Chronic continuous light exposure leads to melatonin deficiency along with complex neurohumoral activation resulting in hypertension development in rats. The aim of this study was to show, whether continuous light in duces fibrotic rebuilding of the aorta and whether the treatment with melatonin or angiotensin converting enzyme inhibitor captopril can prevent these potential alterations. In a six-week experiment, 3-month-old Wistar rats were divided into 4 groups (t en per group): controls, rats exposed to continuous light, exposed to continuous light plus treated with captopril (100 mg/kg/24 h) and exposed to continuous light plus treated with melatonin (10 mg/kg/24 h). Systolic blood pressure (SBP) and collagen type I and III in the media of thoracic aorta were me asured. Continuous light induced hypertension and fibrotic rebuilding of the aorta in terms of enhancement of collagen I and III concentration in the aortic media. Both captopril and melatonin prevented SBP rise and reduced collagen III concentration in the aorta. However, only melatonin reduced collagen I and the sum of collagen I and III in the aortic tissue. We conclude that in continuous light-induced hypertension, administration of melatonin, along with SBP reduction, decreases collagen I and III concentration in the aorta. It is suggested that antifibrotic effect of melatonin may reduce the stiffness of the aorta and small arteries and beneficially influence the nature of the pulse wave and peripheral vascular resistance., K. Repová-Bednárová ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
Cardiovascular pathologies are frequently associated with anxiety
and other behavioral disturbances. Ivabradine, an inhibitor of the
hyperpolarization-activated cyclic nucleotide-gated channels in
the sinoatrial node, decreases heart rate and provides
cardiovascular protection. Although ivabradine is increasingly
used in cardiovascular medicine, the data on its behavioral
effects are lacking. The aim of this work was to show
ivabradine’s potential effect on behavior in healthy and
hypertensive rats. After a four-week treatment period, systolic
blood pressure was increased in the N(G)-nitro-L-arginine methyl
ester (L-NAME)-group and ivabradine significantly reduced it.
Furthermore, it reduced the heart rate in both the control and
L-NAME-group. In the control group, ivabradine enhanced the
time spent in and transition to the open arms of the elevated
plus maze test (EPM). In the L-NAME-group, ivabradine does not
show a significant effect on the time spent in the EPM open arms
and the number of transitions into them. Furthermore, ivabradine
has no impact on cognitive function in both control and L-NAME
groups. We conclude that ivabradine showed no undesirable
effects on anxiety, locomotion or learning; in fact, some of these
parameters were even improved. For the first time it has been
shown that ivabradine is a safe cardiovascular drug regarding its
effect on psycho-behavioral manifestations.