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The objective of this study was to examine the response of tissue steroid sulfatase (STS) levels in hypertensive rat strains, when blood pressure (BP) was lowered by different techniques at an early age. A 4x3 factoral design was used, in which males (n=6-8) from four rat strains (WKY, SHR, SHR/a, SHR/y) at 4 weeks of age, were randomly assigned to one of three treatment groups: a hydralazine group, a castration group and a control group. BP was measured by the tail cuff technique and verified by tail catheter at the end of the experiment. BP was significantly reduced by both treatments in the hypertensive strains (SHR, SHR/a, SHR/y) compared to respective control groups. At 15-17 weeks of age, animals were euthanized and heart, kidney, adrenal glands and liver were assayed for STS levels. The major trend in tissue STS was that castration significantly lowered: adrenal, heart and liver STS in specific strains. In conclusion, castration and hydralazine significantly lowered the BP in the hypertensive rat strains, but only castration consistently lowered STS levels across strains implicating testosterone as a regulator of tissue STS.

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Our hypothesis is that the steroid sulfatase gene (Sts) may indirectly contribute to the modulation of blood pressure (BP) in rats with genetic hypertension. The steroid sulfatase enzyme (STS) catalyzes the conversion of estrone sulfate, dehydroepiandrosterone sulfate, cholesterol sulfate and glucocorticoid sulfates to their active nonconjugated forms. This causes the elevation of biologically active steroids, such as glucocorticoids, mineralcorticoids as well as testosterone, which may lead to increased BP. The main objective was to examine the effects of a steroid sulfatase inhibitor on blood pressure and steroid levels in rats with hypertensive genetic backgrounds. Three treatment groups, 5-15 weeks of age were used: controls, estrone and STS inhibitor (estrone-3-O-sulfamate), (n=8 per group). BP was taken weekly by tail cuff, and serum testosterone (T), estrogens (E), and plasma corticosterone (C) levels were measured by radioimmunoassay. BP was significantly reduced by the STS inhibitor in the strains with genetically elevated BP. Also the inhibitor alone significantly reduced plasma corticosterone in all strains compared to estrone treatment with a concomitant as well as significant rise in estrogens and reduction in testosterone and body weight.

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The tissue biocompatibility of a series of novel rubbery polyisobutylene (PIB)/polydimethylsiloxane (PDMS) bicomponent networks was investigated by in vivo implantation into rats. Bicomponent networks of varying composition (PIB wt%/PDMS wt% = 70/30, 50/50, 35/65) as well as a standard polyethylene control were implanted intraperitoneally. After eight weeks the implants and surrounding tissue were removed for histological evaluation. In all scoring categories (i.e. collagen thickness, fibrous tissue orientation, collagen deposition in muscle tissue, lymphocyte infiltration, angiogenesis) the PIB/PDMS bicomponent network implants elicited either less or similar tissue and cellular response than polyethylene. To determine which implant elicited the least tissue and cellular response overall, a weighted score including collagen thickness, lymphocyte infiltration, and angiogenesis was calculated for each implant. According to these preliminary investigations, PIB/PDMS bicomponent networks are suitable for implant applications.

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The hypothesis was tested that the sympathetic nervous system (SNS) developmentally influences circulating testosterone (T), systolic blood pressure (SBP) and cardio-renal pathology in SHR/y animals. A sympathoplegic drug, guanethidine, and an antibody to nerve growth factor were administered to WKY and borderline hypertensive SHR/y male rats (n = 20/group) for the first 3 weeks of life; control groups (n = 20/group) received saline. SBP, serum T and luteinizing hormone (LH) were measured. SBP in the WKY and SHR/y sympathectomy (sympx) groups decreased 10mmHg (p < 0.001) and 50mmHg (p < 0.001), respectively, when compared to their control groups. Serum T levels in the sympx WKY group were lower (p < 0.01) than those in controls, and the rise of T typically observed in SHR/y from weeks 6-8 was delayed in the sympx SHR/y group, similar to the pattern in WKY. Serum LH levels were increased in the sympx WKY group, but not in the SHR/y group. Sympx caused a greater reduction in renal glomerular changes (p < 0.01), coronary artery collagen deposition (p < 0.01) and myocardial fibrosis (p < 0.01) in SHR/y than WKY rats. In conclusion, the SHR Y chromosome has a locus that enhances SNS activity, which can raise SBP and result in renal and cardiovascular tissue damage.

