RENAL AND URODYNAMIC EFFECTS OF OPIOIDS
μ-Receptor activation causes antidiuresis and decreases electrolyte
excretion. κ-receptor stimulation predominantly produces diuresis with little
change in electrolyte excretion. The stable dynorphin analogue E-2078 causes κ-receptor
mediated diuretic effects in the isolated perfused rat kidney.[254]
Indirect actions may involve inhibiting or altering the secretion of ADH and atrial
natriuretic peptide.[255]
Kien and associates noted a 25% decrease in renal cortical blood
flow that paralleled changes in blood pressure suggesting impairment of autoregulation.
[256]
However, the absence of increases in plasma
ADH, renin, and aldosterone indicates that fentanyl, sufentanil, alfentanil, and
probably remifentanil most likely preserve or minimally alter renal function in humans.
If renal function does change during opioid anesthesia and surgery, it is probably
due to secondary changes in systemic and renal hemodynamics.
Lower urinary tract opioid effects include disturbances of micturition
characterized by urinary retention, especially after intrathecal opioid administration.
Not all opioid agonists behave similarly, and morphine appears to be particularly
potent with regard to producing urodynamic problems.[257]
Malinovsky and colleagues. compared the urodynamic effects of intravenously administered
morphine (10 mg), buprenorphine (0.3 mg), fentanyl (0.35 mg) and nalbuphine (20 mg).
[258]
It was shown that all of the opioids altered
bladder sensations, but that detrusor contraction decreased only after administration
of fentanyl and buprenorphine.
