Resistance vessel structure and the pathogenesis of hypertension.
To review evidence on the influence of resistance vessel structure in the pathogenesis of essential and experimental hypertension. Results of review: In essential hypertension, recent experiments have provided direct evidence that the structure of the more proximal resistance vessels (small arteries) is abnormal, with a reduction in the lumen and an increase in the ratio of medial thickness to lumen diameter (media: lumen ratio). Furthermore, the abnormal structure appears to be due more to 'remodelling' (a rearrangement of a normal amount of material around a smaller lumen), rather than to a growth process, in agreement with the original Folkow hypothesis. These abnormalities are usually closely correlated with blood pressure, but whether the abnormalities cause, or are the effect of, the increased blood pressure remains unclear. However, in animal experiments where procedures have been used to create a discrepancy between blood pressure and small artery structure (e.g., unclipping a rat made hypertensive by the Goldblatt technique), the blood pressure has not been correlated with small artery structure. This suggests that the abnormal structure of small arteries in hypertension is adaptive, rather than causal. Therefore if the resistance vessel structure as a whole is a primary factor in essential hypertension, it seems that it must be the more distal resistance vessels which are responsible. There is evidence that alterations in the structure and function of renal afferent arterioles could have a pathogenetic effect in genetic hypertension, and it is suggested that further work be directed towards testing this possibility.
Mulvany
M J
MJ
Danish Biomembrane Research Centre, Aarhus University.
D000818:Animals; D001158:Arteries / Q000473:pathology* / Q000503:physiopathology; D001160:Arterioles / Q000473:pathology / Q000503:physiopathology; D001794:Blood Pressure / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D008955:Models, Cardiovascular; D051381:Rats; D014655:Vascular Resistance