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OBJECTIVES: To evaluate whether renin and angiotensinogen gene expression in females from two strains of rats that share the same autosomes and X chromosomes differs. Female SHR/y rats have the parental Wistar-Kyoto rat autosomes and X chromosomes and have no chromosomes of spontaneously hypertensive rat origin; thus they are genetically equivalent to female Wistar-Kyoto rats. DESIGN AND METHODS: Because these genes are regulated by steroid hormones, we investigated the effects of removal of estrogen (ovariectomy) and addition of androgen (testosterone implants) on three groups of female SHR/y rats and the parental rat strain Wistar-Kyoto rat with groups of intact (control) rats, rats subjected to ovariectomy at age 3 weeks, and rats subjected to ovariectomy with a testosterone implant at age 3 weeks. RESULTS: The combination of removing estrogen early in development and supplementing the ovariectomized females with testosterone revealed strain differences in response of blood pressure. Renin and angiotensinogen messenger RNA levels appear to be regulated coordinately within each strain, although actual levels of messenger RNA differ between the strains. CONCLUSIONS: Similar patterns of responses of renin and angiotensinogen genes to ovariectomy and ovariectomy plus testosterone suggest that regulation of the genes is likely to be similar or coordinate. Differences in regulation of renin-angiotensin system genes between strains may result from epigenetic mechanisms such as genome imprinting of these genes or of another gene that functions as a common regulator of renin and angiotensinogen.

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BACKGROUND: During long-term in vitro heart preservation and subsequent reperfusion, irreversible tissue damage occurs in part due to reactive oxygen species. Therefore, inhibition of generation of oxygen-derived free radicals and the related oxidative damage of ischemic tissue may be useful in maintaining heart function after long-term preservation. Complexes of Cu(II) may cause disproportionation of superoxide and thus may function as an inhibitor of the effects of oxygen-derived free radicals. METHODS: In this study, 24-h preservation of isolated rat hearts was performed. Using the Langendorff technique, hearts were perfused for 24 h with a hypothermic, moderately hyperkalemic (15 mM KCl) solution containing various metabolic and membrane-stabilizing additives at constant low pressure. In addition, the potential benefit of the addition of two Cu(II) compounds (Cu(II) Cl2 and Cu(II)2Asp4) to the perfusion solution was examined. RESULTS: The Cu(II)Cl2-treated hearts were significantly better preserved than control hearts after 24 h of preservation with regard to recovery of systolic pressure, coronary flow, max +dP/dt, and max -dP/dt. Lipid peroxidation as estimated by myocardial malonaldehyde (both P < 0. 001) and myocardial creatine kinase release (both P < 0.05 vs control) were significantly reduced in the Cu(II)Cl2 and Cu(II)2Asp4 groups. Overall, Cu(II)Cl2 best preserved the heart after 24 h of cold preservation with respect to indices of functional recovery, whereas Cu(II)2Asp4 did not significantly improve functional recovery compared to control. CONCLUSION: Low-pressure, cold perfusion with an enhanced solution is a potential method to preserve donor hearts in preparation for transplantation. The beneficial effect of Cu(II)Cl2 was attributed to (i) SOD activity of the Cu2+ species and/or (ii) termination of chain carriers in the lipid peroxidations by aqueous Cu2+ and Cu+ species. The negation of some of the positive effects of Cu2+ species by the introduction of acetylsalicylate was tentatively assigned to potentiation of the Ca2+ modality for reperfusion injury.

