Hypotensive effect and vascular relaxation in different arteries induced by the nitric oxide donor RuBPY.

NO donors are compounds that release NO that can be used when the endogenous NO bioavailability is impaired. The compound cis-[Ru(bpy)2(py)(NO2)](PF6) (RuBPY) is a nitrite-ruthenium, since it has a NO2 in its molecule. The aim of the present study was to evaluate the effect of RuBPY on arterial pressure, as well as on the vascular relaxation of different vascular arteries in renal hypertensive (2K-1C) and normotensive (2K) rats. We have evaluated the arterial pressure and heart rate changes as well as the RuBPY and SNP-induced relaxation (thoracic aorta, mesenteric resistance, coronary and basilar arteries). The administration of RuBPY in awake rats evoked a smaller but long lasting hypotensive effect when compared to SNP, with no increase in heart rate. The relaxation induced by RuBPY was similar between 2K-1C and 2K rats in thoracic aorta, mesenteric resistance and coronary arteries. However, the relaxation induced by RuBPY was smaller in basilar arteries from 2K-1C than in 2K. Taken together, our results show that RuBPY presents several advantages over SNP, since it does not induce hypotensive effect in normotensive animals, the hypotensive effect is slower, with no reflex tachycardia, and it is long lasting. In addition, RuBPY induces coronary artery relaxation (useful for angina) and presented only a small effect on basilar artery (may not induce headache).

The effects of gap junction modulators on the rhythmic contractions in aortas isolated from rats subjected with sinoaortic denervation.

Following sinoaortic denervation (SAD) rats present intense arterial pressure lability without sustained hypertension. This study aimed to verify the effects of heptanol (a putative gap-junction blocker) and tetraethylammonium (TEA, a putative gap-junction activator) on rhythmic contractions (RCs) and vascular reactivity in the aortas isolated from SAD and Sham-operated (SO) rats. Rhythmic contractions were observed with phenylephrine in endothelium-removed aortic rings from SAD rats. We evaluated the effects of the gap-junction modulators heptanol or TEA on the frequency and amplitude of these oscillations. Additionally, concentration-response curves were constructed to TEA and KCl and in pre-contracted arteries (with phenylephrine or KCl) to heptanol in order to verify the effects of those gap-junction modulators. Comparatively, rhythmic contractions were observed in 10/10 SAD rat aortas vs. 2/10 controls. Heptanol decreased the frequency of oscillations in a concentration-dependent manner. TEA increased the amplitude and frequency of RCs. In the experiments of concentration-response curves to TEA, the maximal contractile effect was similar in both groups, although the potency was lower in SAD than in SO rat aortas. The relaxation to heptanol was different between the groups only after pre-contraction induced by phenylephrine. Heptanol showed higher potency in SAD as compared to SO rat aortas. In conclusion, arterial pressure lability occurs only in SAD rats, and their isolated aortas exhibit intense RCs. These RCs seem to be dependent of the gap-junction communication, since these oscillations are intensified by TEA and inhibited by heptanol. After SAD, aortas are more sensitive to heptanol and less sensitive to TEA.