1. The New Zealand strain of rats with genetic hypertension (GH rats), the Japanese strain with spontaneous hypertension and the salt-sensitive strain of Dahl are now well established as three genetically pure lines for use in hypertensive research. Other pure lines not consciously selected for high blood pressure have also recently been shown to exhibit hypertension.
2. In the GH rats the inheritance of the blood pressure appears to be polygenic; thus a simple causation of the hypertension appears unlikely. The inheritance is also complex in the other pure lines of hypertensive rats.
3. In the GH rats variation in intake of sodium from 0.05% to 1% of the solid diet does not affect the development of the hypertension.
4. The renin-angiotensin-aldosterone system does not appear to play a primary role in the initiation of the hypertension in the GH rats. Compared with normotensive rats of the parent colony, plasma and renal renin are decreased, total exchangeable and carcass sodium are decreased, as are also the plasma volume and total extracellular fluid volume. Plasma sodium is normal and plasma potassium increased.
5. There is no evidence of a primary abnormality of catecholamine storage or turnover. Prevention of the development of the sympathetic nervous system from birth does not entirely abolish the difference in blood pressure between GH rats and comparably treated normotensive rats.
6. The increased peripheral resistance in blood-perfused hind limbs and tails of GH rats is due both to increased neurogenic and myogenic components and to a structural element. Increased vascular reactivity to a variety of constrictor agents is readily demonstrated in saline-perfused preparations.
7. The different strains of hypertensive rats may in their diversity mirror the differences between the various forms of human essential hypertension.