This work aimed to explore the cardiovascular effects induced by freeze-dried juice from Syzygium jambolanum (Lam.) DC fruits (JSJ). JSJ presented high polyphenol content and steroids. HPLC analysis revealed that 2,5-dihydroxybenzoic and caffeic acid were present in higher amounts in the JSJ extract. In rat, JSJ induces hypotension and vasodilatation in mesenteric arteries, with or without vascular endothelium. JSJ-mediated vasodilation response against contractions induced with KCl (60 mM) depolarizing solution was significantly lower than the responses induced by JSJ when evaluated against phenylephrine-induced contractions. To investigate the involvement of potassium channels we used Tyrode's solution with KCl (20 mM) or tetraethylammonium (1.0, 3.0, or 5.0 mM). In these conditions JSJ-induced effects were significantly attenuated. To investigate the potassium channel subtypes involved in the response, we used 4-aminopyridine, glibenclamide, BaCl2, and iberiotoxin. In the presence (simultaneous) of different potassium channel blockers we observed a significant attenuation of JSJ-induced effect. Inhibition was also observed when using BaCl2, glibenclamide, or 4-aminopyridine, separately. However, incubation with iberiotoxin did not promote changes in either maximum effect, or potency. We also evidenced a discrete participation of CaV channels in the JSJ-induced vasorelaxant effect. In addition, patch-clamp studies demonstrated that JSJ could activate potassium channels. In conclusion, JSJ promotes hypotension and vasorelaxation in rats, involving, at least, the activation of potassium channels.

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Carvacrol is a monoterpene found in essential oils from various plants. Several pharmacological properties have already been described for carvacrol, including antimicrobial, anti-inflammatory, anticarcinogenic, antioxidant, vasorelaxant and hypotensive activities. The present study evaluated the effect of carvacrol on hypertensive rats with erectile dysfunction. Twelve-week-old spontaneously hypertensive rats (SHR) were treated with vehicle, carvacrol (50 or 100 mg/kg/day) or sildenafil (1.5 mg/kg/day), intragastrically, for four weeks. Wistar Kyoto (WKY) rats were used as the normotensive controls. All substances tested reduced systolic blood pressure during the treatment period. The intracavernosal pressure/mean arterial pressure ratio of the hypertensive rats was improved by carvacrol and sildenafil treatments. In isolated rat corpora cavernosa, the acetylcholine- and SNP-induced relaxation responses were significantly increased by carvacrol or sildenafil treatments. In SHR corpora cavernosa, treatment with carvacrol attenuated the hypercontractility induced by phenylephrine or electrical field stimulation. Phe-induced hypercontractility in the presence of tempol was not altered when compared to the response induced by carvacrol alone. In rat corpora cavernosa fluorescence intensity emitted by the DHE probe was significantly reduced in SHR treated (carvacrol or sildenafil) groups when compared to that emitted in the SHR-CTL. This study showed that carvacrol improves the erectile function of hypertensive rats and reduces endothelial dysfunction, smooth muscle cell hypercontractility and superoxide anion generation.

Assays in vitro and in vivo were performed on extract from roots and leaves from the Valeriana prionophylla Standl. (VPR and VPF, resp.). In phenylephrine (1 μM) precontracted rings, VPR (0.01–300 μg/mL) induced a concentration-dependent relaxation (maximum response (MR) = 75.4 ± 4.0%, EC50 = 5.97 (3.8–9.3) μg/mL, n = 6]); this effect was significantly modified after removal of the endothelium (EC50 = 39.6 (27.2–57.6) μg/mL, P < 0.05). However, VPF-induced vasorelaxation was less effective compared to VPR. When rings were preincubated with L-NAME (100 μM) or indomethacin (10 μM), the endothelium-dependent relaxation induced by VPR was significantly attenuated (MR = 20.9 ± 2.3%, 34.2 ± 2.9%, resp., P < 0.001). In rings denuded endothelium, precontracted with KCl (80 mM), or in preparations pretreated with KCl (20 mM) or tetraethylammonium (1 or 3 mM), the vasorelaxant activity of VPR was significantly attenuated (MR = 40.0 ± 8.2, n = 5; 50.5 ± 6.0%; 49.3 ± 6.4%; 46.8 ± 6.2%; resp., P < 0.01). In contrast, neither glibenclamide (10 μM), barium chloride (30 μM), nor 4-aminopyridine (1 mM) affected VPR-induced relaxation. Taken together, these results demonstrate that hypotension induced by VPR seems to involve, at least in part, a vascular component. Furthermore, endothelium-independent relaxation induced by VPR involves K+ channels activation, most likely due to BKCa channels, in the rat superior mesenteric artery.