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The battle over salt has changed over the centuries from one of where to find salt sources to one of how much salt to use in a healthful manner. Many questions were answered by the INTERSALT Study across numerous countries and, yet, many questions persist. It is a love-hate relationship, an approach-avoidance paradigm. We need it but in excess it may cause harm. Questions that still remain are, Who is salt sensitive? What are the most appropriate and relevant models to study? What are the functional differences of the many salt effects? Can the data support a single public policy on dietary sodium recommendations? The following review examines some of these questions and the interaction of neural, neuroendocrine, renal, and social factors in the great salt debate. Dietary sodium can alter peripheral and central neurotransmitter concentrations, receptor density, and sensitivity. Low-sodium diets can produce acute neuroendocrine and neural compensations that are different from the chronic effects of low dietary sodium. Chronic high- or low-sodium diets may also cause trophic hormonal changes that can influence resistance vessel structure and, consequently, blood pressure. Both human and animal studies suggest a genetic basis for salt sensitivity. In some cases stress unmasks the salt sensitivity. For instance, the social context can modulate blood pressure responses to a high-sodium diet. Therefore, 24-h monitoring of blood pressure becomes important, especially in salt-sensitive persons.

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The spontaneously hypertensive rat (SHR) has a Y chromosome locus that increases blood pressure. This locus requires an androgen receptor and testosterone for maximum expression. Steroid sulfatase (STS) catalyzes the conversion of steroid sulfates to their active nonconjugated form. In some mammals the steroid sulfatase locus (Sts) is on the Y chromosome, although the rat Sts is on the X chromosome. We measured STS activity levels in SHR and normotensive Wistar Kyoto (WKY) males. SHR had significantly higher STS activity in testes, adrenal gland, liver, and hypothalamus. The Km values for STS in the two strains were not significantly different; thus, activity differences were likely due to differences in enzyme amounts. STS activity was measured in the backcross strains SHR/y and SHR/a to test and/or confirm a Y chromosome influence on STS. STS activity levels in these strains were intermediate between those of SHR and WKY. Because the blood pressures of SHR/y and SHR/a were also intermediate between SHR and WKY, the STS activity could be a secondary response to the hypertension. An alternative hypotheses is that a regulatory locus in addition to the structural locus is responsible for STS activity levels, and this regulatory locus is on the rat Y chromosome. Further study is needed to discriminate between these possibilities, and until the second hypothesis can be eliminated, the Sts locus or its modifier loci remain a potential component of the Y chromosome hypertensive locus.

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OBJECTIVE: To investigate the relationship between testosterone and blood pressure during the rapid development phase of blood pressure rise in four strains of rats: Wistar-Kyoto (WKY) rats; spontaneously hypertensive rats (SHR); SHR/y, a substrain with an SHR Y chromosome and WKY rat autosomes and X chromosomes; and SHR/a, a substrain with SHR autosomes and X chromosomes and the WKY rat Y chromosome. METHODS: Blood pressure was measured every 2 weeks by the tail-cuff method, and was verified in selected rats at 23 weeks by aortic telemetry. Serum testosterone was measured, by radioimmunoassay, every 2 weeks from 5 to 23 weeks of age. RESULTS: During the rapid phase of blood pressure rise, between 5 and 9 weeks of age, there was a significantly larger rise in serum testosterone in SHR and SHR/y than in WKY rats and SHR/a groups. The hypertensive Y chromosome in the SHR and SHR/y accelerated peak testosterone approximately 4 weeks earlier, and blood pressure was increased in these two groups compared with the SHR/a and WKY rat groups, respectively. A gene on the SHR Y chromosome (Tty) affecting the timing of testosterone in development is proposed. At approximately 15 weeks of age testosterone levels decreased sharply towards prepubertal levels in WKY rats and at 23 weeks in SHR/y, whereas testosterone levels were maintained in SHR and SHR/a, which suggests an autosomal component. CONCLUSION: The SHR Y chromosome may accelerate the start of puberty and a cascade of molecular and neuroendocrine events that raise blood pressure.

