The concept of autoregulation of total blood flow and its role in hypertension.
Arterial vascular resistance to blood flow is increased in every known form of established hypertension. The proposed mechanisms responsible for these alterations in vascular resistance include humoral factors, the nervous system and local autoregulatory events. This study focuses on the potential importance of the phenomenon of tissue autoregulation as a factor in vascular resistance. Nearly all individual organ systems can locally adjust their vascular resistance (autoregulate) to maintain appropriate blood flow, so that the sum of all the tissue resistances determines the total blood flow through the circulation (cardiac output). The extent to which these local autoregulatory mechanisms can influence hemodynamic events associated with various types of hypertension is evaulated. It is concluded that even slight fluid retention over periods of weeks and months enables autoregulatory mechanisms to sustain a 50 per cent increase in arterial pressure with only a 5 per cent observed increase in cardiac output. In some forms of hypertension, these mechanisms appear to explain the observed hemodynamic changes (i.e., low renin essential hypertension or primary aldosteronism). In other forms, there may be no reason for autoregulation to occur, so the mechanism might be of no consequence in determining the vascular resistance. The evidence indicates that regulation of cardiac output cannot explain the cause of hypertension, but local autoregulation of flow must be carefully considered if we are to understand fully the hemodynamic events associated with various forms of hypertension.
D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001783:Blood Flow Velocity; D001794:Blood Pressure / Q000187:drug effects; D001810:Blood Volume; D002302:Cardiac Output; D003900:Desoxycorticosterone / Q000494:pharmacology; D004285:Dogs; D005110:Extracellular Space / Q000502:physiology; D006706:Homeostasis; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D006978:Hypertension, Renovascular / Q000503:physiopathology; D007668:Kidney / Q000503:physiopathology; D009638:Norepinephrine / Q000494:pharmacology; D014655:Vascular Resistance; D014664:Vasodilation
D000804:Angiotensin II; D003900:Desoxycorticosterone; D009638:Norepinephrine