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.