Separate sex-influenced and genetic components in spontaneously hypertensive rat hypertension.

A hypertensive father, but not hypertensive mother, determines blood pressure in normotensive male offspring through body mass index

“…These have emphasised the role of autosomal chromosomes and Y chromosome in determination of BP in SHR. 9,10,17,18 Considering these data from backcrossed SHR, Y chromosome from a male rat with hypertension is responsible in part for elevation of BP probably through enhanced adrenergic nerve system or androgen receptor mediated events. 11,19 If hypertensive Y chromosome influences adrenergic nerve activity in human as well, [12][13][14][15] this theory is able to explain the linkage between the genetic loading from a hypertensive father and BMI observed in the present study.…”

Possible Involvement of Androgen in Increased Norepinephrine Synthesis in Blood Vessels of Spontaneously Hypertensive Rats

“…Therefore, it is possible that the changes in NE level and TH activity by testosterone may be induced via alteration of the TH gene transcription in SHR. Turner et al (24) have reported that the blood pressure increase shown by male SHR over WKY was related to the Y chromosome. Furthermore, Ganten et al (11) reported that the blood pressure is higher in male hypertensives than female ones and that this sexual dimorphism is not present in normotensive rats, and they suggested that this sexual dimorphism in SHR is linked to the "hypertensive genes".…”

Genetic isolation of a region of chromosome 8 that exerts major effects on blood pressure and cardiac mass in the spontaneously hypertensive rat.

“…Although this strain has been the subject of extensive physiologic and biochemical investigation, little is known about the primary genetic lesions responsible for the pathogenesis of spontaneous hypertension. Recent linkage studies in recombinant inbred strains and in F2 populations derived from the SHR and normotensive strains have suggested that BP quantitative trait loci (QTLs) may exist on chromosomes 1, 2, 4, 8, 10, 13, 16, 19, and 20 (2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16). However, the individual contributions of each of these chromosomes in the pathogenesis of spontaneous hypertension have not been clearly defined.…”

“…By replacing single chromosome regions in the SHR with the corresponding chromosome regions from an appropriate normotensive strain, it should be possible to confirm the existence of putative QTLs, determine their relative contributions to hypertension, and begin fine genetic mapping of specific variants responsible for increased BP. Although consomic strains derived from SHR and normotensive Wistar Kyoto rats have been used to confirm the existence of BP QTLs on the Y chromosome (8), the near total lack of recombination on the Y chromosome precludes the use of these consomic strains for genetic mapping. In a new congenic strain derived from SHR and normotensive Brown-Norway (BN) rats, we have trapped a QTL regulating blood pressure in a region of chromosome 8 that appears to play a major role in the pathogenesis of spontaneous hypertension.…”