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BACKGROUND: Cardiopulmonary bypass and crystalloid cardioplegia may lead to endothelial dysfunction in the coronary microcirculation. The aim of the present study was to examine whether the alteration of endothelium-dependent microvascular responses may be related to the generation of oxygen-derived free radicals. METHODS AND RESULTS: Pigs (30 kg) were heparinized and placed on cardiopulmonary bypass. The hearts were arrested for 1 hour with either plain hypothermic, hyperkalemic (25 mEq/L) crystalloid cardioplegic solution (n = 10) or crystalloid cardioplegic solution containing either deferoxamine (n = 8) or manganese superoxide dismutase (n = 6). Hearts were then reperfused for 1 hour while the pigs were separated from cardiopulmonary bypass. Noninstrumented pigs were used as controls (n = 8). Coronary microarteries (120 to 190 microns in diameter) were studied in vitro in a pressurized (40 mm Hg), no-flow state with videomicroscopy and electronic dimension analysis. After precontraction of microvessels, the endothelium-dependent and -independent agents were applied extraluminally. Serotonin caused a slight dilation of control vessels (percent dilation of acetylcholine-induced preconstriction at 10 mumol/L drug concentration, 5 +/- 8%; P < .05 versus crystalloid cardioplegia group) and a significant contractile response after crystalloid cardioplegia (-28 +/- 10%). Bradykinin elicited near complete relaxation of control vessels (96 +/- 3%, P < .05), whereas it caused considerably less relaxation after cardioplegia (33 +/- 9%). The addition of either deferoxamine or superoxide dismutase to the cardioplegic solution significantly (but not completely) preserved vasomotor responses of coronary microvessels to serotonin (9 +/- 6% and 11 +/- 4%, respectively; P < .05) or bradykinin (72 +/- 4% and 87 +/- 3%, respectively; P < .05). Endothelium-independent relaxations of vessels in response to sodium nitroprusside were similar in all groups. CONCLUSIONS: Either the hydroxyl radical synthesis inhibitor deferoxamine or manganese superoxide dismutase preserves endothelium-dependent relaxation during crystalloid cardioplegia-reperfusion. Therefore, ischemic cardioplegia-reperfusion-induced endothelial dysfunction is at least partially mediated by the generation of oxygen-derived free radicals.

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We have recently shown that the spontaneously hypertensive rat (SHR) and the Wistar-Kyoto (WKY) rat differ at a frequency of 1 per 62 bases in their nuclear DNA (Hypertension 1992; 19:425-427). Given the origin of these strains this level of divergence was unexpected. To investigate the origin of this nuclear divergence we have examined mitochondrial DNA. Mitochondrial DNA was isolated from SHR and WKY rats, digested with several restriction enzymes, electrophoresed in 1.0% agarose gels, and the fragments visualized with ethidium bromide staining. This approach allowed us to analyze 220 base pairs of mitochondrial DNA. No differences were detected between SHR and WKY rats. Comparison with the King-Holtzman rat strain produced differences at an average of 1 per 52 base pairs. We also examined several SHR and WKY rats from within our colonies and found no differences suggesting intrastrain homogeneity for mitochondrial DNA phenotypes. These data indicate that the SHR and WKY rat share a recent, common maternal ancestor. This result is consistent with the published origins of the SHR and WKY rat strains. Together with the nuclear divergence results, the data suggest that the original Wistar colony from which SHR and WKY rats were derived was probably highly polymorphic for nuclear genes.

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Our laboratory has shown that the Y chromosome has a significant effect on blood pressure in the spontaneously hypertensive rat (SHR) model of hypertension and that the testes and androgen receptor contribute to the blood pressure rise. As an extension of our research, we have developed two new rat strains, SHR/a and SHR/y (F11) to study the Y chromosome. The objectives of the following research were 1) to study the blood pressure of rats with an SHR Y chromosome in a normotensive genetic background (SHR/y) or a normotensive Y chromosome in an SHR genetic background (SHR/a), 2) to determine the effect of male sex phenotype on the blood pressure of these rats, 3) to determine if testosterone replacement in castrated rats would restore blood pressure, and 4) to determine whether the Y chromosome from the SHR/y strain when crossed with a normotensive female can induce hypertension in androgen receptor-deficient male offspring. Blood pressure of male SHR/y rats was significantly higher than that of normotensive Wistar-Kyoto males (p < 0.01), and SHR/a males had significantly lower blood pressure compared with that of the parent SHR strain (p = 0.05). Testosterone replacement in castrated rats of both strains (SHR/a and SHR/y) restored blood pressure to control levels. Normotensive female King-Holtzman rats heterozygous for the testicular feminization gene were crossed with F11 SHR/a and SHR/y males.(ABSTRACT TRUNCATED AT 250 WORDS)

