The incidence of vein diseases (varicosity, thrombophlebitis, phlebosclerosis, orthostatic intolerance) is extremely high. In several countries it may exceed that of the arterial pathology by an order of magnitude. In the last decades, this recognition and the rapid accumulation of experimental data have resulted in a progressive reevaluation of the physiological significance of the venous system, which had been rather neglected earlier by scientists. The major aim of this review is to provide a critical survey of recent selected literature related to different physiological functions of the venous system as well as to biomechanical, metabolic, and humoral (ionic, hormonal) aspects of the local venous control. Local neural control mechanisms, including effects of catecholamines and other transmitters, are regarded to be beyond the scope of this work. At present, the synthesis of information available in the literature meets certain difficulties, because occasionally poorly defined methodological techniques and physiological parameters have been applied. On the other hand, a significant part of works dealing with venous physiology is excellent and inspirational. We have good reason to believe that the fast accumulation of reliable scientific data on this very important field will soon reach a new critical level, then an even more effective integration of knowledge will be possible.

Background:In expression systems diacylglycerol (DAG) produced during AT 1 angiotensin receptor signaling can be converted to 2-arachidonoylglycerol. Results: Inhibition of CB 1 receptors and DAG lipase augmented angiotensin II-induced vasoconstriction in resistance arteries. Conclusion: Angiotensin II-induced vasoconstriction is attenuated via 2-arachidonoylglycerol release and consequent CB 1 receptor activation. Significance: This is the first demonstration that angiotensin II-induced endocannabinoid release can modulate vasoconstriction.

To clarify the mechanism leading to the development and rupture of intracranial aneurysms, tensile strength and viscoelastic parameters of 22 human saccular aneurysms were investigated. Meridional and circumferential strips from the thin and the thick part of the aneurysm sack and 18 control strips from the basilar artery of 8 patients with pathologies not affecting the cerebral arterial system were studied. The length of the strips was increased in 200-µm steps, while distending force was recorded. Tensile strength and viscoelastic parameters were computed. In both directions, tensile strength of thick strips was significantly lower than that of controls. In the meridional direction, tensile strength of thin strips was significantly larger than that of thick ones (14.5 ± 4.1 × 10⁶ vs. 7.5 ± 2.0 × 10⁶ dyn/cm², p < 0.05). In the circumferential direction, thin strips tore at lower strain values than thick ones (29 ± 4 vs. 55 ± 16%, p < 0.05). Viscoelastic parameters changed in parallel. In circumferential direction, values of thick and thin strips were significantly lower than those of controls. In the meridional direction, values of thin strips were significantly higher than those of the thick ones. These observations show that characteristic mechanical deterioration and steric inhomogeneities accompany the loss of smooth muscle cells and the derangement of connective tissue elements in the wall of intracranial aneurysms, which may explain certain steps in their initiation, enlargement and rupture.

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Hyperandrogenic state in females is accompanied with metabolic syndrome, insulin resistance and vascular pathologies. A total of 67%-85% of hyperandrogenic women suffer also from vitamin D deficiency. We aimed to check a potential interplay between hyperandrogenism and vitamin D deficiency in producing insulin resistance and effects on coronary resistance arteries. Adolescent female rats were divided into four groups, 11-12 animals in each. Transdermal testosterone-treated and vehicle-treated animals were kept either on vitamin D-deficient or on vitamin D-supplemented diet for 8 weeks. Plasma sexual steroid, insulin, leptin and vitamin D plasma levels were measured, and oral glucose tolerance test was performed. In coronary arterioles, insulin receptor and vitamin D receptor expressions were tested by immunohistochemistry, and insulin-induced relaxation was measured in vitro on isolated coronary resistance artery segments. Testosterone impaired glucose tolerance, and it diminished insulin relaxation but did not affect the expression of insulin and vitamin D receptors in vascular tissue. Vitamin D deficiency elevated postprandial insulin levels and homeostatic model assessment insulin resistance. It also diminished insulin-induced coronary arteriole relaxation, while it raised the expression of vitamin D and insulin receptors in the endothelial and medial layers. Our conclusion is that both hyperandrogenism and vitamin D deficiency reduce sensitivity of coronary vascular tissue to insulin, but they do it with different mechanisms.

Objective: To investigate the vascular dysfunction caused by insulin resistance in polycystic ovary syndrome (PCOS) and the effectiveness of vitamin D in an animal model. Design: Controlled experimental animal study. Setting: Animal laboratory at a university research institute. Animal(s): Thirty female Wistar rats. Intervention(s): Rats were divided into groups at age 21-28 weeks. Twenty of them were subjected to dihydrotestosterone (DHT) treatment (83 mg/d); ten of them also received parallel vitamin D treatment (120 ng/100 g/wk). Oral glucose tolerance tests with insulin level measurements were performed. Gracilis arterioles were tested for their contractility as well as their nitric oxide (NO)-dependent and insulin-induced dilation using pressure arteriography. Main Outcome Measure(s): Several physiologic parameters, glucose metabolism, and pressure arteriography. Result(s): DHT treatment increased the passive diameter of resistance arterioles, lowered norepinephrine-induced contraction (30.1 AE 4.7% vs. 8.7 AE 3.6%) and reduced acetylcholine-induced (122.0 AE 2.9% vs. 48.0 AE 1.4%) and insulin-induced (at 30 mU/mL: 21.7 AE 5.3 vs. 9.8 AE 5.6%) dilation. Vitamin D treatment restored insulin relaxation and norepinephrine-induced contractility; in contrast, it failed to alter NO-dependent relaxation.

Background and purposeVitamin D deficiency (VDD) is a global health problem, which can lead to several pathophysiological consequences including cardiovascular diseases. Its impact on the cerebrovascular system is not well understood. The goal of the present work was to examine the effects of VDD on the morphological, biomechanical and functional properties of cerebral arterioles.MethodsFour-week-old male Wistar rats (n = 11 per group) were either fed with vitamin D deficient diet or received conventional rat chow with per os vitamin D supplementation. Cardiovascular parameters and hormone levels (testosterone, androstenedione, progesterone and 25-hydroxyvitamin D) were measured during the study. After 8 weeks of treatment anterior cerebral artery segments were prepared and their morphological, biomechanical and functional properties were examined using pressure microangiometry. Resorcin-fuchsin and smooth muscle actin staining were used to detect elastic fiber density and smooth muscle cell counts in the vessel wall, respectively. Sections were immunostained for eNOS and COX-2 as well.ResultsVDD markedly increased the wall thickness, the wall-to-lumen ratio and the wall cross-sectional area of arterioles as well as the number of smooth muscle cells in the tunica media. As a consequence, tangential wall stress was significantly lower in the VDD group. In addition, VDD increased the myogenic as well as the uridine 5’-triphosphate-induced tone and impaired bradykinin-induced relaxation. Decreased eNOS and increased COX-2 expression were also observed in the endothelium of VDD animals.ConclusionsVDD causes inward hypertrophic remodeling due to vascular smooth muscle cell proliferation and enhances the vessel tone probably because of increased vasoconstrictor prostanoid levels in young adult rats. In addition, the decreased eNOS expression results in endothelial dysfunction. These morphological and functional alterations can potentially compromise the cerebral circulation and lead to cerebrovascular disorders in VDD.

Several long-term antigravity defense mechanisms are activated in the lower extremity veins and microvessels when an organism is exposed to chronic orthostatic load. These mechanisms involve acute pressure-induced myogenic response, counterregulatory K+ channels, functional and structural remodeling of sympathetic innervation, and vascular network properties.