BackgroundTestosterone (T) and the sympathetic nervous system each contribute to the pathology of hypertension. Altered blood vessel reactivity is also associated with the pathology of high blood pressure. The purpose of this study was to examine the effects of T manipulation in the regulation of resistance-sized blood vessel reactivity.MethodsAdult spontaneously hypertensive (SHR) and Wistar Kyoto (WKY) male rats at 8 weeks of age were used. The rats were divided into groups consisting of gonadally intact controls (CONT), castrate with sham implant (CAST) and castrate with T implant (CAST + T) (n = 6 to 12 per group). Following a short-term period of T treatment (approximately 4 weeks), plasma norepinephrine (NE) and plasma T were assessed by performing high-performance liquid chromatography and RIA, respectively. Resistance-sized mesenteric artery reactivity was assessed on a pressurized arteriograph for myogenic reactivity (MYO), phenylephrine (PE) responsiveness and passive structural mechanics.ResultsSHR and WKY males exhibited similar physiological trends in T manipulation, with castration significantly lowering plasma T and NE and T replacement significantly increasing plasma T and NE. T manipulation in general resulted in significant alterations in MYO of second-order mesenteric arteries, with T replacement decreasing MYO in SHR (P < 0.05) compared to CONT, T replacement increasing MYO, and CAST decreasing MYO in WKY rats (P < 0.001) compared to CONT rats. Additionally, PE-induced constriction was significantly altered in both strains following T treatment, with the effective concentration of PE to constrict the vessel to 50% of the total diameter significantly increased in the CAST + T SHR compared to CONT (P < 0.05). Comparisons of passive structural mechanics between SHR and WKY treatment groups indicated in SHR a significantly increased wall-to-lumen ratio and decreased circumferential wall stress compared to WKY treatment groups.ConclusionsThese data suggest that T and NE are involved in a complex interaction with both myogenic reactivity and structural alterations of resistance-sized blood vessels and that these factors likely contribute to the development and maintenance of hypertension.

The immune system of the rat undergoes substantial functional and morphological development during the postnatal period. Some aspects of this development are genetically predetermined, while other aspects depend on environmental influences. Detailed information on postnatal development is important in the interpretation of histopathologic findings in juvenile toxicology and pubertal assay studies, as well as other studies conducted in juvenile rats. Studies were conducted to provide detailed characterization of histologic features of the major functional compartments of immune system organs in male and female Sprague-Dawley rats at weekly intervals from the day of birth through postnatal day (PND) 42. Maturation of the individual immune system organs occurred across a range of ages, with histologic maturation of T-cell-related compartments typically occurring prior to maturation of B-cell-related compartments. The sequence of histologic maturation was bone marrow and thymus on PND 14, mesenteric lymph node on PND 21, Peyer's patches and bronchus-associated lymphoid tissue on PND 28, mandibular lymph node, nasopharynx-associated lymphoid tissue, and diffuse mucosal mononuclear cell population of small intestine on PND 35, and spleen on PND 42. An estimation of functional maturation can be made based on the morphological indications of maturity of each compartment of immune system organs, but histologic indications of maturity do not confirm functional immunocompetence.

Background: The Y-chromosome (Yc) and testosterone (T) increase blood pressure and may also influence renal electrolyte excretion. Therefore, the goal of this study was to determine if the Yc combined with T manipulation could influence renal Na and K excretion.

The etiology of preeclampsia remains unknown. However, a contributing factor to this hypertensive disease of pregnancy is a reduction in uterine perfusion pressure resulting in placental ischemia. Uterine arteries may be a major regulator of this process through changes in vascular reactivity and localized blood flow. The reduced uterine perfusion pressure (RUPP) pregnant rat is an established animal model of preeclampsia pathology. Pregnant Sprague Dawley rats were used for this investigation and subjected to RUPP or SHAM surgery on Day 14 of gestation. On Day 21 of gestation, animals were terminated and resistance-caliber uterine arteries were harvested and mounted on a pressurized arteriograph to examine myogenic reactivity, agonist induced vasodilation (methacholine and VEGF), and vasoconstriction (phenylephrine and U-46619). Resistance-caliber uterine arteries from RUPP animals exhibited increased myogenic reactivity and decreased vasodilation (methacholine and VEGF) compared to SHAM uterine arteries (p<0.05). Phenylephrine and U-46619 induced constriction was similar in uterine arteries between RUPP and SHAM rats. These results suggest that resistancecaliber uterine arteries from RUPP pregnant rats are altered to reflect a more constrictive phenotype which may play a role in the development of maternal hypertension demonstrated in these animals and thereby potentially in preeclampsia.

The Spontaneously Hypertensive Rat (SHR) model was used to test the hypothesis that a locus on the SHR Y-chromosome is responsible for increased aggression resulting from increased serum testosterone and decreased amygdala serotonin content compared to the WKY Y-chromosome. To examine the Y-chromosome in SHR and WKY males, consomic Y-chromosome strains were used (WKY.SHR-Y and SHR.WKY-Y). Novel resident intruder tests and intra-colony scarring behavioral paradigms were used to measure aggression in a colony environment. Both resident intruder test attack number and wounding, along with intra-colony scarring scores showed the colony males with the SHR Y-chromosome (SHR and WKY.SHR-Y strains) were more aggressive than the colony males with the WKY Y-chromosome (WKY and SHR.WKY-Y strains). The SHR Y-chromosome colony male animals also had significantly higher serum testosterone, as well as overall lower amygdala serotonin content than the WKY Y-chromosome colony male animals. The results suggest that these behavioral and physiological differences between the SHR and WKY strains are a result of a mutation in the non-pseudoautosomal region unique to the Y-chromosome.