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The pressor response to normal daily behaviors and acute stress was studied in black racer snakes (Coluber constrictor) at 30 degrees C. In addition, hematological changes during the stress response were assessed. Mean nighttime systemic arterial blood pressure (SABP) in undisturbed snakes was lower than daytime pressure (26 +/- 3 vs. 32 +/- 9 mmHg, P < 0.001). When snakes were fed mice, SABP increased 3.5- to 4-fold and heart rate increased approximately 3-fold above resting values within approximately 30 s (peak SABP, 99 +/- 18 mmHg; peak heart rate, 99 +/- 12 beats/min). Killing and ingesting the mice required 6-15 min, during which time mean SABP and heart rate were 84 +/- 16 mmHg and 92 +/- 12 beats/min. Pulmonary blood pressure also increased but remained 40-50 mmHg lower than SABP. During stress elicited by tapping the snakes for 5-8 min, heart rate was 94 +/- 6 beats/min but SABP averaged only 44 +/- 11 mmHg. Plasma norepinephrine and epinephrine increased 51- and 26-fold. Plasma glucose increased 58%, hematocrit increased 19%, and plasma volume decreased 19%. It is concluded that blood pressure is markedly affected by behavior and that the sympathetic nervous system appears to play a key role.

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A method of restriction fragment length polymorphism (RFLP) analysis was used to estimate the amount of genetic divergence between the spontaneously hypertensive rat (SHR) strain and the Wistar-Kyoto (WKY) strain. DNA from each strain was digested with eight restriction endonucleases and hybridized with six single copy gene sequences. The number of hybridization bands in each digestion was used to estimate the total number of bases analyzed and RFLPs were scored as single mutations. Divergence was then estimated by dividing the number of mutations by the number of bases analyzed. In a total of 808 bases analyzed in WKY rats, a minimum of 13 mutations were scored in SHR, which yields a nucleotide divergence of 1 change per 62 bp. This is an extremely high amount of divergence given the known origin of these two strains and is comparable to the maximum divergence possible between unrelated humans.

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Previous results from our laboratory indicated two major genetic components of spontaneously hypertensive rat (SHR) hypertension, an autosomal component and a Y chromosome component. Two new substrains, SHR/a and SHR/y, were developed using a series of backcrosses to isolate each of these components. The SHR/a substrain has the autosomal loci and X chromosome from the SHR strain and the Y chromosome from the Wistar-Kyoto (WKY) rat strain. The SHR/y substrain has only the Y chromosome from the SHR and autosomal loci and X chromosome from the WKY strain. Throughout these breeding programs parents were chosen at random without selection for blood pressure. Males of both substrains maintained blood pressures over 180 mm Hg. Comparisons of blood pressure in these new substrains with the original parental strains can be used to determine the relative proportions of each genetic component in hypertension. The Y chromosome component contributes 34 mm Hg, which is the difference between SHR/y male and WKY male blood pressure. The total autosomal component contributes 46 mm Hg, which is the difference between SHR/a male and WKY male blood pressure. The autosomal component is a sex-influenced trait; males in the SHR/a strain have significantly higher pressures than SHR/a females. Of the 46 mm Hg estimated for the autosomal component, 41 mm Hg is the result of these loci interacting with male phenotypic sex. This sex-influenced component is separate and distinct from the Y chromosome component.

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The objective of this study was to determine if males with a deficient androgen receptor would develop hypertension when crossed with a hypertensive parent. Female King-Holtzman rats (n = 15), heterozygous for the testicular feminization (Tfm) gene, were crossed with male spontaneously hypertensive rats (SHR), and blood pressure was measured weekly from 5-14 weeks in the F1 hybrid males. Approximately 50% of the F1 hybrid males were Tfm males and androgen receptor-deficient, and 50% were normal. Blood pressure in the parent King-Holtzman males, Tfms, and female rats was also followed for the same time period. The F1 normal male hybrids had a significantly higher (p less than 0.05) systolic blood pressure than the Tfm hybrid males after 12 weeks (195 +/- 8 versus 170 +/- 8 mm Hg, respectively). Blood pressure in the male and Tfm Holtzman rats was 120 +/- 5 mm Hg and 110 +/- 6 mm Hg, respectively. Castration lowered blood pressure by 38 mm Hg in the hybrid males and 27 mm Hg in the Tfm hybrids. Female F1 hybrids also showed a pressure rise above that of female Holtzman controls (155 +/- 6 mm Hg versus 110 +/- 6 mm Hg, p less than 0.01) but lower than the F1 males and Tfm hybrids. Ovariectomized females with testosterone implants did not show an elevation in blood pressure. Plasma electrolytes, norepinephrine, and cholesterol were not significantly different between normal and Tfm hybrid males. The results suggest that the presence of an androgen receptor and a testis-derived factor mediate the blood pressure rise in the hybrid males.(ABSTRACT TRUNCATED AT 250 WORDS)

