Kidneys and primary hypertension--initiators, stabilizers or/and victim-aggravators?

As the kidneys so importantly contribute to longterm blood pressure control, and decisively to e.g. Goldblatt hypertension, it is often assumed that they are "prime movers" also in most variants of primary hypertension. The "pros and cons" of such a view are briefly discussed, and not least because strategies in therapy and preventive measures in man greatly depend on the nature, and major sites of expression, of the polygenetic predisposition. It is emphasized how the predisposing elements usually seem to exert their main influences via decidedly extra-renal parts of cardiovascular control systems in general, though soon leading to secondary "upward resetting" of the renal barostat function concerning both salt-water excretion and the renal pressure-regulating hormones. In SHR, for example, all proximal systemic resistance vessels, including the renal preglomerular ones, show an intrinsic tendency towards structural upward resetting quite early in life. Further, already early common variants of human primary hypertension, as well as SHR, exhibit an evidently "primary" central hyper-reactivity to psychosocial stimuli. Via neuro-hormonal pressor and growth-promoting effects such in principle extra-renal influences soon induce the same type of cardiovascular and renovascular structural upward resettings. Therefore the transfer of such kidneys to normotensive organisms here induces hypertension because of the prevailing preglomerular resistance increase, which easily gives the impression that these kidneys must have been the cause of hypertension in the donor organism as well.(ABSTRACT TRUNCATED AT 250 WORDS)