[The effect of blood pressure-lowering treatment of essential hypertension on kidney vasculature and kidney function].

The tight embrace between blood pressure control and renal function makes it extremely difficult, particularly in the case of essential hypertension, to disentangle the reciprocity of cause and effect relationships. Even ingenious models of experimental hypertension have failed to provide a firm answer as to the order of sequence between these two entities. While not excluding the possibility of a subtle renal defect as a prime mover in essential hypertension, we have preliminarily adopted the thesis that hypertension per se is the main condition, which subsequently induces functional changes in the kidney. The latter may then contribute in their turn to the persistence or even the progression of the hypertensive process. The earliest detectable change in the hypertensive kidney is an apparent vasoconstriction. Since glomerular filtration rate appears to be maintained in the face of this, efferent arteriolar tone is likely to be enhanced. Using pharmacological tools we have been able to establish that local pressor systems are responsible for the above vasoconstriction: both alpha-2 receptors and the renin-angiotensin system appear to be involved. From a preventive point of view it might make sense to use antihypertensive drugs in order to abolish the renal vasoconstriction: this way the involvement into structural arteriolar changes could perhaps be prevented. Although indeed currently used antihypertensive drugs facilitate renal blood flow, their ultimate role in salvaging the kidney remains to be established.