Sympathetic and parasympathetic components of reflex cardiostimulation during vasodilator treatment of hypertension

Abstract

1 The alleged importance of cardiac β-adrenoceptors for the baroreceptor induced rise in cardiac output after acute vasodilatation was assessed in 41 patients with essential hypertension.

2 Diazoxide (300 mg i.v.) was given, to patients 1) when untreated (n=29), 2) during treatment with propranolol (320 mg/day), (n=15), or 3) during propranolol plus atropine (0.04 mg/kg), (n=12).

3 Diazoxide-induced reductions in arterial pressure during propranolol, either alone (-23±3%) or combined with atropine (-22±3%), were not significantly different from those without pretreatment (-24±3%, mean±s.e. mean.

4 The response of heart rate to diazoxide was somewhat diminished during propranolol (+14±2 with propranolol ν+21±3% without propranolol, 15 paired observations, P < 0.001).

5 Stroke volume rose more in response to diazoxide after pretreatment with propranolol (+16±11 with propranolol ν+2±5% without propranolol, P < 0.001) so that the response of cardiac output was not altered by β-adrenoceptor blockade (+32±4 with propranolol ν+24±9% without propranolol, P > 0.05).

6 The rise in cardiac output was markedly diminished by additional parasympathetic blockade (+14±5% with propranolol plus atropine, n = 12, ν 32±4% with propranolol alone, n = 15, P < 0.01).

7 Increments in plasma noradrenaline were not significantly different in the three situations, indicating that baroreceptor sensitivity was not altered.

8 We conclude that the baroreflex induced rise in cardiac output during vasodilator treatment of hypertension depends on withdrawal of parasympathetic tone rather than sympathetic stimulation.