The structural cardiovascular factor in primary hypertension--pressure dependence and genetic reinforcement.

Experimental results suggesting a genetic facilitation of cardiovascular structural adaptation in primary hypertension are surveyed. Most such studies have been performed on spontaneously hypertensive rats (SHR), a few on New Zealand genetically hypertensive (GH) and Dahl salt-sensitive (Dahl-S) rats, and primary human hypertension has also been explored. The evidence comes partly from various haemodynamic-morphometric analyses of the relationships between cardiovascular design and pressure level in vivo and partly from in vitro studies of SHR vascular smooth muscle in tissue culture. When combined, the experimental findings from the various approaches strongly suggest that genetic elements can so reinforce the normal process of structural cardiovascular adaptation in primary hypertension, that this factor becomes a primary element of great haemodynamic importance, particularly in SHR, probably in GH rats and perhaps in man, but hardly in Dahl-S rats. The overall support for this type of genetic reinforcement appears, in fact, to be stronger than for any other type of mechanism presently considered to be genetically linked to the induction of primary hypertension. This genetic structural endowment seems to be partly intrinsic in the muscle cells and partly the result of extrinsic 'trophic' effects, e.g. from catecholamines, consequent to a genetically based central accentuation of sympathetic activity, present in SHR and evidently often in man.