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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
Hypertension 1991 Jun
PMID:Separate sex-influenced and genetic components in spontaneously hypertensive rat hypertension. 204 55

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.
Hypertension 1990 Sep
PMID:Hypertension in the spontaneously hypertensive rat is linked to the Y chromosome. 239 86

Gonadal neoplasms developed in three 46, XY females aged 3 yr and 10 mo, 15 yr, and 19 yr. One patient died from metastatic neoplasia. Early diagnosis of 46, XY gonadal dysgenesis is essential, and should be considered in female infants and children with any features of Turner's syndrome, ambiguous genitalia, phallic hypertrophy, excessive height, large hands and feet, failure of development of secondary sexual characteristics, primary amenorrhea, abdominal mass, or unexplained hypertension. Any female with gonadal dysgenesis and a Y chromosome in her karyotype should have prophylactic gonadectomy as soon as possible. The absence of Sertoli cells in these patients, causing lack of androgen binding protein with deficient local concentration of androgens and consequent failure of maturation of spermatogonia, may lead to unregulated proliferation of germ cells, and hence explain the frequency of gonadal neoplasia in the 46, XY female.
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PMID:Importance of early diagnosis and gonadectomy in 46, XY females. 744 56

We used a cross between the stroke-prone spontaneously hypertensive rat (SHRSP) strain and the Wistar-Kyoto (WKY) normotensive strain to elucidate the genetic basis of hypertension. Previous studies have reported conflicting evidence for the contribution of the Y chromosome to hypertension in these models. To investigate further the role of the Y chromosome in hypertension, we performed two large reciprocal crosses: one with the SHRSP as a male progenitor of the cross, yielding 60 F2 rats, and another with the WKY as a male progenitor, yielding 83 F2 rats. The resulting F2 hybrids were phenotyped with the use of a radiotelemetry system (Data Sciences) for measurement of systolic, diastolic, and mean arterial pressures as well as heart rate and motor activity continuously for 96 hours at baseline and after 1% NaCl was added to the rats' drinking water for 12 days. Male F2 hybrids with the SHRSP grandfather had significantly higher average systolic, diastolic, and mean arterial pressures at baseline compared with male F2 hybrids with the WKY grandfather (188.7 +/- 18.1 versus 168.9 +/- 11.5, 130.3 +/- 14 versus 115.7 +/- 7.3, and 159.1 +/- 15.8 versus 141.5 +/- 9.4 mm Hg, respectively). These differences were also observed after salt loading (197.9 +/- 22.1 versus 176.8 +/- 11.7, 136.5 +/- 17.3 versus 120.7 +/- 7.6, and 166.7 +/- 19.5 versus 148 +/- 9.7 mm Hg, respectively; P < .0001 for each comparison). These results suggest that the SHRSP Y chromosome contains a locus or loci that contribute to hypertension in SHRSP/WKY F2 hybrids.
Hypertension 1995 Sep
PMID:Blood pressure in genetically hypertensive rats. Influence of the Y chromosome. 764 81

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)
Hypertension 1993 Jun
PMID:The hypertensive Y chromosome elevates blood pressure in F11 normotensive rats. 850 94

25 adult asymptomatic patients with Turner's syndrome were evaluated by clinical examination, ECG, M-mode and two-dimensional echocardiography and 24 h Holter monitoring. Patients with Turner's syndrome had a significantly higher resting heart rate (83.3 versus 73.7/min in controls, p < 0.01) and a shorter PQ interval (122.3 ms versus 147.1 in controls, p < 0.01). The short PQ interval was not associated with the karyotype (45,X vs. mosaic karyotypes and structural abnormalities of X and Y chromosome), hypertension, estrogen treatment, or congenital valvular abnormalities. No significant arrhythmias were present. On 24 hours ambulatory ECG monitoring the frequency of ectopic supraventricular and ventricular activity was identical as in published controls. The congenital heart abnormalities were detected in 8 (32%) women with T.sy, however, during the follow-up they became significant in only two (8%) of them.
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PMID:[Cardiovascular changes in Turner's syndrome]. 850 69

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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PMID:Steroid sulfatase and the Y chromosome hypertensive locus of the spontaneously hypertensive rat. 853 76

