Vascular smooth muscle in hypertension.
The cause of the elevated arterial pressure in most forms of hypertension is an increase in total peripheral resistance. This brief review is directed toward an assessment of recent investigations contributing information about the factors responsible for this increased vascular resistance. Structural abnormalities in the vasculature that characterize the hypertensive process are 1) changes in the vascular media, 2) rarefication of the resistance vessels, and 3) lesions of the intimal vascular surface. These abnormalities are mainly the result of an adaptive process and are secondary to the increase in wall stress and/or to pathological damage to cellular components in the vessel wall. Functional alterations in the vascular smooth muscle are described as changes in agonist-smooth muscle interaction or plasma membrane permeability. These types of changes appear to play a primary, initiating role in the elevation of vascular resistance of hypertension. These alterations are not the result of an increase in wall stress and they often precede the development of high blood pressure. The functional changes are initiated by abnormal function of neurogenic, humoral, and/or myogenic changes that alter vascular smooth muscle activity.
D000804:Angiotensin II / Q000502:physiology; D000818:Animals; D002118:Calcium / Q000502:physiology; D002412:Cations / Q000502:physiology; D002415:Cats; D002463:Cell Membrane Permeability; D006973:Hypertension / Q000209:etiology*; D006984:Hypertrophy / Q000473:pathology; D066298:In Vitro Techniques; D007473:Ion Channels / Q000502:physiology; D009131:Muscle, Smooth, Vascular / Q000503:physiopathology*; D009638:Norepinephrine / Q000502:physiology; D051381:Rats; D011919:Rats, Inbred Strains; D013552:Swine; D014655:Vascular Resistance; D014661:Vasoconstriction; D014662:Vasoconstrictor Agents / Q000494:pharmacology
D002412:Cations; D007473:Ion Channels; D014662:Vasoconstrictor Agents; D000804:Angiotensin II; D002118:Calcium; D009638:Norepinephrine