RESPONSES OF THE CARDIOVASCULAR SYSTEM OF THE RAT TO NORADRENALINE INFUSIONS AND THEIR MODIFICATION BY ADRENOCEPTOR BLOCKING AGENTS

1 The effects of noradrenaline upon the cardiovascular system of the rat, anaesthetized with pentobarbitone, have been investigated. 2 Noradrenaline produces a dose‐dependent increase in mean arterial blood pressure (MABP) which is due entirely to an increase in cardiac output; total peripheral vascular resistance (TPR) remains unchanged. 3 Following β‐adrenoceptor blockade the pressor response to infused noradrenaline is enhanced and is now due mainly to an increase in TPR; the increment in cardiac output is reduced. 4 After α‐adrenoceptor blockade the pressor response is greatly reduced; the residual increase in MABP is due solely to an increase in cardiac output. 5 After ganglion blockade resting cardiac output and TPR both fall, resulting in a reduction in MABP. The pressor response to noradrenaline is enhanced and is now due to increases in both TPR and in cardiac output. 6 The cardiovascular response of the anaesthetized rat to noradrenaline can be explained in terms of classical α‐ and β‐adrenoceptor stimulation by the amine; the unusual form of the response may be due to an effective predominance of β‐adrenoceptor‐mediated effects in this species. 7 It is suggested that the failure of exogenous noradrenaline to produce a rise in TPR results from a balance between the α‐adrenoceptor‐mediated increase and β‐adrenoceptor‐mediated decrease in this variable. However, this proposed balance is lost if resting vasoconstrictor tone is reduced by ganglion blockade.