Coronary and carotid artery structure was studied in rats in order to analyze the processes in the cardiovascular system in NO-deficient hypertension model. Long-term inhibition of NO synthase was induced by L-nitro arginine methyl ester (L-NAME, 50 mg/kg/day p.o.) for a period of 8 weeks. An increase in blood pressure and heart/body weight ratio confirmed the reliability of the model. The wall thickness as well as the calculated wall area of the coronary artery increased by 70 % and 50 %, respectively, in comparison to control vessels. The wall thickness and the calculated wall area of the carotid artery increased by 73 % and 70 %, respectively. Further analysis indicated that both the tunica intima and tunica media in the coronary and the carotid artery increased quantitatively in a similar manner. Remarkable differences were found in the contribution of cellular and noncellular components in the tunica media of the coronary and carotid arteries of experimental animals. The calculated extracellular area increased by 116 % in comparison to the control coronary artery and by 97 % in comparison to the control carotid artery. The increase in extracellular matrix of the tunica media of coronary and carotid arteries seems to be basic cause of the remodelling of the vessels studied.
We investigated the effect of pertussis toxin (PTX) on hypotensive response induced by acetylcholine (ACh) and bradykinin (BK) and on noradrenaline (NA)-induced pressor response in spontaneously hypertensive rats (SHR). Fifteen-week-old Wistar rats and age-matched SHR were used. Half of SHR received PTX (10 μg/kg/i.v.) and the experiments were performed 48 h later. After the anesthesia the right carotid artery was cannulated in order to record blood pressure (BP). The hypotensive response to ACh was enhanced in SHR compared to Wistar rats. After pretreatment of SHR with PTX the hypotensive response to ACh was reduced compared to untreated SHR and it was also diminished in comparison to Wistar rats. Similarly, the hypotensive response to BK was also decreased after PTX pretreatment. The pressor response to NA was increased in SHR compared to Wistar rats. NA-induced pressor response was considerably decreased after PTX pretreatment compared to untreated SHR. In conclusion, the enhancement of hypotensive and pressor responses in SHR was abolished after PTX pretreatment. Our results suggested that the activation of PTX-sensitive inhibitory Gi proteins is involved in the regulation of integrated vasoactive responses in SHR and PTX pretreatment could be effectively used for modification of BP regulation in this type of experimental hypertension., S. Čačányiová, F. Kristek, J. Kuneš, J. Zicha., and Obsahuje bibliografii a bibliografické odkazy
Cardiovascular studies have confirmed that hydrogen sulphide (H2S) is involved in various signaling pathways in both physiological and pathological conditions, including hypertension. In contrast to nitric oxide (NO), which has a clear vasorelaxant action, H2S has both vasorelaxing and vasoconstricting effects on the cardiovascular system. H2S is an important antihypertensive agent, and the reduced production of H2S and the
alterations in its functions are involved in the initiation of spontaneous
hypertension. Moreover, cross-talk between H2S and NO has been reported. NO-H2S interactions include reactions between the molecules themselves, and each has been shown to regulate the endogenous production of the other. In addition, NO and H2S can interact to form a nitrosothiol/s complex, which has original properties and represents a novel nitroso-sulphide signaling pathway. Furthermore, recent results have shown that the interaction between H2S and NO could be involved in the endothelium-regulated compensatory mechanisms that are observed in juvenile spontaneously hypertensive rats. The present review is devoted to role of H2S in vascular tone regulation. We primarily focus on the mechanisms of H2S-NO interactions and on the role of H2S in blood pressure regulation in normotensive and spontaneously hypertensive rats.