The population genetic consequences of nearestneighbor pollination in an outcrossing plant species were investigated through computer simulations. The genetic system consisted of two alleles at a single locus in a self-incompatible plant that mates by random pollen transfer from a neighboring individual. Beginning with a random distribution ofgenotypes, restricted pollen and seed dispersal were applied each generation to 10,000 individuals spaced uniformly on a square grid. This restricted gene flow caused inbreeding, a rapid increase in homozygosity, and striking microgeographic differentiation of the populations. Patches of homozygotes bordered by heterozygotes formed quickly and persisted for many generations. Thus, high levels of inbreeding, homozygosity, and patchiness in the spatial distribution of genotypes are expected in plant populations with breeding systems based on nearest-neighbor pollination, and such observations require no explanation by natural selection or other deterministic forces.Genetic differentiation of populations over the habitats they occupy is a major factor in the processes of adaptation and evolution. For populations subdivided into small colonies, it is easy to picture this differentiation as the result of genetic drift. Wright (1-3) showed that even large populations distributed continuously over an area will differentiate if gene dispersal within them is sufficiently restricted. He termed this process isolation by distance. Many genetic characteristics of such continuous populations depend on the size of local breeding units, or neighborhoods, within them. In particular, the smaller the neighborhoods, the greater the genetic differentiation in the population, so these neighborhoods are essentially subdivisions created by limited gene dispersal. Inbreeding and increased homozygosity result, as does a spatial differentiation ofgene and genotype frequencies. The genetic structure of a population departs considerably from that expected in a random-mating population. Rohlf and Schnell (4), using computer simulations of Wright's model to examine spatial patterning and genetic differentiation in populations with various neighborhood sizes, observed rapid establishment of spatial patterns in gene frequency, which persisted for many generations.Many plant species have reproductive systems ideally suited to isolation by distance. Pollinator flight behavior and seed dispersal determine gene flow, and both are often severely limited. The restriction on pollen movement is particularly strong when pollinators fly between nearest-neighboring plants, a common behavior. Levin and Kerster (5), for example, observed almost exclusively nearest-neighbor pollination (NNP) in Liatris aspera (Compositae), as well as highly localized dispersal of seeds. Even with some carryover ofpollen from previous visits, gene dispersal was highly leptokurtic (6). NNP has been reported sufficiently often for other plants and pollinators (5-15) that it is clearly an important characteristic of pollination bio...

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 mothersxWKY fathers (180±4 versus 160±5 well-studied animal model of human essential hypertension. This inbred strain was developed by selective breeding of the Wistar-Kyoto (WKY) stock for higher blood pressure.1 The response to this selection was rapid, with almost 100% hypertension by generation three.2 This quick selective response indicates that only a few genetic loci were involved. This genetically selected SHR strain spontaneously and consistently develops moderate-to-severe hypertension between 7 and 15 weeks of age and has served as one model of genetic hypertension in humans. 34 Several studies have shown that, although the SHR is stress responsive, it is actually quite resistant to elevated dietary sodium unless coupled with high stress.5 -7 However, the genetic mechanism of hypertension in the SHR model is not yet understood, and comparative studies of various genetic hypertensive rat strains suggest several different pathogenic mechanisms.8 A few studies have used crosses of closely related strains and subsequent backcrosses that further support the idea that very few loci (from one to four) appear to be Received October 2,1989; accepted in revised form April 19,1990. involved in the development of SHR hypertension. -12Also, a few studies have examined genetic markers of hypertension using different animal models. 13-19 However, no consistent trends have emerged across rat models and specifically in the SHR as to the specific genes responsible for hypertension.One of the more studied rat models with regard to the genetics of hypertension is the Dahl salt-sensitive (DS) and salt-resistant (DR) rat. In the DS rat there is no reported evidence for sex-linked loci controlling blood pressure.20 Sex steroids do, however, exert effects as female DS rats show slower sodiuminduced rises in blood pressure than males and castration of females altered their blood pressure to respond like that of males to salt. 21 Endocrine studies have shown that the adrenals are necessary for the development of hypertension in DS rats, 22 and genetic studies have shown that the characteristic steroid patterns of DS and DR rats are controlled by a single genetic locus (HYP-1) with two codominant alleles.14 However, there are other loci involved as the HYP-1 locus accounted for a 16 mm Hg blood pressure difference between DS and DR rats and the remaining difference was due to other unidentified genetic loci (see Reference 23 for a comprehensive review on DS and DR rats).Also, in the psychosocial stress hypertension mouse model, 24 the rat model, 2 -25 and in human hypertension, there is highe...

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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.

We demonstrated that the Sry gene complex on the SHR Y chromosome is a candidate locus for hypertension that accounts for the SHR Y chromosome blood pressure effect. All rat strains examined to date share 6 Sry loci, and a seventh Sry locus (Sry3) appears to be unique to SHR males. Previously, we showed that Sry1 increased activity of the tyrosine hydroxylase promoter in transfected PC12 cells, and Sry1 delivered to adrenal gland of WKY rats increased blood pressure and sympathetic nervous system activity. The objective of this study was to determine whether renin-angiotensin system genes participate in Sry-mediated effects. Sry expression vectors were co-transfected into CHO cells with luciferase reporter constructs containing promoters of angiotensinogen (Agt −1430/ +22), renin (Ren −1050/−1), ACE (ACE −1677/+21) and ACE2 (ACE2 −1091/+83). Sry1, Sry2 and Sry3 differentially up-regulated activity of the promoters of angiotensinogen, renin and ACE genes, and down-regulated ACE2 promoter activity. The largest effect was seen with Sry3, which increased activity of angiotensinogen promoter by 1.7 fold, renin promoter by 1.3 fold, ACE promoter by 2.6 fold, and decreased activity of ACE2 promoter by 0.5 fold. The effect of Sry1 on promoter activity was significantly less than Sry3. Sry2 activated promoters at a significantly lower level than Sry1. The result of either an additive effect of Sry regulation of multiple genes in the renin-angiotensin system or alterations in expression of a single gene could favor increased levels of Ang II and decreased levels of Ang-(1-7). These actions of Sry could result in increased blood pressure in males and contribute to gender differences in blood pressure.