor function.

The increase in NO-mediated vasodilator tone and the possible decrease in adrenergic vasoconstriction induced by NAC treatment in SHR could explain the hypotensive effect of NAC in this model of hypertension.

4 The effect of BK was not affected by diclofenac (1 fiM), a cyclo-oxygenase inhibitor. Bisindolylmaleimide (1 gLM), a protein kinase C inhibitor, significantly reduced the facilitatory effect of BK (10 nM), angiotensin II (0.3 p4M) and phorbol dibutyrate (0.1 and 1 f1M) but not of fenoterol (1 fM). 5 The results suggest that BK enhances noradrenaline release via a prejunctional B2 kinin receptor in the rat atrium. The effect appears to involve protein kinase C as a second messenger.