Nifedipine, a calcium ion influx inhibitor (Ca-channel blocker), selectively inhibits calcium ion influx across the cell membrane of cardiac muscle and vascular smooth muscle while maintaining serum calcium concentrations. In humans, Nifedipine decreases peripheral vascular resistance and creates a modest fall in systolic and diastolic pressure (5-10mm Hg systolic although sometimes larger). Nifedipine is generally given using the “bite and swallow” method, in a dose of 10 mg.
Five studies (n=59) (Steinberger et al. 1990; Lindan et al. 1985; Thyberg et al. 1994; Kabalin et al. 1993; Dykstra et al. 1987) have evaluated the effects of Nifedipine; two level 2 controlled but not randomized trials (Steinberger et al. 1990; Lindan et al. 1985), and three level 4 studies (Thyberg et al. 1994; Kabalin et al. 1993; Dykstra et al. 1987). Four of these five studies saw a reduction or alleviation of AD with nifedipine (Steinberger et al. 1990; Thyberg et al. 1994; Kabalin et al. 1993; Dykstra et al. 1987). In their non-randomized control trial, Steinberger and co-investigators (1990) reported that sublingual nifedipine decreased peak systolic, diastolic, and mean blood pressure in SCI individuals undergoing electroejaculation. Braddom and Rocco (1991) surveyed 86 physicians with an average of 16.8 years of experience in managing AD in patients with SCI. While pharmacologic treatment of AD varied greatly from physician to physician, antihypertensive medications were the most frequently used medications with Nifedipine being a drug of choice for 48% of physicians for minor AD cases and for 58% of physicians for severe symptomatic AD cases. Although nifedipine has been the most commonly used agent for management of AD in individuals with SCI (Thyberg et al. 1994; Dykstra et al. 1987; Esmail et al. 2002; Braddom & Rocco 1991), its use has declined recently (Frost 2002; Anton & Townson 2004). There have been no reported adverse events from the use of nifedipine in the treatment of AD (Blackmer 2003), although all studies had a very small sample size. However, a review of nifedipine for the management of hypertensive emergencies not specific to SCI found serious adverse effects such as stroke, acute myocardial infarction, death and numerous instances of severe hypotension (Grossman et al. 1996). Due to several reports of serious adverse reactions occurring after administration of immediate-release nifedipine, the Joint National Committee on Detection, Evaluation and Treatment of High Blood Pressure (1997) has discouraged use of this drug.
There is level 2 evidence (from 2 prospective controlled trials: Steinberger et al. 1990; Lindan et al. 1985) that Nifedipine may be useful to prevent dangerous blood pressure reactions, e.g. during cystoscopy and other diagnostic or therapeutic procedures in SCI injured patients with AD.
There is level 5 evidence (from clinical consensus: Joint National Committee on Detection, Evaluation and Treatment of High Blood Pressure 1997), that serious adverse effects from Nifedipine may occur and these have been reported in other populations.