Changes in cardiovascular responsiveness caused by age and high blood pressure: implications for therapy.
With older age and higher blood pressure, defective cardiovascular responses to beta-adrenergic activation allow unopposed alpha 1- and alpha 2-adrenoceptor-mediated vasoconstriction to occur. This helps to explain the transition from early hypertension resulting from an increase in cardiac output and renin secretion to a later form caused by an augmented peripheral vascular resistance. The status of the beta-adrenoceptors aids in determining the response to antihypertensive drugs. Thus, the predominance of beta-adrenergic responses to sympathetic stimulation renders the younger patient more susceptible to antihypertensive therapy with beta-adrenergic blockers or inhibitors of converting enzyme; the latter eliminates the amplifying effect of angiotension II on sympathetic neurotransmission. The blunted cardiovascular counterregulation observed in the older patients favors a response to antihypertensive drugs acting mainly by peripheral vasodilatation, including alpha-adrenergic antagonists and calcium-entry blockers.
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D000375:Aging; D000818:Animals; D002319:Cardiovascular System / Q000503:physiopathology*; D004837:Epinephrine / Q000097:blood; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000503:physiopathology*; D011942:Receptors, Adrenergic, alpha / Q000502:physiology; D011943:Receptors, Adrenergic, beta / Q000502:physiology
D011942:Receptors, Adrenergic, alpha; D011943:Receptors, Adrenergic, beta; D004837:Epinephrine