The present study was undertaken to investigate whether the development of proteinuria in the borderline hypertensive rat (BHR) is influenced by the Y chromosome and to determine if the onset of proteinuria in the BHR is delayed when blood pressure is lowered with enalapril, an angiotensin I converting enzyme inhibitor. Male F1, rats were the first-generation offspring of the mating of spontaneously hypertensive (SHR) females and Wistar-Kyoto (WKY) males and the mating of SHR males and WKY females. At 20 weeks of age, enalapril (125 mg/l) was added to the drinking water. Untreated BHR and enalapril-treated BHR (BHRE) were followed to 90-100 weeks of age. Urine was collected every 10-20 weeks for determination of protein, albumin, and nitric oxide (NO2/NO3) metabolite excretion. Indirect blood pressure in BHR from both crosses was approximately 175 mm Hg from 20 to 90-100 weeks of age. Enalapril lowered blood pressure by about 30 mm Hg, but was ineffective in reducing urinary protein or albumin excretion rates at any age. Urinary excretion of nitric oxide metabolites was similar in all groups at all time periods. There were significant differences in the percent of glomerulosclerosis between the two matings. Based on these results, renal injury in the BHR is not associated with the Y chromosome and can be dissociated from hypertension. Further studies using congenic and transgenic technology will be necessary to identify functions of genes and associations with hypertension in order to understand the kidney disease in this model of hypertension.
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PMID:Sex chromosomes do not influence renal injury in borderline hypertensive rats. 885 66

Previous studies have revealed conflicting evidence concerning a Y-chromosome effect on blood pressure (BP) in genetic crosses involving different strains of spontaneously hypertensive rats (SHR or SHRSP). We had previously found an approximately 16 mm Hg difference in systolic BP (P < 10(-7)) at baseline but not after dietary salt loading (P = .82) between F2 males derived from an SHRSPHD grandfather and a Wistar-Kyoto (WKYHD-0) grandmother and F2 males from a reciprocal cross (WKYHD-0 grandfather). When we examined F2 animals from reciprocal crosses between SHRSPHD and a congenic strain, WKYHD-1, which carries a 6-centimorgan-long SHRSPHD-homologous genomic fragment on chromosome 10 that contains a quantitative trait locus linked to BP (BP/SP-la), we found no significant differences either at baseline (P = .39) or after salt loading (P = .51) in the two reciprocal F2 cohorts. To test the hypothesis that Y-chromosome-autosomal epistasis accounts for the discrepant Y-chromosome effects on BP, we analyzed the interaction between BP/SP-1a and reciprocal cross status on BP in the two crosses. In the F2 (WKYHD-0xSHRSPHD) cross, no significant interaction was found for basal systolic BP (P = .89), arguing against a major influence of BP/SP-1a on the Y-chromosome effects on basal BP. However, a significant interaction between zygosity at the BP/SP-1a locus and reciprocal cross status for systolic BP after salt loading (P = .022) indicated that the BP/SP-1a-SHRSPHD allele exhibited a significant effect on BP after dietary excess salt only in males that inherited the SHRSP Y chromosome. These results support the relevance of a Y-chromosome effect on BP and suggest that a complex interplay of epistatic and ecogenetic interactions governs its effect on phenotype.
Hypertension 1996 Nov
PMID:The Y chromosome. Epistatic and ecogenetic interactions in genetic hypertension. 890 41

Previous studies from our laboratory have demonstrated that the Y chromosome from the spontaneously hypertensive rat (SHR) is responsible for a significant portion of the elevated blood pressure and also produces an earlier pubertal rise in plasma testosterone. We performed the following studies to determine whether the SHR Y chromosome raises blood pressure by sympathetic nervous system responses as measured by adrenal chromogranin A and plasma and tissue catecholamines. Male SHR from the University of Akron colony were studied from 5 to 20 weeks of age. Blood pressure was measured by tail-cuff, tail artery cannulation, and aortic telemetry (Data Sciences); acute (air stress) and chronic (territorial colony) social stressors were compared; blood was collected for determination of plasma catecholamines; and adrenal glands were analyzed at 15 weeks for catecholamines. Rats with the SHR Y chromosome had higher blood pressure and plasma norepinephrine than those with the normotensive Wistar-Kyoto (WKY) Y chromosome. However, the SHR Y chromosome did not significantly change responsiveness to acute or chronic stressors. Phentolamine and clonidine prevented the stress responses. Adrenal chromogranin A levels were elevated 37% and 40% and adrenal norepinephrine content 29% and 100% at 4 and 10 weeks of age, respectively, in rats with an SHR Y chromosome compared with WKY. Chemical sympathectomy normalized blood pressure in all strains and significantly reduced norepinephrine (36% to 41%) in all strains except in WKY, which already had a normal blood pressure. In conclusion, the SHR Y chromosome appears to increase the chronic sympathetic nervous system. A potential mechanism could be a Y locus that influences chronic sympathetic nervous system activity, which may reinforce neurohumoral factors and structural components of the vessel wall, accelerating the development of hypertension.
Hypertension 1997 Feb
PMID:Spontaneously hypertensive rat Y chromosome increases indexes of sympathetic nervous system activity. 904 Apr 47


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