Structure and function of small arteries in hypertension.
Both direct in vitro evidence and histological evidence strongly suggest that in essential hypertensive patients there is an alteration in the structure of proximal resistance vessels (small arteries); the media: lumen ratio is increased and the lumen volume is decreased. Although it may be supposed that essential hypertension is related to an increased sensitivity in the resistance vasculature, there is little evidence for this view, either from haemodynamic investigations, or from in vitro experiments. What evidence there is appears to be based primarily on results from the spontaneously hypertensive rat (SHR), but even here small artery sensitivity does not seem to be related to blood pressure. However, two functional abnormalities of the small arteries may be associated with hypertension. First, in small arteries from both essential hypertensive patients and SHR, cocaine has a greater ability to increase the noradrenaline sensitivity than in normotensive subjects, possibly due to increased innervation. Second, genetic experiments with SHR show that the oscillatory activity of small arteries (rhythmic changes in tone in response to agonist activation) is correlated with blood pressure. The role of these structural and functional abnormalities in the pathogenesis of hypertension is not clear. In particular, although the structural changes could account for the increased peripheral resistance, evidence that they are a primary cause of hypertension is lacking. However, the structural changes could play an important role in the morbid consequences of hypertension. Failure to normalize vascular structure with antihypertensive treatment could be one reason why treatment does not improve the prognosis as much as expected.
Mulvany
M J
MJ
Danish Biomembrane Research Centre, Aarhus University.
D000818:Animals; D001158:Arteries / Q000473:pathology* / Q000503:physiopathology; D001794:Blood Pressure / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000473:pathology / Q000503:physiopathology*; D009638:Norepinephrine / Q000502:physiology; D051381:Rats; D011918:Rats, Inbred SHR; D014655:Vascular Resistance / Q000502:physiology*
D009638:Norepinephrine