1988 Volume 25 Issue 2 Pages 160-168
Hemodynamic effects of upright posture, isometric exercise and norepinephrine infusion were investigated before and after subligual administratin of calcium antagonist nifedipine 10mg in elderly hypertensives and normotensives, aged 65 to 85 years. Hypertensives (n=12) responded to upright posture (60° head-up tilt) with increase in systolic blood pressure, diastolic blood pressure, heart rate, total peripheral resistance and decrease in cardiac output. Nifedipine decreased blood pressure and total peripheral resistance and increased heart rate and cardiac output. Hemodynamic responses to upright posture were not different before or after administration of nifedipine. Plasma norepinephrine levels were significantly higher during upright posture than at supine position. Hypertensives (n=10) responded to isometric exercise (weight susteining isometric exercise) with increase in blood pressure, heart rate, cardiac output and total peripheral resistance. Although nifedipine reduced the absolute values of blood pressure, the rates of hemodynamic responses to isometric exercise were unchanged before or after administration of nifedipine. Plamsa norepinephrine levels were significantl highery during isometric exercise than at rest. Normotensives (n=7) responded intravenous norepinephrine infusion of 0.2μg/kg/min with increase in blood pressure and total peripheral resistance and decrease in heart rate and cardiac output. After administration of nifedipine, norenephrine slightly elevated blood pressure and total peripheral resistance and did not change heart rate or cardiac output. The rates of blood pressure and total peripheral resistance rises in response to norepinephrine were significantly lower after administraiton of nifedipine than before administration. Nifedipine did not suppress the increase in vascular resistance during upright posture or isometric exercise. However, the drug inhibited the increase in vascular resistance to the infused norepinephrine. The sympathetic effects are mediated predominantly via postjunctional alpha-1-adrenoceptors and postjunctional alpha-2-adrenoceptors are preferentially stimulated by circulating norepinephrine because of their extrajunctional location. The discrepancy in response to endogenous sympathetic stimulation by physical exercise and intravenously infused norepinephrine might be due to the fact that postjunctional alpha-2-rather than postjunctional alpha-1-adrenoceptor-mediated vasoconstriction is suppressed by calcium antagonist. In conclusion, calcium antagonist had no adverse hemodynamic effects during upright posture or isometric exercising in elderly patients with hypertension. Calcium antagonist may dominantly inhibit the effects of intravenously administered norepinephrine rather than those of norepinephrine released from sympathetic nerve ending.
