A sub-strain of male and female spontaneously hypertensive rats (SHR) capable of having massively obese or non-obese offspring were bred repeatedly or were maintained as virgin controls. When the male and female breeders had sired or given birth to 5 litters of young, they were autopsied along with their 10-month-old celibate brothers and sisters. Virgin and breeder SHR developed high blood pressure (250 +/- 10 mm Hg). Breeder rats were significantly heavier than their virgin cohorts; pituitary and adrenal glands, hearts, and kidneys were significantly enlarged while thymi were severely involuted in breeder vs virgin SHR. The hyperlipidemia, fatty liver, hyperglycemia, and islet hyperplasia, characteristic of virgin SHR, were greatly exacerbated in breeder SHR. Blood levels of corticosterone, deoxycorticosterone, and aldosterone were greatly elevated in breeder vs virgin SHR. Although breeder rats of genetically normotensive strains develop aortic sclerosis, none of the breeder SHR developed aortic sclerosis. Instead, intimal fibrinohyalin lesions appeared confined to the testes and ovaries. It is suggested that the anatomical appearance or resistance of the arterial wall to the development of lesions is genetically mediated but this genetic programming may be modified by metabolic and hormonal factors with particular emphasis on the participation of adrenocorticoids.