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Sodium (Na) balance is maintained by a complex set of genetic, hemodynamic, hormonal and neural mechanisms that affect intake, reabsorption and excretion. This research focused on the role of a reduction in dietary Na on cardiovascular and neuroeffector function in normotensive (WKY) and spontaneously hypertensive rats (SHR) raised from 5-20 weeks on a control Na diet (12 mmol per 100 g food) or various low Na diets (0.5-2 mmol per 100 g food). For comparison purposes, high Na (140 mmol per 100 g food) results are reported. With regards to hemodynamics and volume regulation, the lowest Na diet reduced blood pressure 15% in SHRs but not in WKYs. Body weights, blood volume, hematocrit, plasma electrolytes, extracellular volume, and cardiac output were not different between diets or strains. However, both SHR and WKY low Na groups were abnormally sensitive to blood loss and showed attenuated pressor responses, mediated by the sympathetic nervous system, to both acute and chronic stress situations. Low Na treatment significantly attenuated the pressor response during stress, which was primarily due to reduction in noradrenergic transmitter release. In spite of depressed function during restriction of dietary Na, compensatory responses were adequate to maintain homeostasis, but the neurohumoral compensatory reserve was thereby markedly curtailed. The data suggest that risks are associated with a reduced intake of dietary Na. These findings imply that the "hygienic" Na intake in man should be carefully experimentally defined before generalized measures are taken to reduce dietary Na in society.

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The objective of our study was to determine the genetic influence on blood pressure in spontaneously hypertensive rats (SHR), and normotensive Wistar-Kyoto (WKY) rats using genetic crosses. Blood pressure was measured by tail sphygmomanometry from 8 to 20 weeks of age. Blood pressure was significantly higher from 12 to 20 weeks in the male offspring derived from WKY mothers x SHR fathers as compared with male offspring derived from SHR mothers X WKY fathers (180 +/- 4 versus 160 +/- 5 mm Hg, p less than 0.01). There was no significant difference between the blood pressure of the F1 females, further supporting Y chromosome linkage and not parental imprinting. The blood pressure data from F2 males derived from reciprocal crosses of parental strains were consistent with the presence of a Y-linked locus, but not with an X-linked locus controlling blood pressure. The data strongly suggest that hypertension in the SHR has two primary components of equal magnitude, one consisting of a small number of autosomal loci with a second Y-linked component.

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Sodium balance is maintained by a complex set up of hemodynamic, hormonal and neural mechanisms that affect intake, reabsorption and excretion. The focus of the following research was on the cardiovascular and neuroeffector effects of dietary Na reduction primarily in normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR) raised from 4 to 15 weeks on a control Na diet (CNa: 12 mmol per 100 g food) or various low Na diets (LNa: 0.5 to 3 mmol per 100 g food). With regards to hemodynamics and volume regulation, the lowest Na diet reduced blood pressure 15% and raised resting heart rate (20%) in SHRs but not WKYs. Blood volume, hematocrit, plasma electrolytes, extracellular volume, and cardiac output were not different between diets or strains. However, both LNa strains were abnormally sensitive to blood loss and showed attenuated pressor responses to both acute and chronic stress situations. Cardiac function was not altered by LNa treatment in either rat strain although structural compensations occurred. LNa treatment significantly attenuated the pressor reduction in mesenteric blood flow during stress which was primarily due to reduction in noradrenergic transmitter release and not due to altered receptor sensitivity, density, or Na/K ATPase activity. Compensatory sympathetic activity was increased as was sodium conservation through humoral mechanisms which maintained homeostasis. However, further neurohumoral compensation was markedly reduced. The data suggests that the hygienic sodium intake in humans should be experimentally defined before generalized measures are taken to reduced dietary sodium use throughout society.

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